TY  - CONF
AU  - Petrović, Anja
AU  - Bogojević, Desanka
AU  - Ivanović-Matić, Svetlana
AU  - Martinović, Vesna
AU  - Korać, Aleksandra
AU  - Jovanović-Stojanov, Sofija
AU  - Grigorov, Ilijana
PY  - 2018
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5660
AB  - Oxidative stress. cell damage and cell death underlies the etiology of liver damage/dysfunction  in  diabetes.  Bigh  Mobility  Group  Box 1 (HMGB1) is a nuclear protein that is  released  from damaged/stressed  liver cells during, diabetes and  contributes to oxidative  stresse-mediated autophagy  an cell death/survival. Since ethyl pyruvate (EP) an HMGB1 relase/expession and autophagy in the liver of diabetic rats. Diabetes was indused by streptozotocin(65mg/kg). Pretreated group of diabetes rats- (EP+D) startedl treatment  with EP (80mg/kg/daily) three·days before
diabetes induction,  while  in  the  second  group  (D+EP}  treatment  start   ten  days after diabetes induuction. In compcarison with D+EP group, EP+D group had better glycemic  status  and  higher  activity  of  antioxidative enzyme  SOD  and CAT in diabetic  liver.  According  to  western  immunoblot   analyses,  EP+D  group   sliowed higher     expression     of     extracellular    HMGB l     in    comparison      with D+EP. Consequently  detected increase in HMGB1/RAGE interactions in EP+D group were followed  by higher expression of LC3-II, HMGB1/Beclin 1 interaction and activation  of  autophagy.  Expression  of  LC3-II  and   HMGB1/Beclin 1 interaction were  at  the  control  level  in  D+EP.  Preserved  liver   morphology  in  both  EP   treated groups, observed  by  electron  microscopy,   implicated  existence   of   adaptive mechanisms  in EP+D  group.  Further  analyses  showed that  protective autophagy (mitophagy) was enhanced in EP+D group compared with diabetic and D+EP groups. Thus treatment of  diabetic  patients  with  EP  may  constitute  a  new strategy for the treatment  of  diabetes related  tissue  injury.
PB  - Belgrade: Serbian Physiological Society
C3  - Abstract book: 4th Congress of Physiological Sciences of Serbia with International Participation: Current Trends in Physiological Sciences: from cell signals to the biology of aging; 2018 Sep 19-23; Niš, Serbia
T1  - Pretreatment of diabetic rats with ethyl piruvate upregulates HMGB-driven protective autophagy in the liver
SP  - 108
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5660
ER  - 

@conference{
author = "Petrović, Anja and Bogojević, Desanka and Ivanović-Matić, Svetlana and Martinović, Vesna and Korać, Aleksandra and Jovanović-Stojanov, Sofija and Grigorov, Ilijana",
year = "2018",
abstract = "Oxidative stress. cell damage and cell death underlies the etiology of liver damage/dysfunction  in  diabetes.  Bigh  Mobility  Group  Box 1 (HMGB1) is a nuclear protein that is  released  from damaged/stressed  liver cells during, diabetes and  contributes to oxidative  stresse-mediated autophagy  an cell death/survival. Since ethyl pyruvate (EP) an HMGB1 relase/expession and autophagy in the liver of diabetic rats. Diabetes was indused by streptozotocin(65mg/kg). Pretreated group of diabetes rats- (EP+D) startedl treatment  with EP (80mg/kg/daily) three·days before
diabetes induction,  while  in  the  second  group  (D+EP}  treatment  start   ten  days after diabetes induuction. In compcarison with D+EP group, EP+D group had better glycemic  status  and  higher  activity  of  antioxidative enzyme  SOD  and CAT in diabetic  liver.  According  to  western  immunoblot   analyses,  EP+D  group   sliowed higher     expression     of     extracellular    HMGB l     in    comparison      with D+EP. Consequently  detected increase in HMGB1/RAGE interactions in EP+D group were followed  by higher expression of LC3-II, HMGB1/Beclin 1 interaction and activation  of  autophagy.  Expression  of  LC3-II  and   HMGB1/Beclin 1 interaction were  at  the  control  level  in  D+EP.  Preserved  liver   morphology  in  both  EP   treated groups, observed  by  electron  microscopy,   implicated  existence   of   adaptive mechanisms  in EP+D  group.  Further  analyses  showed that  protective autophagy (mitophagy) was enhanced in EP+D group compared with diabetic and D+EP groups. Thus treatment of  diabetic  patients  with  EP  may  constitute  a  new strategy for the treatment  of  diabetes related  tissue  injury.",
publisher = "Belgrade: Serbian Physiological Society",
journal = "Abstract book: 4th Congress of Physiological Sciences of Serbia with International Participation: Current Trends in Physiological Sciences: from cell signals to the biology of aging; 2018 Sep 19-23; Niš, Serbia",
title = "Pretreatment of diabetic rats with ethyl piruvate upregulates HMGB-driven protective autophagy in the liver",
pages = "108",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5660"
}

Petrović, A., Bogojević, D., Ivanović-Matić, S., Martinović, V., Korać, A., Jovanović-Stojanov, S.,& Grigorov, I.. (2018). Pretreatment of diabetic rats with ethyl piruvate upregulates HMGB-driven protective autophagy in the liver. in Abstract book: 4th Congress of Physiological Sciences of Serbia with International Participation: Current Trends in Physiological Sciences: from cell signals to the biology of aging; 2018 Sep 19-23; Niš, Serbia
Belgrade: Serbian Physiological Society., 108.
https://hdl.handle.net/21.15107/rcub_ibiss_5660

Petrović A, Bogojević D, Ivanović-Matić S, Martinović V, Korać A, Jovanović-Stojanov S, Grigorov I. Pretreatment of diabetic rats with ethyl piruvate upregulates HMGB-driven protective autophagy in the liver. in Abstract book: 4th Congress of Physiological Sciences of Serbia with International Participation: Current Trends in Physiological Sciences: from cell signals to the biology of aging; 2018 Sep 19-23; Niš, Serbia. 2018;:108.
https://hdl.handle.net/21.15107/rcub_ibiss_5660 .

Petrović, Anja, Bogojević, Desanka, Ivanović-Matić, Svetlana, Martinović, Vesna, Korać, Aleksandra, Jovanović-Stojanov, Sofija, Grigorov, Ilijana, "Pretreatment of diabetic rats with ethyl piruvate upregulates HMGB-driven protective autophagy in the liver" in Abstract book: 4th Congress of Physiological Sciences of Serbia with International Participation: Current Trends in Physiological Sciences: from cell signals to the biology of aging; 2018 Sep 19-23; Niš, Serbia (2018):108,
https://hdl.handle.net/21.15107/rcub_ibiss_5660 .

TY  - CONF
AU  - Petrović, Anja
AU  - Bogojević, Desanka
AU  - Ivanović Matić, Svetlana
AU  - Martinović, Vesna
AU  - Korać, Aleksandra
AU  - Jovanović Stojanov, Sofija
AU  - Poznanović, Goran
AU  - Grigorov, Ilijana
PY  - 2018
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5237
AB  - Oxidative stress through changes in antioxidative enzyme activities, glutathione metabolism and lipid peroxidation, leads to cell damage and even cell death. These changes are integrated in the pathogenetic mechanisms of the long-term, specific complications of diabetes, such as neuropathy, retinopathy, cardiomyopathy, nephropathy and hepatopathy. Recent studies have shed light on new redox sensitive endogenous targets which are important regulators of oxidative stress-induced damage. HMGB1 is a nuclear chaperone with an inflammatory function when released in the extracellular space. Extracellular HMGB1, through interaction with TLR4 receptors in its oxidized state, and with RAGE in its reduced state, controls the equilibrium between apoptosis and autophagy. HMGB1 is  a redox sensitive protein with a potentially harmful role. We therefore analyzed the changes in HMGB1 regulated signaling pathways by immunoprecipitation and Western blot that can lead to cell death or cell survival in the liver of streptozotocin (STZ)-induced diabetic rats during decreased oxidative stress after melatonin administration, and when HMGB1 release was inhibited by ethyl pyruvate. Inhibition of HMGB1 release decreased both apoptosis and autophagy, and supported the unchanged state in liver cells in STZ-treated rats as compared to the control animals. The decrease in oxidative stress achieved with melatonin decreased HMGB1 driven apoptosis but upregulated HMGB1 regulated protective autophagy, mitophagy in particular as the second level of antioxidative defense which was detected by electron microscopy. It provided a selective advantage, minimizing oxidant insults when primary antioxidant activities are compromised during oxidative stress. This adaptation led to improved cell survival in the liver of STZ-treated rats. These results showed that modulation of the role of HMGB1 in the extracellular space that was achieved by a decrease in oxidative stress is more desirable than complete inhibition of its release because HMGB1 has a protective role against oxidative injuries in diabetic liver.
PB  - Belgrade: Serbian Society for Mitochondrial and Free Radical Physiology
C3  - Book of Abstracts: Fourth Congress Challenges in Redox Biology: SSMFRP-2018; 2018 Sep 28-30; Belgrade, Serbia
T1  - The level of oxidative stress determines the role of extracellular HMGB1 protein in diabetic liver
SP  - 43
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5237
ER  - 

@conference{
author = "Petrović, Anja and Bogojević, Desanka and Ivanović Matić, Svetlana and Martinović, Vesna and Korać, Aleksandra and Jovanović Stojanov, Sofija and Poznanović, Goran and Grigorov, Ilijana",
year = "2018",
abstract = "Oxidative stress through changes in antioxidative enzyme activities, glutathione metabolism and lipid peroxidation, leads to cell damage and even cell death. These changes are integrated in the pathogenetic mechanisms of the long-term, specific complications of diabetes, such as neuropathy, retinopathy, cardiomyopathy, nephropathy and hepatopathy. Recent studies have shed light on new redox sensitive endogenous targets which are important regulators of oxidative stress-induced damage. HMGB1 is a nuclear chaperone with an inflammatory function when released in the extracellular space. Extracellular HMGB1, through interaction with TLR4 receptors in its oxidized state, and with RAGE in its reduced state, controls the equilibrium between apoptosis and autophagy. HMGB1 is  a redox sensitive protein with a potentially harmful role. We therefore analyzed the changes in HMGB1 regulated signaling pathways by immunoprecipitation and Western blot that can lead to cell death or cell survival in the liver of streptozotocin (STZ)-induced diabetic rats during decreased oxidative stress after melatonin administration, and when HMGB1 release was inhibited by ethyl pyruvate. Inhibition of HMGB1 release decreased both apoptosis and autophagy, and supported the unchanged state in liver cells in STZ-treated rats as compared to the control animals. The decrease in oxidative stress achieved with melatonin decreased HMGB1 driven apoptosis but upregulated HMGB1 regulated protective autophagy, mitophagy in particular as the second level of antioxidative defense which was detected by electron microscopy. It provided a selective advantage, minimizing oxidant insults when primary antioxidant activities are compromised during oxidative stress. This adaptation led to improved cell survival in the liver of STZ-treated rats. These results showed that modulation of the role of HMGB1 in the extracellular space that was achieved by a decrease in oxidative stress is more desirable than complete inhibition of its release because HMGB1 has a protective role against oxidative injuries in diabetic liver.",
publisher = "Belgrade: Serbian Society for Mitochondrial and Free Radical Physiology",
journal = "Book of Abstracts: Fourth Congress Challenges in Redox Biology: SSMFRP-2018; 2018 Sep 28-30; Belgrade, Serbia",
title = "The level of oxidative stress determines the role of extracellular HMGB1 protein in diabetic liver",
pages = "43",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5237"
}

Petrović, A., Bogojević, D., Ivanović Matić, S., Martinović, V., Korać, A., Jovanović Stojanov, S., Poznanović, G.,& Grigorov, I.. (2018). The level of oxidative stress determines the role of extracellular HMGB1 protein in diabetic liver. in Book of Abstracts: Fourth Congress Challenges in Redox Biology: SSMFRP-2018; 2018 Sep 28-30; Belgrade, Serbia
Belgrade: Serbian Society for Mitochondrial and Free Radical Physiology., 43.
https://hdl.handle.net/21.15107/rcub_ibiss_5237

Petrović A, Bogojević D, Ivanović Matić S, Martinović V, Korać A, Jovanović Stojanov S, Poznanović G, Grigorov I. The level of oxidative stress determines the role of extracellular HMGB1 protein in diabetic liver. in Book of Abstracts: Fourth Congress Challenges in Redox Biology: SSMFRP-2018; 2018 Sep 28-30; Belgrade, Serbia. 2018;:43.
https://hdl.handle.net/21.15107/rcub_ibiss_5237 .

Petrović, Anja, Bogojević, Desanka, Ivanović Matić, Svetlana, Martinović, Vesna, Korać, Aleksandra, Jovanović Stojanov, Sofija, Poznanović, Goran, Grigorov, Ilijana, "The level of oxidative stress determines the role of extracellular HMGB1 protein in diabetic liver" in Book of Abstracts: Fourth Congress Challenges in Redox Biology: SSMFRP-2018; 2018 Sep 28-30; Belgrade, Serbia (2018):43,
https://hdl.handle.net/21.15107/rcub_ibiss_5237 .

TY  - JOUR
AU  - Jovanović Stojanov, Sofija
AU  - Martinović, Vesna
AU  - Bogojević, Desanka
AU  - Poznanović, Goran
AU  - Petrović, Anja
AU  - Ivanović Matić, Svetlana
AU  - Grigorov, Ilijana
PY  - 2018
UR  - http://link.springer.com/10.1007/s13105-018-0626-0
UR  - http://www.ncbi.nlm.nih.gov/pubmed/29611132
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3068
AB  - Chronic inflammation plays an essential role in the development of diabetic complications. Understanding the molecular mechanisms that support inflammation is a prerequisite for the design of novel anti-inflammatory therapies. These would take into consideration circulating levels of cytokines and damage-associated molecular patterns (DAMPs) that include the high mobility group box 1 (HMGB1) protein which, in part, promotes the inflammatory response through TLR4 signaling. The liver, as the source of circulating cytokines and acute-phase proteins, contributes to the control of systemic inflammation. We previously found that liver injury in streptozotocin-induced diabetic rats correlated with the level of oxidative stress, increased expression of HMGB1, and with the activation of TLR4-mediated cell death pathways. In the present work, we examined the effects of ethyl pyruvate (EP), an inhibitor of HMGB1 release/expression, on the modulation of activation of the HMGB1/TLR4 inflammatory cascade in diabetic liver. We observed that increased expression of inflammatory markers, TNF-α, IL-6, and haptoglobin in diabetic liver was associated with increased HMGB1/TLR4 interaction, activation of MAPK (p38, ERK, JNK)/NF-κB p65 and JAK1/STAT3 signaling pathways, and with decreased expression of Nrf2-regulated antioxidative enzymes. The reduction in HMGB1 expression as the result of EP administration reduced the pro-inflammatory activity of HMGB1 and exerted a protective effect on diabetic liver, which was observed as improved liver histology and antioxidant and inflammatory statuses. Our results suggest that prevention of HMGB1 release and blockage of the HMGB/TLR4 axis represents a potentially effective therapeutic strategy aimed at ameliorating diabetes-induced inflammation and ensuing liver injury.
T2  - Journal of Physiology and Biochemistry
T1  - Modulation of diabetes-related liver injury by the HMGB1/TLR4 inflammatory pathway.
IS  - 2
VL  - 74
DO  - 10.1007/s13105-018-0626-0
SP  - 345
EP  - 358
ER  - 

@article{
author = "Jovanović Stojanov, Sofija and Martinović, Vesna and Bogojević, Desanka and Poznanović, Goran and Petrović, Anja and Ivanović Matić, Svetlana and Grigorov, Ilijana",
year = "2018",
abstract = "Chronic inflammation plays an essential role in the development of diabetic complications. Understanding the molecular mechanisms that support inflammation is a prerequisite for the design of novel anti-inflammatory therapies. These would take into consideration circulating levels of cytokines and damage-associated molecular patterns (DAMPs) that include the high mobility group box 1 (HMGB1) protein which, in part, promotes the inflammatory response through TLR4 signaling. The liver, as the source of circulating cytokines and acute-phase proteins, contributes to the control of systemic inflammation. We previously found that liver injury in streptozotocin-induced diabetic rats correlated with the level of oxidative stress, increased expression of HMGB1, and with the activation of TLR4-mediated cell death pathways. In the present work, we examined the effects of ethyl pyruvate (EP), an inhibitor of HMGB1 release/expression, on the modulation of activation of the HMGB1/TLR4 inflammatory cascade in diabetic liver. We observed that increased expression of inflammatory markers, TNF-α, IL-6, and haptoglobin in diabetic liver was associated with increased HMGB1/TLR4 interaction, activation of MAPK (p38, ERK, JNK)/NF-κB p65 and JAK1/STAT3 signaling pathways, and with decreased expression of Nrf2-regulated antioxidative enzymes. The reduction in HMGB1 expression as the result of EP administration reduced the pro-inflammatory activity of HMGB1 and exerted a protective effect on diabetic liver, which was observed as improved liver histology and antioxidant and inflammatory statuses. Our results suggest that prevention of HMGB1 release and blockage of the HMGB/TLR4 axis represents a potentially effective therapeutic strategy aimed at ameliorating diabetes-induced inflammation and ensuing liver injury.",
journal = "Journal of Physiology and Biochemistry",
title = "Modulation of diabetes-related liver injury by the HMGB1/TLR4 inflammatory pathway.",
number = "2",
volume = "74",
doi = "10.1007/s13105-018-0626-0",
pages = "345-358"
}

Jovanović Stojanov, S., Martinović, V., Bogojević, D., Poznanović, G., Petrović, A., Ivanović Matić, S.,& Grigorov, I.. (2018). Modulation of diabetes-related liver injury by the HMGB1/TLR4 inflammatory pathway.. in Journal of Physiology and Biochemistry, 74(2), 345-358.
https://doi.org/10.1007/s13105-018-0626-0

Jovanović Stojanov S, Martinović V, Bogojević D, Poznanović G, Petrović A, Ivanović Matić S, Grigorov I. Modulation of diabetes-related liver injury by the HMGB1/TLR4 inflammatory pathway.. in Journal of Physiology and Biochemistry. 2018;74(2):345-358.
doi:10.1007/s13105-018-0626-0 .

Jovanović Stojanov, Sofija, Martinović, Vesna, Bogojević, Desanka, Poznanović, Goran, Petrović, Anja, Ivanović Matić, Svetlana, Grigorov, Ilijana, "Modulation of diabetes-related liver injury by the HMGB1/TLR4 inflammatory pathway." in Journal of Physiology and Biochemistry, 74, no. 2 (2018):345-358,
https://doi.org/10.1007/s13105-018-0626-0 . .

TY  - CONF
AU  - Jovanović Stojanov, Sofija
AU  - Grigorov, Ilijana
AU  - Petrović, Anja
AU  - Bogojević, Desanka
AU  - Ivanović Matić, Svetlana
AU  - Martinović, Vesna
PY  - 2017
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5246
AB  - Introduction: Oxidative stress and chronic low-grade inflammation in diabetes leads to liver injury. During diabetes, extracellular level of high-mobility group box-1 (HMGB1) protein increases. Considering that extracellular HMGB1 (eHMGB1) protein functions as an pro-inflammatory mediator, triggering inflammatory responses by promoting the expression of inflammatory cytokines, the aim of this study was to investigate its contribution to the maintenance of inflammatory condition in the liver of diabetic rats. This may help to better understand diabetes-induced liver pathologies and potentially provide target to develop efficient therapies. Methods: Diabetes was induced by a single intraperitoneal (ip) injection of STZ (65 mg/kg). Inflammatory status in the rat liver was determined in the fourth week after diabetes induction by measuring expression of pro-inflammatory cytokines (TNFα, IL- 6) and related production of anti-inflammatory protein haptoglobin (Hp). We also studied the effects of HMGB1 on inflammation through its interaction with TLR4 and related downstream signaling pathways in terms of inhibited HMGB1 secretion in diabetic rats by ethyl pyruvate (EP) treatment (80 mg/kg/ip/daily). Results: The results show that decrease in eHMGB1 expression caused by EP treatment, correlates with reduced level of TNFα, IL-6 and Hp in the serum and liver of diabetic rats. These changes are in accordance with significant decrease in HMGB1/TLR4 interaction and decreased activation of MAPK (p38, ERK, JNK), NF-κB p65 and JAK1/STAT3 signaling pathways in diabetic liver. Conclusion: In diabetic liver eHMGB1 is involved in the inflammatory response dually. It acts pro-inflammatory by enhancing production of inflammatory mediators and anti-inflammatory by increasing Hp expression.
PB  - Belgrade: University of Belgrade, Faculty of Biology
C3  - Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.
T1  - Pro-inflamatory and anti-inflamatory role of HMGB1 in the liver of diabetic rats
SP  - 44
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5246
ER  - 

@conference{
author = "Jovanović Stojanov, Sofija and Grigorov, Ilijana and Petrović, Anja and Bogojević, Desanka and Ivanović Matić, Svetlana and Martinović, Vesna",
year = "2017",
abstract = "Introduction: Oxidative stress and chronic low-grade inflammation in diabetes leads to liver injury. During diabetes, extracellular level of high-mobility group box-1 (HMGB1) protein increases. Considering that extracellular HMGB1 (eHMGB1) protein functions as an pro-inflammatory mediator, triggering inflammatory responses by promoting the expression of inflammatory cytokines, the aim of this study was to investigate its contribution to the maintenance of inflammatory condition in the liver of diabetic rats. This may help to better understand diabetes-induced liver pathologies and potentially provide target to develop efficient therapies. Methods: Diabetes was induced by a single intraperitoneal (ip) injection of STZ (65 mg/kg). Inflammatory status in the rat liver was determined in the fourth week after diabetes induction by measuring expression of pro-inflammatory cytokines (TNFα, IL- 6) and related production of anti-inflammatory protein haptoglobin (Hp). We also studied the effects of HMGB1 on inflammation through its interaction with TLR4 and related downstream signaling pathways in terms of inhibited HMGB1 secretion in diabetic rats by ethyl pyruvate (EP) treatment (80 mg/kg/ip/daily). Results: The results show that decrease in eHMGB1 expression caused by EP treatment, correlates with reduced level of TNFα, IL-6 and Hp in the serum and liver of diabetic rats. These changes are in accordance with significant decrease in HMGB1/TLR4 interaction and decreased activation of MAPK (p38, ERK, JNK), NF-κB p65 and JAK1/STAT3 signaling pathways in diabetic liver. Conclusion: In diabetic liver eHMGB1 is involved in the inflammatory response dually. It acts pro-inflammatory by enhancing production of inflammatory mediators and anti-inflammatory by increasing Hp expression.",
publisher = "Belgrade: University of Belgrade, Faculty of Biology",
journal = "Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.",
title = "Pro-inflamatory and anti-inflamatory role of HMGB1 in the liver of diabetic rats",
pages = "44",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5246"
}

Jovanović Stojanov, S., Grigorov, I., Petrović, A., Bogojević, D., Ivanović Matić, S.,& Martinović, V.. (2017). Pro-inflamatory and anti-inflamatory role of HMGB1 in the liver of diabetic rats. in Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.
Belgrade: University of Belgrade, Faculty of Biology., 44.
https://hdl.handle.net/21.15107/rcub_ibiss_5246

Jovanović Stojanov S, Grigorov I, Petrović A, Bogojević D, Ivanović Matić S, Martinović V. Pro-inflamatory and anti-inflamatory role of HMGB1 in the liver of diabetic rats. in Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.. 2017;:44.
https://hdl.handle.net/21.15107/rcub_ibiss_5246 .

Jovanović Stojanov, Sofija, Grigorov, Ilijana, Petrović, Anja, Bogojević, Desanka, Ivanović Matić, Svetlana, Martinović, Vesna, "Pro-inflamatory and anti-inflamatory role of HMGB1 in the liver of diabetic rats" in Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia. (2017):44,
https://hdl.handle.net/21.15107/rcub_ibiss_5246 .

TY  - CONF
AU  - Petrović, Anja
AU  - Ivanović Matić, Svetlana
AU  - Bogojević, Desanka
AU  - Martinović, Vesna
AU  - Korać, Aleksandra
AU  - Jovanović Stojanov, Sofija
AU  - Stevanović, Jelena
AU  - Grigorov, Ilijana
PY  - 2017
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5244
AB  - Introduction: Hepatocellular death is the main trigger of liver disease. Since diabetic patients are very prone to liver diseases there is a urgent need to identify key regulators of cell death processes. High-mobility group box protein 1 (HMGB1) is a non-histone nuclear protein with a role in apoptotic and autophagic activation when it is present in cytosol and extracellular space. The aim of this study was to elucidate HMGB1 contribution to liver injury trough activation of apoptosis and autophagy in streptozotocin (STZ)-induced diabetic rats since the role of HMGB1 in hepatic cell death during diabetes is partially known. Methods: Diabetes was induced with a single intraperitoneal (i.p.) injection of STZ (65 mg/kg). Inhibition of HMGB1 release was achieved by ethyl pyruvate (80 mg/kg/i.p./daily). We followed changes in expression of serum and cytosolic HMGB1 and its interaction with TLR4 and RAGE and how these changes affect on apoptotic and autophagic activity and liver morphology. Results: In the serum of diabetic rats elevated levels of HMGB1 were accompanied by increased HMGB1 interactions with TLR4 and RAGE receptors. Enhancement in these interactions led to increased activity of both apoptotic and autophagic signaling pathways resulting in altered liver morphology and acummulation of autophagosomes in hepatocytes. Inhibition of HMGB1 release caused reduction in apoptotic and autophagic activity which resulted in preservation of normal liver architecture and decreased number of autophagosomes. Conclusion: HMGB1 causes liver damage through activation of apoptosis and autophagy, therefore it’s a suitable new target for prevention of liver diseases in diabetic patients.
PB  - Belgrade: University of Belgrade, Faculty of Biology
C3  - Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.
T1  - Inhibition of HMGB1 release decreases both apoptopic and autophagic activity in the hepatocytes and reduce liver injury in streptozotocin treated rats
SP  - 65
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5244
ER  - 

@conference{
author = "Petrović, Anja and Ivanović Matić, Svetlana and Bogojević, Desanka and Martinović, Vesna and Korać, Aleksandra and Jovanović Stojanov, Sofija and Stevanović, Jelena and Grigorov, Ilijana",
year = "2017",
abstract = "Introduction: Hepatocellular death is the main trigger of liver disease. Since diabetic patients are very prone to liver diseases there is a urgent need to identify key regulators of cell death processes. High-mobility group box protein 1 (HMGB1) is a non-histone nuclear protein with a role in apoptotic and autophagic activation when it is present in cytosol and extracellular space. The aim of this study was to elucidate HMGB1 contribution to liver injury trough activation of apoptosis and autophagy in streptozotocin (STZ)-induced diabetic rats since the role of HMGB1 in hepatic cell death during diabetes is partially known. Methods: Diabetes was induced with a single intraperitoneal (i.p.) injection of STZ (65 mg/kg). Inhibition of HMGB1 release was achieved by ethyl pyruvate (80 mg/kg/i.p./daily). We followed changes in expression of serum and cytosolic HMGB1 and its interaction with TLR4 and RAGE and how these changes affect on apoptotic and autophagic activity and liver morphology. Results: In the serum of diabetic rats elevated levels of HMGB1 were accompanied by increased HMGB1 interactions with TLR4 and RAGE receptors. Enhancement in these interactions led to increased activity of both apoptotic and autophagic signaling pathways resulting in altered liver morphology and acummulation of autophagosomes in hepatocytes. Inhibition of HMGB1 release caused reduction in apoptotic and autophagic activity which resulted in preservation of normal liver architecture and decreased number of autophagosomes. Conclusion: HMGB1 causes liver damage through activation of apoptosis and autophagy, therefore it’s a suitable new target for prevention of liver diseases in diabetic patients.",
publisher = "Belgrade: University of Belgrade, Faculty of Biology",
journal = "Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.",
title = "Inhibition of HMGB1 release decreases both apoptopic and autophagic activity in the hepatocytes and reduce liver injury in streptozotocin treated rats",
pages = "65",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5244"
}

Petrović, A., Ivanović Matić, S., Bogojević, D., Martinović, V., Korać, A., Jovanović Stojanov, S., Stevanović, J.,& Grigorov, I.. (2017). Inhibition of HMGB1 release decreases both apoptopic and autophagic activity in the hepatocytes and reduce liver injury in streptozotocin treated rats. in Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.
Belgrade: University of Belgrade, Faculty of Biology., 65.
https://hdl.handle.net/21.15107/rcub_ibiss_5244

Petrović A, Ivanović Matić S, Bogojević D, Martinović V, Korać A, Jovanović Stojanov S, Stevanović J, Grigorov I. Inhibition of HMGB1 release decreases both apoptopic and autophagic activity in the hepatocytes and reduce liver injury in streptozotocin treated rats. in Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.. 2017;:65.
https://hdl.handle.net/21.15107/rcub_ibiss_5244 .

Petrović, Anja, Ivanović Matić, Svetlana, Bogojević, Desanka, Martinović, Vesna, Korać, Aleksandra, Jovanović Stojanov, Sofija, Stevanović, Jelena, Grigorov, Ilijana, "Inhibition of HMGB1 release decreases both apoptopic and autophagic activity in the hepatocytes and reduce liver injury in streptozotocin treated rats" in Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia. (2017):65,
https://hdl.handle.net/21.15107/rcub_ibiss_5244 .

TY  - CONF
AU  - Martinović, Vesna
AU  - Jovanović Stojanov, Sofija
AU  - Bogojević, Desanka
AU  - Ivanović Matić, Svetlana
AU  - Petrović, Anja
AU  - Poznanović, Goran
AU  - Grigorov, Ilijana
PY  - 2017
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5245
AB  - Introduction: Oxidative stress and inflammation are involved in the pathogenesis of diabetes. Previously, we showed that melatonin exerts potent anti-oxidative and anti-inflammatory actions in the liver of streptozotocin (STZ)-induced diabetic rats, thus correcting diabetes-associated abnormalities. The concept of a liver-spleen axis has been proposed as an intersection linking immunity and metabolism in various conditions, including chronic liver diseases. We therefore compared the effect of melatonin on oxidative stress and the inflammatory response in the liver and spleen of STZ-induced diabetic rats. Methods: Male Wistar rats were injected with 65 mg/kg STZ to induce diabetes. Melatonin was administrated daily (0.2 mg/kg/i.p) until the end of the study at 4 weeks after diabetes induction. Oxidative stress was assessed by measuring the level of lipid peroxidation and the changes in antioxidative enzyme activities. Inflammation was evaluated by examining the levels of proinflammatory cytokines, inflammatory mediators and the acute-phase protein haptoglobin (Hp). Results: In both tissues, melatonin lowered oxidative stress, which was observed as a decrease in lipid peroxidation and increased expression and activity of CAT, MnSOD and CuZnSOD. By suppressing the activation of NF-κB p65 and MAPK (p38, JNK, ERK) signaling cascades and by decreasing the production of TNF-α, IL-6, HMGB1 and Hp, melatonin also reduced inflammation. Conclusion: Melatonin stimulated the antioxidative defense in both, the spleen and liver of diabetic rats and attenuated inflammation via the same molecular mechanisms.
PB  - Belgrade: University of Belgrade, Faculty of Biology
C3  - Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.
T1  - Effect of melatonin on oxdative and inflammatory stress in spleen and liver of streptozotocin -induced diabetic rats
SP  - 55
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5245
ER  - 

@conference{
author = "Martinović, Vesna and Jovanović Stojanov, Sofija and Bogojević, Desanka and Ivanović Matić, Svetlana and Petrović, Anja and Poznanović, Goran and Grigorov, Ilijana",
year = "2017",
abstract = "Introduction: Oxidative stress and inflammation are involved in the pathogenesis of diabetes. Previously, we showed that melatonin exerts potent anti-oxidative and anti-inflammatory actions in the liver of streptozotocin (STZ)-induced diabetic rats, thus correcting diabetes-associated abnormalities. The concept of a liver-spleen axis has been proposed as an intersection linking immunity and metabolism in various conditions, including chronic liver diseases. We therefore compared the effect of melatonin on oxidative stress and the inflammatory response in the liver and spleen of STZ-induced diabetic rats. Methods: Male Wistar rats were injected with 65 mg/kg STZ to induce diabetes. Melatonin was administrated daily (0.2 mg/kg/i.p) until the end of the study at 4 weeks after diabetes induction. Oxidative stress was assessed by measuring the level of lipid peroxidation and the changes in antioxidative enzyme activities. Inflammation was evaluated by examining the levels of proinflammatory cytokines, inflammatory mediators and the acute-phase protein haptoglobin (Hp). Results: In both tissues, melatonin lowered oxidative stress, which was observed as a decrease in lipid peroxidation and increased expression and activity of CAT, MnSOD and CuZnSOD. By suppressing the activation of NF-κB p65 and MAPK (p38, JNK, ERK) signaling cascades and by decreasing the production of TNF-α, IL-6, HMGB1 and Hp, melatonin also reduced inflammation. Conclusion: Melatonin stimulated the antioxidative defense in both, the spleen and liver of diabetic rats and attenuated inflammation via the same molecular mechanisms.",
publisher = "Belgrade: University of Belgrade, Faculty of Biology",
journal = "Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.",
title = "Effect of melatonin on oxdative and inflammatory stress in spleen and liver of streptozotocin -induced diabetic rats",
pages = "55",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5245"
}

Martinović, V., Jovanović Stojanov, S., Bogojević, D., Ivanović Matić, S., Petrović, A., Poznanović, G.,& Grigorov, I.. (2017). Effect of melatonin on oxdative and inflammatory stress in spleen and liver of streptozotocin -induced diabetic rats. in Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.
Belgrade: University of Belgrade, Faculty of Biology., 55.
https://hdl.handle.net/21.15107/rcub_ibiss_5245

Martinović V, Jovanović Stojanov S, Bogojević D, Ivanović Matić S, Petrović A, Poznanović G, Grigorov I. Effect of melatonin on oxdative and inflammatory stress in spleen and liver of streptozotocin -induced diabetic rats. in Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.. 2017;:55.
https://hdl.handle.net/21.15107/rcub_ibiss_5245 .

Martinović, Vesna, Jovanović Stojanov, Sofija, Bogojević, Desanka, Ivanović Matić, Svetlana, Petrović, Anja, Poznanović, Goran, Grigorov, Ilijana, "Effect of melatonin on oxdative and inflammatory stress in spleen and liver of streptozotocin -induced diabetic rats" in Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia. (2017):55,
https://hdl.handle.net/21.15107/rcub_ibiss_5245 .

TY  - JOUR
AU  - Petrović, Anja
AU  - Bogojević, Desanka
AU  - Korać, Aleksandra
AU  - Golić, Igor
AU  - Jovanović Stojanov, Sofija
AU  - Martinović, Vesna
AU  - Ivanović Matić, Svetlana
AU  - Stevanović, Jelena
AU  - Poznanović, Goran
AU  - Grigorov, Ilijana
PY  - 2017
UR  - http://link.springer.com/10.1007/s13105-017-0574-0
UR  - http://www.ncbi.nlm.nih.gov/pubmed/28695466
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2787
AB  - The progression of oxidative stress, resulting cell damage, and cell death underlies the etiology of liver damage/dysfunction as a complication of diabetes. High-mobility group box 1 (HMGB1) protein, a chromatin-binding nuclear protein and damage-associated molecular pattern molecule, is integral to oxidative stress and signaling pathways regulating cell death and cell survival. We previously found that in streptozotocin (STZ)-induced diabetic rats, reduction of oxidative stress after melatonin administration lowered necrotic cell death and increased expression of HMGB1 and hepatocellular damage. In the present study, we examined whether alleviation of diabetes-attendant oxidative stress and ensuing change in HMGB1 expression influence the dynamic equilibrium between apoptosis/autophagy and liver damage. We observed that elevated HMGB1 protein levels in diabetic rat liver accompanied increased interactions of HMGB1 with TLR4 and RAGE, and activation of the intrinsic apoptotic pathway and Beclin 1-dependent autophagy. The absence of p62 degradation in diabetic rat liver pointed to defective autophagy which was responsible for lower autophagosome/autophagolysosome formation and an increased apoptosis/autophagy ratio. Compared to diabetic rats, in melatonin-treated diabetic rats, the structure of liver cells was preserved, HMGB1/TLR4 interaction and downstream apoptotic signaling were significantly reduced, HMGB1/Beclin 1 colocalization and interactions were augmented and Beclin 1-mediated autophagy, mithophagy in particular, were increased. We concluded that in mild oxidative stress, HMGB1 is cytoprotective, whereas in intense oxidative stress, HMGB1 actions promote cell death and liver damage. Since reduced HMGB1 binds to RAGE but not to TLR4, redox modification of HMGB1 as a mechanism regulating the cross-talk between apoptosis and autophagy in diabetes is discussed.
T2  - Journal of Physiology and Biochemistry
T1  - Oxidative stress-dependent contribution of HMGB1 to the interplay between apoptosis and autophagy in diabetic rat liver.
DO  - 10.1007/s13105-017-0574-0
ER  - 

@article{
author = "Petrović, Anja and Bogojević, Desanka and Korać, Aleksandra and Golić, Igor and Jovanović Stojanov, Sofija and Martinović, Vesna and Ivanović Matić, Svetlana and Stevanović, Jelena and Poznanović, Goran and Grigorov, Ilijana",
year = "2017",
abstract = "The progression of oxidative stress, resulting cell damage, and cell death underlies the etiology of liver damage/dysfunction as a complication of diabetes. High-mobility group box 1 (HMGB1) protein, a chromatin-binding nuclear protein and damage-associated molecular pattern molecule, is integral to oxidative stress and signaling pathways regulating cell death and cell survival. We previously found that in streptozotocin (STZ)-induced diabetic rats, reduction of oxidative stress after melatonin administration lowered necrotic cell death and increased expression of HMGB1 and hepatocellular damage. In the present study, we examined whether alleviation of diabetes-attendant oxidative stress and ensuing change in HMGB1 expression influence the dynamic equilibrium between apoptosis/autophagy and liver damage. We observed that elevated HMGB1 protein levels in diabetic rat liver accompanied increased interactions of HMGB1 with TLR4 and RAGE, and activation of the intrinsic apoptotic pathway and Beclin 1-dependent autophagy. The absence of p62 degradation in diabetic rat liver pointed to defective autophagy which was responsible for lower autophagosome/autophagolysosome formation and an increased apoptosis/autophagy ratio. Compared to diabetic rats, in melatonin-treated diabetic rats, the structure of liver cells was preserved, HMGB1/TLR4 interaction and downstream apoptotic signaling were significantly reduced, HMGB1/Beclin 1 colocalization and interactions were augmented and Beclin 1-mediated autophagy, mithophagy in particular, were increased. We concluded that in mild oxidative stress, HMGB1 is cytoprotective, whereas in intense oxidative stress, HMGB1 actions promote cell death and liver damage. Since reduced HMGB1 binds to RAGE but not to TLR4, redox modification of HMGB1 as a mechanism regulating the cross-talk between apoptosis and autophagy in diabetes is discussed.",
journal = "Journal of Physiology and Biochemistry",
title = "Oxidative stress-dependent contribution of HMGB1 to the interplay between apoptosis and autophagy in diabetic rat liver.",
doi = "10.1007/s13105-017-0574-0"
}

Petrović, A., Bogojević, D., Korać, A., Golić, I., Jovanović Stojanov, S., Martinović, V., Ivanović Matić, S., Stevanović, J., Poznanović, G.,& Grigorov, I.. (2017). Oxidative stress-dependent contribution of HMGB1 to the interplay between apoptosis and autophagy in diabetic rat liver.. in Journal of Physiology and Biochemistry.
https://doi.org/10.1007/s13105-017-0574-0

Petrović A, Bogojević D, Korać A, Golić I, Jovanović Stojanov S, Martinović V, Ivanović Matić S, Stevanović J, Poznanović G, Grigorov I. Oxidative stress-dependent contribution of HMGB1 to the interplay between apoptosis and autophagy in diabetic rat liver.. in Journal of Physiology and Biochemistry. 2017;.
doi:10.1007/s13105-017-0574-0 .

Petrović, Anja, Bogojević, Desanka, Korać, Aleksandra, Golić, Igor, Jovanović Stojanov, Sofija, Martinović, Vesna, Ivanović Matić, Svetlana, Stevanović, Jelena, Poznanović, Goran, Grigorov, Ilijana, "Oxidative stress-dependent contribution of HMGB1 to the interplay between apoptosis and autophagy in diabetic rat liver." in Journal of Physiology and Biochemistry (2017),
https://doi.org/10.1007/s13105-017-0574-0 . .

TY  - CONF
AU  - Petrović, Anja
AU  - Bogojević, Desanka
AU  - Ivanović Matić, Svetlana
AU  - Martinović, Vesna
AU  - Jovanović Stojanov, Sofija
AU  - Stevanović, Jelena
AU  - Blagojević, Duško
AU  - Grigorov, Ilijana
PY  - 2016
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4280
AB  - Melatonin, a hormone secreted primarly by pineal gland,exhibitsantioxidative and anti-inflammatory properties. We have previously reported antinecrotic effect of melatonin in the liver of streptozotocin (STZ) treated rats. However, molecular mechanisms underlyingmelatonin hepatoprotective rolein oxidative enviroment are still partially known. In this study we investigated effects of melatonin on the role of nuclear factor-kappa B (NF-κB) p65 and nuclear erythroid 2-related factor 2 (Nrf2) in the liver of STZ treated rats.Melatonin at doses of 2 mg/kg/i.p was administrated daily, 3 days before STZ treatment (65mg/kg, i.p), and continued until the end of study at 4 weeks after STZ injection. STZ treatment causeshypoinsulinemia followed by hyperglycemia which increases the production of reactive oxidative species (ROS) leading tooxidative stress. ROS activatedNF-κB p65 in hepatocytes and increased its nuclear expresssion where it enhances expression of genes of proinflammatory cytokines leading to elevated presence of TNFα and IL-6. High TNFα has a cytotoxic activity and may potentiate liver damage.Melatonin reduced the elevated expression of NF-κB p65, TNFα and IL-6.STZ treatmentincreased expression of Nrf2 but reduced its activation which is followed by decrease in superoxide dismutase (SOD), glutathione-S-transferase (GST) and catalase (CAT) expression and activity. Melatonin significantly increases nuclear expression of Nrf2 which enhances the up-regulation of SOD, GST and CAT expression and activity.The results of this study suggest that melatonin improves oxidative–induced liver damage by attenuation of proinflammatory stimuli through decreasing of NF-κB activation cascade and strengthens antioxidative defence through activation of Nrf2 cascade.
PB  - Bratislava: Institute of Normal and Pathological Physiology, Slovak Academy of Sciences
C3  - 2nd Joint Meeting of Slovak and Serbian Physiological Societies “Physiology Without Frontiers“, Book of Abstracts
T1  - Melatonin attenuates streptozotocin induced inflammation and oxidative stress in the rat liver by modulation of NF-kB and Nrf2 signaling
SP  - 39
EP  - 39
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_4280
ER  - 

@conference{
author = "Petrović, Anja and Bogojević, Desanka and Ivanović Matić, Svetlana and Martinović, Vesna and Jovanović Stojanov, Sofija and Stevanović, Jelena and Blagojević, Duško and Grigorov, Ilijana",
year = "2016",
abstract = "Melatonin, a hormone secreted primarly by pineal gland,exhibitsantioxidative and anti-inflammatory properties. We have previously reported antinecrotic effect of melatonin in the liver of streptozotocin (STZ) treated rats. However, molecular mechanisms underlyingmelatonin hepatoprotective rolein oxidative enviroment are still partially known. In this study we investigated effects of melatonin on the role of nuclear factor-kappa B (NF-κB) p65 and nuclear erythroid 2-related factor 2 (Nrf2) in the liver of STZ treated rats.Melatonin at doses of 2 mg/kg/i.p was administrated daily, 3 days before STZ treatment (65mg/kg, i.p), and continued until the end of study at 4 weeks after STZ injection. STZ treatment causeshypoinsulinemia followed by hyperglycemia which increases the production of reactive oxidative species (ROS) leading tooxidative stress. ROS activatedNF-κB p65 in hepatocytes and increased its nuclear expresssion where it enhances expression of genes of proinflammatory cytokines leading to elevated presence of TNFα and IL-6. High TNFα has a cytotoxic activity and may potentiate liver damage.Melatonin reduced the elevated expression of NF-κB p65, TNFα and IL-6.STZ treatmentincreased expression of Nrf2 but reduced its activation which is followed by decrease in superoxide dismutase (SOD), glutathione-S-transferase (GST) and catalase (CAT) expression and activity. Melatonin significantly increases nuclear expression of Nrf2 which enhances the up-regulation of SOD, GST and CAT expression and activity.The results of this study suggest that melatonin improves oxidative–induced liver damage by attenuation of proinflammatory stimuli through decreasing of NF-κB activation cascade and strengthens antioxidative defence through activation of Nrf2 cascade.",
publisher = "Bratislava: Institute of Normal and Pathological Physiology, Slovak Academy of Sciences",
journal = "2nd Joint Meeting of Slovak and Serbian Physiological Societies “Physiology Without Frontiers“, Book of Abstracts",
title = "Melatonin attenuates streptozotocin induced inflammation and oxidative stress in the rat liver by modulation of NF-kB and Nrf2 signaling",
pages = "39-39",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_4280"
}

Petrović, A., Bogojević, D., Ivanović Matić, S., Martinović, V., Jovanović Stojanov, S., Stevanović, J., Blagojević, D.,& Grigorov, I.. (2016). Melatonin attenuates streptozotocin induced inflammation and oxidative stress in the rat liver by modulation of NF-kB and Nrf2 signaling. in 2nd Joint Meeting of Slovak and Serbian Physiological Societies “Physiology Without Frontiers“, Book of Abstracts
Bratislava: Institute of Normal and Pathological Physiology, Slovak Academy of Sciences., 39-39.
https://hdl.handle.net/21.15107/rcub_ibiss_4280

Petrović A, Bogojević D, Ivanović Matić S, Martinović V, Jovanović Stojanov S, Stevanović J, Blagojević D, Grigorov I. Melatonin attenuates streptozotocin induced inflammation and oxidative stress in the rat liver by modulation of NF-kB and Nrf2 signaling. in 2nd Joint Meeting of Slovak and Serbian Physiological Societies “Physiology Without Frontiers“, Book of Abstracts. 2016;:39-39.
https://hdl.handle.net/21.15107/rcub_ibiss_4280 .

Petrović, Anja, Bogojević, Desanka, Ivanović Matić, Svetlana, Martinović, Vesna, Jovanović Stojanov, Sofija, Stevanović, Jelena, Blagojević, Duško, Grigorov, Ilijana, "Melatonin attenuates streptozotocin induced inflammation and oxidative stress in the rat liver by modulation of NF-kB and Nrf2 signaling" in 2nd Joint Meeting of Slovak and Serbian Physiological Societies “Physiology Without Frontiers“, Book of Abstracts (2016):39-39,
https://hdl.handle.net/21.15107/rcub_ibiss_4280 .

TY  - JOUR
AU  - Martinović, Vesna
AU  - Ivanović, Žarko
AU  - Mihailović, Mirjana
AU  - Ivanović Matić, Svetlana
AU  - Poznanović, Goran
AU  - Vidaković, Melita
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2073
AB  - We examined the functions of the rat lymphocyte nuclear matrix after a single exposure to total body irradiation with doses ranging from sublethal to lethal. Irradiation induced systemic oxidative stress, detected as increased activities of serum SOD and catalase, lymphocyte DNA damage, detected by the Comet assay, and apoptosis. After irradiation with lower doses, the recruitment of DNA repair centers on the matrix was observed by Western analysis as increased levels of matrix-associated PARP-1, p53 and PCNA. Augmented partitioning of the pro-survival transcription factor NF-κB on the matrix was also detected after irradiation. Exposure to a lethal dose caused breakdown of the matrix, observed as lamin B cleavage, and of the matrix-associated DNA repair centers, detected as caspase-mediated PARP-1 proteolysis and loss of protein associations with the matrix. These findings suggest that the nuclear matrix establishes functional 2 interactions in a defensive mechanism, integrated in a decision-making process that resolves cell fate
PB  - Belgrade: Serbian Biological Society
T2  - Archives of Biological Sciences
T1  - Lymphocytes' 'Last Stand' on the Nuclear Matrix After Whole Body Exposure of Rats To Low-Let Ionizing Radiation
IS  - 1
VL  - 67
DO  - 10.2298/ABS140124002M
SP  - 69
EP  - 81
ER  - 

@article{
author = "Martinović, Vesna and Ivanović, Žarko and Mihailović, Mirjana and Ivanović Matić, Svetlana and Poznanović, Goran and Vidaković, Melita",
year = "2015",
abstract = "We examined the functions of the rat lymphocyte nuclear matrix after a single exposure to total body irradiation with doses ranging from sublethal to lethal. Irradiation induced systemic oxidative stress, detected as increased activities of serum SOD and catalase, lymphocyte DNA damage, detected by the Comet assay, and apoptosis. After irradiation with lower doses, the recruitment of DNA repair centers on the matrix was observed by Western analysis as increased levels of matrix-associated PARP-1, p53 and PCNA. Augmented partitioning of the pro-survival transcription factor NF-κB on the matrix was also detected after irradiation. Exposure to a lethal dose caused breakdown of the matrix, observed as lamin B cleavage, and of the matrix-associated DNA repair centers, detected as caspase-mediated PARP-1 proteolysis and loss of protein associations with the matrix. These findings suggest that the nuclear matrix establishes functional 2 interactions in a defensive mechanism, integrated in a decision-making process that resolves cell fate",
publisher = "Belgrade: Serbian Biological Society",
journal = "Archives of Biological Sciences",
title = "Lymphocytes' 'Last Stand' on the Nuclear Matrix After Whole Body Exposure of Rats To Low-Let Ionizing Radiation",
number = "1",
volume = "67",
doi = "10.2298/ABS140124002M",
pages = "69-81"
}

Martinović, V., Ivanović, Ž., Mihailović, M., Ivanović Matić, S., Poznanović, G.,& Vidaković, M.. (2015). Lymphocytes' 'Last Stand' on the Nuclear Matrix After Whole Body Exposure of Rats To Low-Let Ionizing Radiation. in Archives of Biological Sciences
Belgrade: Serbian Biological Society., 67(1), 69-81.
https://doi.org/10.2298/ABS140124002M

Martinović V, Ivanović Ž, Mihailović M, Ivanović Matić S, Poznanović G, Vidaković M. Lymphocytes' 'Last Stand' on the Nuclear Matrix After Whole Body Exposure of Rats To Low-Let Ionizing Radiation. in Archives of Biological Sciences. 2015;67(1):69-81.
doi:10.2298/ABS140124002M .

Martinović, Vesna, Ivanović, Žarko, Mihailović, Mirjana, Ivanović Matić, Svetlana, Poznanović, Goran, Vidaković, Melita, "Lymphocytes' 'Last Stand' on the Nuclear Matrix After Whole Body Exposure of Rats To Low-Let Ionizing Radiation" in Archives of Biological Sciences, 67, no. 1 (2015):69-81,
https://doi.org/10.2298/ABS140124002M . .

TY  - CONF
AU  - Petrović, Anja
AU  - Bogojević, Desanka
AU  - Ivanović-Matić, Svetlana
AU  - Martinović, Vesna
AU  - Korać, Aleksandra
AU  - Jovanović-Stojanov, Sofija
AU  - Stevanović, Jelena
AU  - Poznanović, Goran
AU  - Grigorov, Ilijana
PY  - 2015
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5654
AB  - Autophagy is a cellular process that involves lysosomal degradation and recycling of intracellular
organelles and proteins. By removing damaged and dysfunctional cellular components in order to
maintain energy homeostasis during cellular stress, autophagy can serve as a cytoprotective
mechanism. Also, it could lead to cell death if it‟s overactive or defective. Molecular mechanisms
responsible for the two faces of autophagy are still partially known. Therefore, for the development of
therapy based on autophagy modulation, it‟s necessary to fully define these processes. This study
investigated the role of oxidative stress on autophagic processes in the liver of diabetic rats and effects
of melatonin, as an antioxidant, on autophagy initiation/modulation. The liver, as one of the main
target organs of insulin, takes an important role in regulation of glucose homeostasis. In diabetes,
hypoinsulinemia followed by hyperglycemia increases mitochondrial proton gradient within the cells.
In this state organelles become the source of reactive oxidative species leading to macromolecule
damage which may cause necrotic, apoptotic or autophagic cell death. In the liver of diabetic rats
obtained four weeks after diabetes induction with streptozotocin (65 mg/kg, i.p.), light and electron
transmission microscopy showed significant changes in the structure of the cells and a large number of
necrotic cells. By using Western blot, immunoprecipitation and confocal microscopy analyses,
autophagy in diabetic liver was confirmed by increased expression of proteins required for
autophagosome formation, LC3B and Beclin1, and by the presence of Beclin1 interactions with its
activator HMGB1. In the state of oxidative stress HMGB1 is relocated from the nucleus to the
cytoplasm. Continuous melatonin treatment of diabetic rats (2mg/kg/daily, i.p.) leads to significant
reduction of liver damage, presumably through elevated mitochondrial autophagy. Melatonin
additionally contributes to elevated expression of LC3B and Beclin1, HMGB1-Beclin1 interactions
and autophagosome formation. Thus, it seems that melatonin protects the liver from diabetes induced
damage by favoring autophagy as a protective mechanism.
PB  - Belgrade : Serbian Society for Mitochondrial and Free-Radical Physiology
C3  - Book of Abstracts: Third Congress Redox Medicine: Reactive Species Signaling, Analytical Methods, Phytopharmacy, Molecular Mechanisms of Disease - SSMFRP-2015; 2015 Sep 25-26; Belgrade, Serbia
T1  - Effects of melatonin on autophagic processes in the liver of diabetic rats
SP  - 33
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5654
ER  - 

@conference{
author = "Petrović, Anja and Bogojević, Desanka and Ivanović-Matić, Svetlana and Martinović, Vesna and Korać, Aleksandra and Jovanović-Stojanov, Sofija and Stevanović, Jelena and Poznanović, Goran and Grigorov, Ilijana",
year = "2015",
abstract = "Autophagy is a cellular process that involves lysosomal degradation and recycling of intracellular
organelles and proteins. By removing damaged and dysfunctional cellular components in order to
maintain energy homeostasis during cellular stress, autophagy can serve as a cytoprotective
mechanism. Also, it could lead to cell death if it‟s overactive or defective. Molecular mechanisms
responsible for the two faces of autophagy are still partially known. Therefore, for the development of
therapy based on autophagy modulation, it‟s necessary to fully define these processes. This study
investigated the role of oxidative stress on autophagic processes in the liver of diabetic rats and effects
of melatonin, as an antioxidant, on autophagy initiation/modulation. The liver, as one of the main
target organs of insulin, takes an important role in regulation of glucose homeostasis. In diabetes,
hypoinsulinemia followed by hyperglycemia increases mitochondrial proton gradient within the cells.
In this state organelles become the source of reactive oxidative species leading to macromolecule
damage which may cause necrotic, apoptotic or autophagic cell death. In the liver of diabetic rats
obtained four weeks after diabetes induction with streptozotocin (65 mg/kg, i.p.), light and electron
transmission microscopy showed significant changes in the structure of the cells and a large number of
necrotic cells. By using Western blot, immunoprecipitation and confocal microscopy analyses,
autophagy in diabetic liver was confirmed by increased expression of proteins required for
autophagosome formation, LC3B and Beclin1, and by the presence of Beclin1 interactions with its
activator HMGB1. In the state of oxidative stress HMGB1 is relocated from the nucleus to the
cytoplasm. Continuous melatonin treatment of diabetic rats (2mg/kg/daily, i.p.) leads to significant
reduction of liver damage, presumably through elevated mitochondrial autophagy. Melatonin
additionally contributes to elevated expression of LC3B and Beclin1, HMGB1-Beclin1 interactions
and autophagosome formation. Thus, it seems that melatonin protects the liver from diabetes induced
damage by favoring autophagy as a protective mechanism.",
publisher = "Belgrade : Serbian Society for Mitochondrial and Free-Radical Physiology",
journal = "Book of Abstracts: Third Congress Redox Medicine: Reactive Species Signaling, Analytical Methods, Phytopharmacy, Molecular Mechanisms of Disease - SSMFRP-2015; 2015 Sep 25-26; Belgrade, Serbia",
title = "Effects of melatonin on autophagic processes in the liver of diabetic rats",
pages = "33",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5654"
}

Petrović, A., Bogojević, D., Ivanović-Matić, S., Martinović, V., Korać, A., Jovanović-Stojanov, S., Stevanović, J., Poznanović, G.,& Grigorov, I.. (2015). Effects of melatonin on autophagic processes in the liver of diabetic rats. in Book of Abstracts: Third Congress Redox Medicine: Reactive Species Signaling, Analytical Methods, Phytopharmacy, Molecular Mechanisms of Disease - SSMFRP-2015; 2015 Sep 25-26; Belgrade, Serbia
Belgrade : Serbian Society for Mitochondrial and Free-Radical Physiology., 33.
https://hdl.handle.net/21.15107/rcub_ibiss_5654

Petrović A, Bogojević D, Ivanović-Matić S, Martinović V, Korać A, Jovanović-Stojanov S, Stevanović J, Poznanović G, Grigorov I. Effects of melatonin on autophagic processes in the liver of diabetic rats. in Book of Abstracts: Third Congress Redox Medicine: Reactive Species Signaling, Analytical Methods, Phytopharmacy, Molecular Mechanisms of Disease - SSMFRP-2015; 2015 Sep 25-26; Belgrade, Serbia. 2015;:33.
https://hdl.handle.net/21.15107/rcub_ibiss_5654 .

Petrović, Anja, Bogojević, Desanka, Ivanović-Matić, Svetlana, Martinović, Vesna, Korać, Aleksandra, Jovanović-Stojanov, Sofija, Stevanović, Jelena, Poznanović, Goran, Grigorov, Ilijana, "Effects of melatonin on autophagic processes in the liver of diabetic rats" in Book of Abstracts: Third Congress Redox Medicine: Reactive Species Signaling, Analytical Methods, Phytopharmacy, Molecular Mechanisms of Disease - SSMFRP-2015; 2015 Sep 25-26; Belgrade, Serbia (2015):33,
https://hdl.handle.net/21.15107/rcub_ibiss_5654 .

TY  - CONF
AU  - Mihailović, Mirjana
AU  - Petrović, Miodrag
AU  - Grdović, Nevena
AU  - Dinić, Svetlana
AU  - Uskoković, Aleksandra
AU  - Vidaković, Melita
AU  - Grigorov, Ilijana
AU  - Bogojević, Desanka
AU  - Ivanović-Matić, Svetlana
AU  - Martinović, Vesna
AU  - Arambašić Jovanović, Jelena
AU  - Poznanović, Goran
PY  - 2014
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5653
AB  - Metallothioneins (MTs) constitute a family of low-molecular  weight, cysteine­ rich and heat stable 
proteins involved in the binding and regulation of essential metals, such as copper and zinc, and 
in the detoxification of these and other non-essential metals, such as cadmium and mercury. 
Previously we showed that the induction of MTs in Merluccius merluccius and Mui/us barbatus 
correlated with elevated concentrations of Cu and Pb, determined by chemical analysis of the 
seawater from Bar and Valdanos. In the present study we studied protein expression of MTs in the 
hepatopancreas of several seawater fish species: Red mullet (Mui/us barbatus), European hake 
(Merluccius merluccius), Tub gurnard (Trig/a lucerna) and Thinlip mullet  (Liza ramada), from the 
Monetengrin Adriatic coastline. Western blot analysis revealed the highest induction of MTs in the 
hepatopancreas in the following order: Merluccius merluccius, Trig/a lucerna, Mui/us barbatus and 
Liza ramada. Considering that MTs play a role in the metabolism of essential metals, they  are 
constitutively expressed. The presence of elevated concentrations of both essential and toxic 
metals provokes the induction of MTs. These results are in correlation with literature data showing 
that fish species differ in their detoxification capacities and amounts of accumulated  metals.  We 
 conclude that the level of induction of MTs in the hepatopancreas of the examined fish species 
correlates with the level of their reliability as bioindicator species in heavy metal 
biomonitoring.
PB  - Kotor, Montenegro : University of Montenegro, Institute of Marine Biology
C3  - Book of Abstracts: 1st International scientific conference integrated coastal zone management in the Adriatic sea; 2014 Sep 29 - Oct 1; Kotor, Montenegro
T1  - Species-specific expression of metallothionein in the hepatopancreas of seawater fish from the Montenegrin Adriatic coastline
SP  - 28
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5653
ER  - 

@conference{
author = "Mihailović, Mirjana and Petrović, Miodrag and Grdović, Nevena and Dinić, Svetlana and Uskoković, Aleksandra and Vidaković, Melita and Grigorov, Ilijana and Bogojević, Desanka and Ivanović-Matić, Svetlana and Martinović, Vesna and Arambašić Jovanović, Jelena and Poznanović, Goran",
year = "2014",
abstract = "Metallothioneins (MTs) constitute a family of low-molecular  weight, cysteine­ rich and heat stable 
proteins involved in the binding and regulation of essential metals, such as copper and zinc, and 
in the detoxification of these and other non-essential metals, such as cadmium and mercury. 
Previously we showed that the induction of MTs in Merluccius merluccius and Mui/us barbatus 
correlated with elevated concentrations of Cu and Pb, determined by chemical analysis of the 
seawater from Bar and Valdanos. In the present study we studied protein expression of MTs in the 
hepatopancreas of several seawater fish species: Red mullet (Mui/us barbatus), European hake 
(Merluccius merluccius), Tub gurnard (Trig/a lucerna) and Thinlip mullet  (Liza ramada), from the 
Monetengrin Adriatic coastline. Western blot analysis revealed the highest induction of MTs in the 
hepatopancreas in the following order: Merluccius merluccius, Trig/a lucerna, Mui/us barbatus and 
Liza ramada. Considering that MTs play a role in the metabolism of essential metals, they  are 
constitutively expressed. The presence of elevated concentrations of both essential and toxic 
metals provokes the induction of MTs. These results are in correlation with literature data showing 
that fish species differ in their detoxification capacities and amounts of accumulated  metals.  We 
 conclude that the level of induction of MTs in the hepatopancreas of the examined fish species 
correlates with the level of their reliability as bioindicator species in heavy metal 
biomonitoring.",
publisher = "Kotor, Montenegro : University of Montenegro, Institute of Marine Biology",
journal = "Book of Abstracts: 1st International scientific conference integrated coastal zone management in the Adriatic sea; 2014 Sep 29 - Oct 1; Kotor, Montenegro",
title = "Species-specific expression of metallothionein in the hepatopancreas of seawater fish from the Montenegrin Adriatic coastline",
pages = "28",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5653"
}

Mihailović, M., Petrović, M., Grdović, N., Dinić, S., Uskoković, A., Vidaković, M., Grigorov, I., Bogojević, D., Ivanović-Matić, S., Martinović, V., Arambašić Jovanović, J.,& Poznanović, G.. (2014). Species-specific expression of metallothionein in the hepatopancreas of seawater fish from the Montenegrin Adriatic coastline. in Book of Abstracts: 1st International scientific conference integrated coastal zone management in the Adriatic sea; 2014 Sep 29 - Oct 1; Kotor, Montenegro
Kotor, Montenegro : University of Montenegro, Institute of Marine Biology., 28.
https://hdl.handle.net/21.15107/rcub_ibiss_5653

Mihailović M, Petrović M, Grdović N, Dinić S, Uskoković A, Vidaković M, Grigorov I, Bogojević D, Ivanović-Matić S, Martinović V, Arambašić Jovanović J, Poznanović G. Species-specific expression of metallothionein in the hepatopancreas of seawater fish from the Montenegrin Adriatic coastline. in Book of Abstracts: 1st International scientific conference integrated coastal zone management in the Adriatic sea; 2014 Sep 29 - Oct 1; Kotor, Montenegro. 2014;:28.
https://hdl.handle.net/21.15107/rcub_ibiss_5653 .

Mihailović, Mirjana, Petrović, Miodrag, Grdović, Nevena, Dinić, Svetlana, Uskoković, Aleksandra, Vidaković, Melita, Grigorov, Ilijana, Bogojević, Desanka, Ivanović-Matić, Svetlana, Martinović, Vesna, Arambašić Jovanović, Jelena, Poznanović, Goran, "Species-specific expression of metallothionein in the hepatopancreas of seawater fish from the Montenegrin Adriatic coastline" in Book of Abstracts: 1st International scientific conference integrated coastal zone management in the Adriatic sea; 2014 Sep 29 - Oct 1; Kotor, Montenegro (2014):28,
https://hdl.handle.net/21.15107/rcub_ibiss_5653 .

TY  - JOUR
AU  - Grigorov, Ilijana
AU  - Bogojević, Desanka
AU  - Jovanović Stojanov, Sofija
AU  - Petrović, Anja
AU  - Ivanović Matić, Svetlana
AU  - Zolotarevski, Lidija
AU  - Poznanović, Goran
AU  - Martinović, Vesna
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2210
AB  - Oxidative stress-mediated damage to liver tissue underlies the
   pathological alterations in liver morphology and function that are
   observed in diabetes. We examined the effects of the antioxidant action
   of melatonin against necrosis-inducing DNA damage in hepatocytes of
   streptozotocin (STZ)-induced diabetic rats. Daily administration of
   melatonin (0.2 mg/kg) was initiated 3 days before diabetes induction and
   maintained for 4 weeks. Melatonin-treated diabetic rats exhibited
   improved markers of liver injury (P<0.05), alkaline phosphatase, and
   alanine and aspartate aminotransferases. Melatonin prevented the
   diabetes-related morphological deterioration of hepatocytes, DNA damage
   (P<0.05), and hepatocellular necrosis. The improvement was due to
   containment of the pronecrotic oxygen radical load, observed as
   inhibition (P<0.05) of the diabetes-induced rise in lipid peroxidation
   and hydrogen peroxide increase in the liver. This was accompanied by
   improved necrotic markers of cellular damage: a significant reduction in
   cleavage of the DNA repair enzyme poly(ADP-ribose) polymerase 1 (PARP-1)
   into necrotic 55- and 62-kDa fragments, and inhibition of
   nucleus-to-cytoplasm translocation and accumulation in the serum of the
   high-mobility group box 1 (HMGB1) protein. We conclude that melatonin is
   hepatoprotective in diabetes. It reduces extensive DNA damage and
   resulting necrotic processes. Melatonin application could thus present a
   viable therapeutic option in the management of diabetes-induced liver
   injury.
T2  - Journal of Physiology and Biochemistry
T1  - Hepatoprotective effects of melatonin against pronecrotic cellular
 events in streptozotocin-induced diabetic rats
IS  - 2
VL  - 70
DO  - 10.1007/s13105-014-0322-7
SP  - 441
EP  - 450
ER  - 

@article{
author = "Grigorov, Ilijana and Bogojević, Desanka and Jovanović Stojanov, Sofija and Petrović, Anja and Ivanović Matić, Svetlana and Zolotarevski, Lidija and Poznanović, Goran and Martinović, Vesna",
year = "2014",
abstract = "Oxidative stress-mediated damage to liver tissue underlies the
   pathological alterations in liver morphology and function that are
   observed in diabetes. We examined the effects of the antioxidant action
   of melatonin against necrosis-inducing DNA damage in hepatocytes of
   streptozotocin (STZ)-induced diabetic rats. Daily administration of
   melatonin (0.2 mg/kg) was initiated 3 days before diabetes induction and
   maintained for 4 weeks. Melatonin-treated diabetic rats exhibited
   improved markers of liver injury (P<0.05), alkaline phosphatase, and
   alanine and aspartate aminotransferases. Melatonin prevented the
   diabetes-related morphological deterioration of hepatocytes, DNA damage
   (P<0.05), and hepatocellular necrosis. The improvement was due to
   containment of the pronecrotic oxygen radical load, observed as
   inhibition (P<0.05) of the diabetes-induced rise in lipid peroxidation
   and hydrogen peroxide increase in the liver. This was accompanied by
   improved necrotic markers of cellular damage: a significant reduction in
   cleavage of the DNA repair enzyme poly(ADP-ribose) polymerase 1 (PARP-1)
   into necrotic 55- and 62-kDa fragments, and inhibition of
   nucleus-to-cytoplasm translocation and accumulation in the serum of the
   high-mobility group box 1 (HMGB1) protein. We conclude that melatonin is
   hepatoprotective in diabetes. It reduces extensive DNA damage and
   resulting necrotic processes. Melatonin application could thus present a
   viable therapeutic option in the management of diabetes-induced liver
   injury.",
journal = "Journal of Physiology and Biochemistry",
title = "Hepatoprotective effects of melatonin against pronecrotic cellular
 events in streptozotocin-induced diabetic rats",
number = "2",
volume = "70",
doi = "10.1007/s13105-014-0322-7",
pages = "441-450"
}

Grigorov, I., Bogojević, D., Jovanović Stojanov, S., Petrović, A., Ivanović Matić, S., Zolotarevski, L., Poznanović, G.,& Martinović, V.. (2014). Hepatoprotective effects of melatonin against pronecrotic cellular
 events in streptozotocin-induced diabetic rats. in Journal of Physiology and Biochemistry, 70(2), 441-450.
https://doi.org/10.1007/s13105-014-0322-7

Grigorov I, Bogojević D, Jovanović Stojanov S, Petrović A, Ivanović Matić S, Zolotarevski L, Poznanović G, Martinović V. Hepatoprotective effects of melatonin against pronecrotic cellular
 events in streptozotocin-induced diabetic rats. in Journal of Physiology and Biochemistry. 2014;70(2):441-450.
doi:10.1007/s13105-014-0322-7 .

Grigorov, Ilijana, Bogojević, Desanka, Jovanović Stojanov, Sofija, Petrović, Anja, Ivanović Matić, Svetlana, Zolotarevski, Lidija, Poznanović, Goran, Martinović, Vesna, "Hepatoprotective effects of melatonin against pronecrotic cellular
 events in streptozotocin-induced diabetic rats" in Journal of Physiology and Biochemistry, 70, no. 2 (2014):441-450,
https://doi.org/10.1007/s13105-014-0322-7 . .

TY  - JOUR
AU  - Ivanović Matić, Svetlana
AU  - Bogojević, Desanka
AU  - Martinović, Vesna
AU  - Petrovic, Anja
AU  - Jovanovic-Stojanov, Sofija
AU  - Poznanović, Goran
AU  - Grigorov, Ilijana
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2117
AB  - Diabetes is a risk factor for cardiovascular disease that has a
   multifactorial etiology, with oxidative stress as an important
   component. Our previous observation of a significant diabetes-related
   increase in rat cardiac catalase (CAT) activity suggested that CAT could
   play a major role in delaying the development of diabetic
   cardiomyopathy. Thus, in the present work, we examined the effects of
   the daily administration of the CAT inhibitor, 3-amino-1,2,4-triazole (1
   mg/g), on the hearts of streptozotocin (STZ)-induced diabetic rats.
   Administration of CAT inhibitor was started from the 15th day after the
   last STZ treatment (40 mg/kg/5 days), and maintained until the end of
   the 4th or 6th weeks of diabetes. Compared to untreated diabetic rats,
   at the end of the observation period, CAT inhibition lowered the induced
   level of cardiac CAT activity to the basal level and decreased CAT
   protein expression, mediated through a decline in the nuclear factor
   erythroid-derived 2-like 2 /nuclear factor-kappa B p65 (Nrf2/NF-kappa B
   p65) subunit ratio. The perturbed antioxidant defenses resulting from
   CAT inhibition promoted increased H2O2 production (P < 0.05) and lipid
   peroxidation (P < 0.05). Generated cytotoxic stimuli increased DNA
   damage (P < 0.05) and activated pro-apoptotic events, observed as a
   decrease (P < 0.05) in the ratio of the apoptosis regulator proteins
   Bcl-2/Bax, increased (P < 0.05) presence of the poly(ADP-ribose)
   polymerase-1 (PARP-1) 85 kDa apoptotic fragment and cytoplasmic levels
   of cytochrome C. These findings confirm an important function of CAT in
   the suppression of events leading to diabetes-promoted cardiac
   dysfunction and cardiomyopathy.
T2  - Journal of Physiology and Biochemistry
T1  - Catalase inhibition in diabetic rats potentiates DNA damage and
 apoptotic cell death setting the stage for cardiomyopathy
IS  - 4
VL  - 70
DO  - 10.1007/s13105-014-0363-y
SP  - 947
EP  - 959
ER  - 

@article{
author = "Ivanović Matić, Svetlana and Bogojević, Desanka and Martinović, Vesna and Petrovic, Anja and Jovanovic-Stojanov, Sofija and Poznanović, Goran and Grigorov, Ilijana",
year = "2014",
abstract = "Diabetes is a risk factor for cardiovascular disease that has a
   multifactorial etiology, with oxidative stress as an important
   component. Our previous observation of a significant diabetes-related
   increase in rat cardiac catalase (CAT) activity suggested that CAT could
   play a major role in delaying the development of diabetic
   cardiomyopathy. Thus, in the present work, we examined the effects of
   the daily administration of the CAT inhibitor, 3-amino-1,2,4-triazole (1
   mg/g), on the hearts of streptozotocin (STZ)-induced diabetic rats.
   Administration of CAT inhibitor was started from the 15th day after the
   last STZ treatment (40 mg/kg/5 days), and maintained until the end of
   the 4th or 6th weeks of diabetes. Compared to untreated diabetic rats,
   at the end of the observation period, CAT inhibition lowered the induced
   level of cardiac CAT activity to the basal level and decreased CAT
   protein expression, mediated through a decline in the nuclear factor
   erythroid-derived 2-like 2 /nuclear factor-kappa B p65 (Nrf2/NF-kappa B
   p65) subunit ratio. The perturbed antioxidant defenses resulting from
   CAT inhibition promoted increased H2O2 production (P < 0.05) and lipid
   peroxidation (P < 0.05). Generated cytotoxic stimuli increased DNA
   damage (P < 0.05) and activated pro-apoptotic events, observed as a
   decrease (P < 0.05) in the ratio of the apoptosis regulator proteins
   Bcl-2/Bax, increased (P < 0.05) presence of the poly(ADP-ribose)
   polymerase-1 (PARP-1) 85 kDa apoptotic fragment and cytoplasmic levels
   of cytochrome C. These findings confirm an important function of CAT in
   the suppression of events leading to diabetes-promoted cardiac
   dysfunction and cardiomyopathy.",
journal = "Journal of Physiology and Biochemistry",
title = "Catalase inhibition in diabetic rats potentiates DNA damage and
 apoptotic cell death setting the stage for cardiomyopathy",
number = "4",
volume = "70",
doi = "10.1007/s13105-014-0363-y",
pages = "947-959"
}

Ivanović Matić, S., Bogojević, D., Martinović, V., Petrovic, A., Jovanovic-Stojanov, S., Poznanović, G.,& Grigorov, I.. (2014). Catalase inhibition in diabetic rats potentiates DNA damage and
 apoptotic cell death setting the stage for cardiomyopathy. in Journal of Physiology and Biochemistry, 70(4), 947-959.
https://doi.org/10.1007/s13105-014-0363-y

Ivanović Matić S, Bogojević D, Martinović V, Petrovic A, Jovanovic-Stojanov S, Poznanović G, Grigorov I. Catalase inhibition in diabetic rats potentiates DNA damage and
 apoptotic cell death setting the stage for cardiomyopathy. in Journal of Physiology and Biochemistry. 2014;70(4):947-959.
doi:10.1007/s13105-014-0363-y .

Ivanović Matić, Svetlana, Bogojević, Desanka, Martinović, Vesna, Petrovic, Anja, Jovanovic-Stojanov, Sofija, Poznanović, Goran, Grigorov, Ilijana, "Catalase inhibition in diabetic rats potentiates DNA damage and
 apoptotic cell death setting the stage for cardiomyopathy" in Journal of Physiology and Biochemistry, 70, no. 4 (2014):947-959,
https://doi.org/10.1007/s13105-014-0363-y . .

TY  - CONF
AU  - Petrović, Anja
AU  - Martinović, Vesna
AU  - Bogojević, Desanka
AU  - Jovanović Stojanov, Sofija
AU  - Ivanović-Matić, Svetlana
AU  - Poznanović, Goran
AU  - Grigorov, Ilijana
PY  - 2013
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5430
AB  - Dijabetes predstavlja metabolički poremećaj koji je okarakterisan hiperglikemijom i sa njom udruženim oksidativnim stresom koji dovodi do oštećenja i disfunkcije mnogih organa. Patološke promene morfologije i funkcije jetre tokom razvoja dijabetesa glavni su uzroci različitih bolesti jetre. Kod dijabetičnih pacijenata dolazi do promena u veličini jetre kao rezultat izmenjenog broja ćelija usled njihovog rasta ili ćelijske smrti. U osnovi üelijske smrti putem nekroze nalaze se DNK oštećenja. Obzirom da tokom dijabetesa dolazi do smanjenja nivoa melatonina, u ovom radu ispitivan je antioksidativni uticaj dnevnog unosa melatonina na stepen DNK oštećenja i prisustvo nekrotskih promena u ćelijama jetre pacova kod kojih je dijabetes izazvan jednokratnim injeciranjem streptozotocina u dozi od 65 mg/kg. Eksperiment su činile kontrolna grupa pacova soja Wistar, grupa koja je primala melatonin (0.2 mg/kg), grupa sa dijabetesom i grupa dijabetičnih pacova tretiranih melatoninom. Tretman melatoninom počeo je tri dana pre injeciranja streptozotocina i trajao je četiri nedelje. Stepen oksidativnog stresa praćen je određivanjem lipidnog statusa i merenjem koncentracije vodonik peroksida (H2O2) u cirkulaciji i jetri. Oštećenje jetre je utvrđivano histološki i preko serumskog nivoa alanin aminotransferaze, aspartat aminotransferaze i alkalne fosfataze. Oštećenja DNK ispitivana su Komet analizom. Prisustvo nekrotskih promena praćeno je histološki i imunoblot analizom profila sečenja DNK reparacionog enzima, PARP-1 (engl. Poly(ADP-ribose)polymerase-1) i subćelijske lokalizacije i ekstraćelijskog prisustva signalnog proteina nekroze, HMGB1 (engl. High Mobility Group Box 1). Dijabetični pacovi tretirani melatoninom ispoljavali su značajno niži nivo oksidativnog stresa i oštećenja jetre u odnosu na dijabetične. Melatonin je očuvao strukturu jetre dijabetičnih pacova i značajno smanjio nivo hidropsne degeneracije i broj nekrotičnih ćelija što korelira sa smanjenjem DNK oštećenja za 77%, redukovanom pojavom nekrotskih fragmenata PARP-1 (55kDa i 62 kDa) i zadržavanjem HMGB1 proteina u jedru. Zaključeno je da melatonin svojim antioksidativnim delovanjem štiti jetru od oštećenja uzrokovanih dijabetičnim stanjem i da bi mogao biti od koristi kao vid terapije kod obolelih od dijabetesa.
PB  - Beograd: Srpsko društvo za mitohondrijalnu i slobodno-radikalsku fiziologiju
PB  - Beograd: Ministarstvo prosvete, nauke i tehnološkog razvoja
PB  - Beograd: Biološki fakultet
PB  - Niš: Medicinski fakultet
C3  - Knjiga sažetaka: Drugi kongres Život sa slobodnim radikalima: Hemija, Biologija, Medicina, SDMSRF-2013; 2013 Sep 28; Niš, Serbia
T1  - Antinekrotski efekat melatonina u jetri dijabetičnih pacova
SP  - 35
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5430
ER  - 

@conference{
author = "Petrović, Anja and Martinović, Vesna and Bogojević, Desanka and Jovanović Stojanov, Sofija and Ivanović-Matić, Svetlana and Poznanović, Goran and Grigorov, Ilijana",
year = "2013",
abstract = "Dijabetes predstavlja metabolički poremećaj koji je okarakterisan hiperglikemijom i sa njom udruženim oksidativnim stresom koji dovodi do oštećenja i disfunkcije mnogih organa. Patološke promene morfologije i funkcije jetre tokom razvoja dijabetesa glavni su uzroci različitih bolesti jetre. Kod dijabetičnih pacijenata dolazi do promena u veličini jetre kao rezultat izmenjenog broja ćelija usled njihovog rasta ili ćelijske smrti. U osnovi üelijske smrti putem nekroze nalaze se DNK oštećenja. Obzirom da tokom dijabetesa dolazi do smanjenja nivoa melatonina, u ovom radu ispitivan je antioksidativni uticaj dnevnog unosa melatonina na stepen DNK oštećenja i prisustvo nekrotskih promena u ćelijama jetre pacova kod kojih je dijabetes izazvan jednokratnim injeciranjem streptozotocina u dozi od 65 mg/kg. Eksperiment su činile kontrolna grupa pacova soja Wistar, grupa koja je primala melatonin (0.2 mg/kg), grupa sa dijabetesom i grupa dijabetičnih pacova tretiranih melatoninom. Tretman melatoninom počeo je tri dana pre injeciranja streptozotocina i trajao je četiri nedelje. Stepen oksidativnog stresa praćen je određivanjem lipidnog statusa i merenjem koncentracije vodonik peroksida (H2O2) u cirkulaciji i jetri. Oštećenje jetre je utvrđivano histološki i preko serumskog nivoa alanin aminotransferaze, aspartat aminotransferaze i alkalne fosfataze. Oštećenja DNK ispitivana su Komet analizom. Prisustvo nekrotskih promena praćeno je histološki i imunoblot analizom profila sečenja DNK reparacionog enzima, PARP-1 (engl. Poly(ADP-ribose)polymerase-1) i subćelijske lokalizacije i ekstraćelijskog prisustva signalnog proteina nekroze, HMGB1 (engl. High Mobility Group Box 1). Dijabetični pacovi tretirani melatoninom ispoljavali su značajno niži nivo oksidativnog stresa i oštećenja jetre u odnosu na dijabetične. Melatonin je očuvao strukturu jetre dijabetičnih pacova i značajno smanjio nivo hidropsne degeneracije i broj nekrotičnih ćelija što korelira sa smanjenjem DNK oštećenja za 77%, redukovanom pojavom nekrotskih fragmenata PARP-1 (55kDa i 62 kDa) i zadržavanjem HMGB1 proteina u jedru. Zaključeno je da melatonin svojim antioksidativnim delovanjem štiti jetru od oštećenja uzrokovanih dijabetičnim stanjem i da bi mogao biti od koristi kao vid terapije kod obolelih od dijabetesa.",
publisher = "Beograd: Srpsko društvo za mitohondrijalnu i slobodno-radikalsku fiziologiju, Beograd: Ministarstvo prosvete, nauke i tehnološkog razvoja, Beograd: Biološki fakultet, Niš: Medicinski fakultet",
journal = "Knjiga sažetaka: Drugi kongres Život sa slobodnim radikalima: Hemija, Biologija, Medicina, SDMSRF-2013; 2013 Sep 28; Niš, Serbia",
title = "Antinekrotski efekat melatonina u jetri dijabetičnih pacova",
pages = "35",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5430"
}

Petrović, A., Martinović, V., Bogojević, D., Jovanović Stojanov, S., Ivanović-Matić, S., Poznanović, G.,& Grigorov, I.. (2013). Antinekrotski efekat melatonina u jetri dijabetičnih pacova. in Knjiga sažetaka: Drugi kongres Život sa slobodnim radikalima: Hemija, Biologija, Medicina, SDMSRF-2013; 2013 Sep 28; Niš, Serbia
Beograd: Srpsko društvo za mitohondrijalnu i slobodno-radikalsku fiziologiju., 35.
https://hdl.handle.net/21.15107/rcub_ibiss_5430

Petrović A, Martinović V, Bogojević D, Jovanović Stojanov S, Ivanović-Matić S, Poznanović G, Grigorov I. Antinekrotski efekat melatonina u jetri dijabetičnih pacova. in Knjiga sažetaka: Drugi kongres Život sa slobodnim radikalima: Hemija, Biologija, Medicina, SDMSRF-2013; 2013 Sep 28; Niš, Serbia. 2013;:35.
https://hdl.handle.net/21.15107/rcub_ibiss_5430 .

Petrović, Anja, Martinović, Vesna, Bogojević, Desanka, Jovanović Stojanov, Sofija, Ivanović-Matić, Svetlana, Poznanović, Goran, Grigorov, Ilijana, "Antinekrotski efekat melatonina u jetri dijabetičnih pacova" in Knjiga sažetaka: Drugi kongres Život sa slobodnim radikalima: Hemija, Biologija, Medicina, SDMSRF-2013; 2013 Sep 28; Niš, Serbia (2013):35,
https://hdl.handle.net/21.15107/rcub_ibiss_5430 .

TY  - JOUR
AU  - Arambašić Jovanović, Jelena
AU  - Mihailović, Mirjana
AU  - Bogojević, Desanka
AU  - Ivanović Matić, Svetlana
AU  - Uskoković, Aleksandra
AU  - Poznanović, Goran
AU  - Grigorov, Ilijana
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1040
AB  - Haptoglobin is a hemoglobin-binding acute-phase protein which possesses anti-inflammatory and antioxidative properties. In this study, we investigated changes in protein expression of rat haptoglobin under diabetes-related inflammatory and oxidative stress conditions induced by an i.p. injection of streptozotocin. The progress of diabetes during an 8-week follow-up period was associated with the increased presence of haptoglobin in the serum and in the liver. This increase was most prominent during the first 2 weeks after which it started to decline. Temporary changes in haptoglobin expression strongly correlated with the serum levels of TNF-alpha and IL-6. Lower haptoglobin expression at the fourth week and thereafter correlated with a decrease in TNF-alpha concentration and changes in the TNF-alpha/IL-6 ratio. Based on the decrease of GSH/GSSG ratio and antioxidant enzyme activities in the liver until the end of fourth week, it was concluded that the liver was exposed to oxidative stress and injury which in the presence of the abovementioned inflammatory mediators lead to different haptoglobin expression profiles at different stages of diabetes. An inverse correlation was observed between the haptoglobin and free iron serum levels in diabetic rats. The higher levels of haptoglobin during the first 2 weeks were accompanied by a lower level of free iron. In view of the established function of haptoglobin, we discuss its possible role in decreasing oxidative stress during the early stage of diabetes.
PB  - Springer Nature
T2  - Journal of Physiology and Biochemistry
T1  - Haptoglobin and the inflammatory and oxidative status in experimental diabetic rats: antioxidant role of haptoglobin
IS  - 1
VL  - 69
DO  - 10.1007/s13105-012-0186-7
SP  - 45
EP  - 58
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1040
ER  - 

@article{
author = "Arambašić Jovanović, Jelena and Mihailović, Mirjana and Bogojević, Desanka and Ivanović Matić, Svetlana and Uskoković, Aleksandra and Poznanović, Goran and Grigorov, Ilijana",
year = "2013",
abstract = "Haptoglobin is a hemoglobin-binding acute-phase protein which possesses anti-inflammatory and antioxidative properties. In this study, we investigated changes in protein expression of rat haptoglobin under diabetes-related inflammatory and oxidative stress conditions induced by an i.p. injection of streptozotocin. The progress of diabetes during an 8-week follow-up period was associated with the increased presence of haptoglobin in the serum and in the liver. This increase was most prominent during the first 2 weeks after which it started to decline. Temporary changes in haptoglobin expression strongly correlated with the serum levels of TNF-alpha and IL-6. Lower haptoglobin expression at the fourth week and thereafter correlated with a decrease in TNF-alpha concentration and changes in the TNF-alpha/IL-6 ratio. Based on the decrease of GSH/GSSG ratio and antioxidant enzyme activities in the liver until the end of fourth week, it was concluded that the liver was exposed to oxidative stress and injury which in the presence of the abovementioned inflammatory mediators lead to different haptoglobin expression profiles at different stages of diabetes. An inverse correlation was observed between the haptoglobin and free iron serum levels in diabetic rats. The higher levels of haptoglobin during the first 2 weeks were accompanied by a lower level of free iron. In view of the established function of haptoglobin, we discuss its possible role in decreasing oxidative stress during the early stage of diabetes.",
publisher = "Springer Nature",
journal = "Journal of Physiology and Biochemistry",
title = "Haptoglobin and the inflammatory and oxidative status in experimental diabetic rats: antioxidant role of haptoglobin",
number = "1",
volume = "69",
doi = "10.1007/s13105-012-0186-7",
pages = "45-58",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1040"
}

Arambašić Jovanović, J., Mihailović, M., Bogojević, D., Ivanović Matić, S., Uskoković, A., Poznanović, G.,& Grigorov, I.. (2013). Haptoglobin and the inflammatory and oxidative status in experimental diabetic rats: antioxidant role of haptoglobin. in Journal of Physiology and Biochemistry
Springer Nature., 69(1), 45-58.
https://doi.org/10.1007/s13105-012-0186-7
https://hdl.handle.net/21.15107/rcub_ibiss_1040

Arambašić Jovanović J, Mihailović M, Bogojević D, Ivanović Matić S, Uskoković A, Poznanović G, Grigorov I. Haptoglobin and the inflammatory and oxidative status in experimental diabetic rats: antioxidant role of haptoglobin. in Journal of Physiology and Biochemistry. 2013;69(1):45-58.
doi:10.1007/s13105-012-0186-7
https://hdl.handle.net/21.15107/rcub_ibiss_1040 .

Arambašić Jovanović, Jelena, Mihailović, Mirjana, Bogojević, Desanka, Ivanović Matić, Svetlana, Uskoković, Aleksandra, Poznanović, Goran, Grigorov, Ilijana, "Haptoglobin and the inflammatory and oxidative status in experimental diabetic rats: antioxidant role of haptoglobin" in Journal of Physiology and Biochemistry, 69, no. 1 (2013):45-58,
https://doi.org/10.1007/s13105-012-0186-7 .,
https://hdl.handle.net/21.15107/rcub_ibiss_1040 .

TY  - CONF
AU  - Petrović, Anja
AU  - Ivanović-Matić, Svetlana
AU  - Bogojević, Desanka
AU  - Martinović, Vesna
AU  - Jovanović-Stojanov, Sofija
AU  - Poznanović, Goran
AU  - Grigorov, Ilijana
PY  - 2013
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5651
AB  - Oxidative stress-related cardiomyocyte damage in diabetes represents a major risk factor for heart disease. Reactive oxygen species triggers a series of deleterious stimuli that result in protein and DNA damage, cell dysfunction and cell death. Our previous study showed that the absence of cardiomyopathy in rats with streptozotocin (STZ)-induced diabetes is accompanied with significantly higher antioxidative activity of catalase (CAT), suggesting that CAT may be one of the key enzymes in heart protection during diabetes. To confirm this hypothesis we analysed oxidative status and extent of DNA damage in cardiomyocytes of diabetic rats with inhibited CAT activity. Diabetes was induced by intraperitoneal (i.p.) injection of ST2 at 40 mg/kg/day for five consecutive days. Inhibition of CAT activity was established by daily i.p. administration of 1 mg/kg 3-amino-1,2,4 triazole throughout the 4 week period, starting from the 15th day of STZ administration. Increased lipid per-oxidation and H2O2, concentration in the heart of diabetic rats with inhibited CAT activity indicated higher level of oxidative stress when compared with diabetic ones. This is followed with decline of glutathione level, activity of glutathione peroxidase and total superoxide dismutase and increased activity of manganese superoxide dismutase whose overexpression could potentiate cardiac CAT activity. According to comet assay, impairment in antioxidant defense system led to significantly increased DNA damage in cardiomyocytes of rats with inhibited CAT activity in comparison with cardiomyocytes of diabetic rats. Also, Western immunoblot revealed that inhibition of CAT activity in diabetic heart was followed by twofold decrease in CAT expression as a result of the decrease in expression of Nrf2, the main transcription factor involved in CAT gene induction. These results suggest that. CAT expression and activity is crucial in prevention of heart damage during diabetes.
PB  - Heidelberg, Germany: EMBL
C3  - Abstracts presented at the 15th international EMBL PhD Symposium: Competition in Biology: The race for survival from molecules to systems; 2013 Nov 21-23; Heidelberg, Germany
T1  - Catalase prevents cardiomyocyte DNA damage during diabetes
SP  - 55
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5651
ER  - 

@conference{
author = "Petrović, Anja and Ivanović-Matić, Svetlana and Bogojević, Desanka and Martinović, Vesna and Jovanović-Stojanov, Sofija and Poznanović, Goran and Grigorov, Ilijana",
year = "2013",
abstract = "Oxidative stress-related cardiomyocyte damage in diabetes represents a major risk factor for heart disease. Reactive oxygen species triggers a series of deleterious stimuli that result in protein and DNA damage, cell dysfunction and cell death. Our previous study showed that the absence of cardiomyopathy in rats with streptozotocin (STZ)-induced diabetes is accompanied with significantly higher antioxidative activity of catalase (CAT), suggesting that CAT may be one of the key enzymes in heart protection during diabetes. To confirm this hypothesis we analysed oxidative status and extent of DNA damage in cardiomyocytes of diabetic rats with inhibited CAT activity. Diabetes was induced by intraperitoneal (i.p.) injection of ST2 at 40 mg/kg/day for five consecutive days. Inhibition of CAT activity was established by daily i.p. administration of 1 mg/kg 3-amino-1,2,4 triazole throughout the 4 week period, starting from the 15th day of STZ administration. Increased lipid per-oxidation and H2O2, concentration in the heart of diabetic rats with inhibited CAT activity indicated higher level of oxidative stress when compared with diabetic ones. This is followed with decline of glutathione level, activity of glutathione peroxidase and total superoxide dismutase and increased activity of manganese superoxide dismutase whose overexpression could potentiate cardiac CAT activity. According to comet assay, impairment in antioxidant defense system led to significantly increased DNA damage in cardiomyocytes of rats with inhibited CAT activity in comparison with cardiomyocytes of diabetic rats. Also, Western immunoblot revealed that inhibition of CAT activity in diabetic heart was followed by twofold decrease in CAT expression as a result of the decrease in expression of Nrf2, the main transcription factor involved in CAT gene induction. These results suggest that. CAT expression and activity is crucial in prevention of heart damage during diabetes.",
publisher = "Heidelberg, Germany: EMBL",
journal = "Abstracts presented at the 15th international EMBL PhD Symposium: Competition in Biology: The race for survival from molecules to systems; 2013 Nov 21-23; Heidelberg, Germany",
title = "Catalase prevents cardiomyocyte DNA damage during diabetes",
pages = "55",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5651"
}

Petrović, A., Ivanović-Matić, S., Bogojević, D., Martinović, V., Jovanović-Stojanov, S., Poznanović, G.,& Grigorov, I.. (2013). Catalase prevents cardiomyocyte DNA damage during diabetes. in Abstracts presented at the 15th international EMBL PhD Symposium: Competition in Biology: The race for survival from molecules to systems; 2013 Nov 21-23; Heidelberg, Germany
Heidelberg, Germany: EMBL., 55.
https://hdl.handle.net/21.15107/rcub_ibiss_5651

Petrović A, Ivanović-Matić S, Bogojević D, Martinović V, Jovanović-Stojanov S, Poznanović G, Grigorov I. Catalase prevents cardiomyocyte DNA damage during diabetes. in Abstracts presented at the 15th international EMBL PhD Symposium: Competition in Biology: The race for survival from molecules to systems; 2013 Nov 21-23; Heidelberg, Germany. 2013;:55.
https://hdl.handle.net/21.15107/rcub_ibiss_5651 .

Petrović, Anja, Ivanović-Matić, Svetlana, Bogojević, Desanka, Martinović, Vesna, Jovanović-Stojanov, Sofija, Poznanović, Goran, Grigorov, Ilijana, "Catalase prevents cardiomyocyte DNA damage during diabetes" in Abstracts presented at the 15th international EMBL PhD Symposium: Competition in Biology: The race for survival from molecules to systems; 2013 Nov 21-23; Heidelberg, Germany (2013):55,
https://hdl.handle.net/21.15107/rcub_ibiss_5651 .

TY  - CONF
AU  - Jovanović Stojanov, Sofija
AU  - Martinović, Vesna
AU  - Bogojević, Desanka
AU  - Ivanović-Matić, Svetlana
AU  - Petrović, Anja
AU  - Poznanović, Goran
AU  - Grigorov, Ilijana
PY  - 2013
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5429
AB  - Hipoinsulinemija i hiperglikemija koje nastaju tokom dijabetesa, uzrokuju pojavu metaboličkog i oksidativnog stresa koji dovode do stanja hronične inflamacije, progresivne disfunkcije i oštećenja jetre. Za predikciju i prevenciju pojave dijabetičnih komplikacija u jetri od interesa je identifikacija endogenih molekula koji svojim delovanjem doprinose njenom oštećenju. U tom smislu izdvaja se protein HMGB1. Prvobitno okarakterisan kao DNK- vezujući protein sa ulogom u organizaciji hromatinske strukture, HMGB1 može biti prisutan u ekstraćelijskom miljeu gde ima ulogu proinflamatornog citokina i medijatora tkivnih oštećenja. U vanćelijsku sredinu HMGB1 dospeva pasivno iz nekroznih ili oštećenih ćelija ili regulisanom sekrecijom iz ćelija izloženih stresu. U ovom radu ispitivan je uticaj oksidativnog statusa na subćelijsku lokalizaciju i ukupno prisustvo HMGB1 proteina u jetri i serumu pacova sa dijabetesom tipa I i promene nastale nakon tretmana dijabetičnih pacova sa antioksidansom melatoninom.
Dijabetes tipa I uspostavljen je davanjem jednokratne doze streptozotocina (65 mg/kg) pacovima soja Wistar. Tretman kontrolnih i dijabetičnih pacova melatoninom (0.2 mg/kg) započet je tri dana pre indukcije dijabetesa i vršen je svakodnevno tokom 4   nedelje.
Dijabetično stanje karakteriše značajan porast koncentracije vodonik peroksida (H2O2), i superoksid anjon radikala (O .-) u serumu, porast lipidne peroksidacije i pad aktivnosti antioksidativnih enzima katalaze, superoksid dismutaza i glutation S transferaze u serumu i
jetri. Ovakav oksidativni status prati značajni porast koncentracije alanin aminotransferaze (ALT), pokazatelja oštećenja jetre, za oko 3.2 puta kao i značajan porast nivoa HMGB1 proteina (2.1 put) u serumu i ukupnim homogenatima jetre (2.3 puta). Imunohistohemijski utvrđena je prevashodno citoplazmatska lokalizacija HMGB1 proteina tokom dijabetesa. Bolji oksidativni status uspostavljen tretmanom sa melatoninom dovodi do smanjenja ošteüenja jetre što je praćeno značajnim smanjenjem nivoa HMGB1 proteina u serumu i jetri i njegovim zadržavanjem u jedru ćelija jetre.
Dobijeni rezultati ukazuju da prisustvo HMGB1 proteina u serumu korelira sa stepenom oksidativnog stresa i oštećenjem jetre što navodi na zaključak da HMGB1 protein može biti potencijalni prognostički indikator tkivnih oštećenja kao i meta terapeutskog delovanja kojim bi se menjala njegova lokalizovanost i aktivnost, a time i redukovala disfunkcija jetre tokom dijabetesa.
PB  - Beograd: Srpsko društvo za mitohondrijalnu i slobodno-radikalsku fiziologiju
PB  - Beograd: Ministarstvo prosvete, nauke i tehnološkog razvoja
PB  - Beograd: Biološki fakultet
PB  - Niš: Medicinski fakultet
C3  - Knjiga sažetaka: Drugi kongres Život sa slobodnim radikalima: Hemija, Biologija, Medicina, SDMSRF-2013; 2013 Sep 28; Niš, Serbia
T1  - HMGB1 kao indikator oštećenja jetre uzrokovanog oksidativnim stresom tokom dijabetesa
SP  - 79
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5429
ER  - 

@conference{
author = "Jovanović Stojanov, Sofija and Martinović, Vesna and Bogojević, Desanka and Ivanović-Matić, Svetlana and Petrović, Anja and Poznanović, Goran and Grigorov, Ilijana",
year = "2013",
abstract = "Hipoinsulinemija i hiperglikemija koje nastaju tokom dijabetesa, uzrokuju pojavu metaboličkog i oksidativnog stresa koji dovode do stanja hronične inflamacije, progresivne disfunkcije i oštećenja jetre. Za predikciju i prevenciju pojave dijabetičnih komplikacija u jetri od interesa je identifikacija endogenih molekula koji svojim delovanjem doprinose njenom oštećenju. U tom smislu izdvaja se protein HMGB1. Prvobitno okarakterisan kao DNK- vezujući protein sa ulogom u organizaciji hromatinske strukture, HMGB1 može biti prisutan u ekstraćelijskom miljeu gde ima ulogu proinflamatornog citokina i medijatora tkivnih oštećenja. U vanćelijsku sredinu HMGB1 dospeva pasivno iz nekroznih ili oštećenih ćelija ili regulisanom sekrecijom iz ćelija izloženih stresu. U ovom radu ispitivan je uticaj oksidativnog statusa na subćelijsku lokalizaciju i ukupno prisustvo HMGB1 proteina u jetri i serumu pacova sa dijabetesom tipa I i promene nastale nakon tretmana dijabetičnih pacova sa antioksidansom melatoninom.
Dijabetes tipa I uspostavljen je davanjem jednokratne doze streptozotocina (65 mg/kg) pacovima soja Wistar. Tretman kontrolnih i dijabetičnih pacova melatoninom (0.2 mg/kg) započet je tri dana pre indukcije dijabetesa i vršen je svakodnevno tokom 4   nedelje.
Dijabetično stanje karakteriše značajan porast koncentracije vodonik peroksida (H2O2), i superoksid anjon radikala (O .-) u serumu, porast lipidne peroksidacije i pad aktivnosti antioksidativnih enzima katalaze, superoksid dismutaza i glutation S transferaze u serumu i
jetri. Ovakav oksidativni status prati značajni porast koncentracije alanin aminotransferaze (ALT), pokazatelja oštećenja jetre, za oko 3.2 puta kao i značajan porast nivoa HMGB1 proteina (2.1 put) u serumu i ukupnim homogenatima jetre (2.3 puta). Imunohistohemijski utvrđena je prevashodno citoplazmatska lokalizacija HMGB1 proteina tokom dijabetesa. Bolji oksidativni status uspostavljen tretmanom sa melatoninom dovodi do smanjenja ošteüenja jetre što je praćeno značajnim smanjenjem nivoa HMGB1 proteina u serumu i jetri i njegovim zadržavanjem u jedru ćelija jetre.
Dobijeni rezultati ukazuju da prisustvo HMGB1 proteina u serumu korelira sa stepenom oksidativnog stresa i oštećenjem jetre što navodi na zaključak da HMGB1 protein može biti potencijalni prognostički indikator tkivnih oštećenja kao i meta terapeutskog delovanja kojim bi se menjala njegova lokalizovanost i aktivnost, a time i redukovala disfunkcija jetre tokom dijabetesa.",
publisher = "Beograd: Srpsko društvo za mitohondrijalnu i slobodno-radikalsku fiziologiju, Beograd: Ministarstvo prosvete, nauke i tehnološkog razvoja, Beograd: Biološki fakultet, Niš: Medicinski fakultet",
journal = "Knjiga sažetaka: Drugi kongres Život sa slobodnim radikalima: Hemija, Biologija, Medicina, SDMSRF-2013; 2013 Sep 28; Niš, Serbia",
title = "HMGB1 kao indikator oštećenja jetre uzrokovanog oksidativnim stresom tokom dijabetesa",
pages = "79",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5429"
}

Jovanović Stojanov, S., Martinović, V., Bogojević, D., Ivanović-Matić, S., Petrović, A., Poznanović, G.,& Grigorov, I.. (2013). HMGB1 kao indikator oštećenja jetre uzrokovanog oksidativnim stresom tokom dijabetesa. in Knjiga sažetaka: Drugi kongres Život sa slobodnim radikalima: Hemija, Biologija, Medicina, SDMSRF-2013; 2013 Sep 28; Niš, Serbia
Beograd: Srpsko društvo za mitohondrijalnu i slobodno-radikalsku fiziologiju., 79.
https://hdl.handle.net/21.15107/rcub_ibiss_5429

Jovanović Stojanov S, Martinović V, Bogojević D, Ivanović-Matić S, Petrović A, Poznanović G, Grigorov I. HMGB1 kao indikator oštećenja jetre uzrokovanog oksidativnim stresom tokom dijabetesa. in Knjiga sažetaka: Drugi kongres Život sa slobodnim radikalima: Hemija, Biologija, Medicina, SDMSRF-2013; 2013 Sep 28; Niš, Serbia. 2013;:79.
https://hdl.handle.net/21.15107/rcub_ibiss_5429 .

Jovanović Stojanov, Sofija, Martinović, Vesna, Bogojević, Desanka, Ivanović-Matić, Svetlana, Petrović, Anja, Poznanović, Goran, Grigorov, Ilijana, "HMGB1 kao indikator oštećenja jetre uzrokovanog oksidativnim stresom tokom dijabetesa" in Knjiga sažetaka: Drugi kongres Život sa slobodnim radikalima: Hemija, Biologija, Medicina, SDMSRF-2013; 2013 Sep 28; Niš, Serbia (2013):79,
https://hdl.handle.net/21.15107/rcub_ibiss_5429 .

TY  - JOUR
AU  - Martinović, Vesna
AU  - Grigorov, Ilijana
AU  - Bogojević, Desanka
AU  - Petrović, Anja
AU  - Jovanović Stojanov, Sofija
AU  - Ilić, Mirka
AU  - Ivanović-Matić, Svetlana
PY  - 2012
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6069
AB  - Aims: Diabetes-related oxidative stress conditions lead to progressive tissue damage and
disfunctionality. Mechanisms underlying liver pathophysiology during diabetes are not
fully understood. The aim of this study was to find relationship between diabetes-related
DNA damage in the rat liver and activities of prosurvival signaling pathways. Methods:
Diabetes, induced by single intraperitoneal injection of streptozotocin, was analyzed two
(development stage) and eight weeks after treatment (stable diabetes). Extent of DNA
damage, analysed by commet assay, was corelated with oxidative status (plasma level of
ROS, liver antioxidant capacity) and activity/abundance of kinases (Akt, p38, ERK1,
JNK, JAK) and transcription factors NF-kB p65 and STAT3. Results: Significant DNA
damage in development stage is accompanied by elevated plasma levels of O2
- and H2O2,
decreased activities of CAT, MnSOD, and GST in the liver and increased activation of
proapoptotic JNK signal pathway. Lower DNA damage in stable diabetes, is
accompanied by elevated plasma level of O2
-, restored antioxidative liver enzyme
activity, decreased activation of JNK and increased activation of prosurvival Akt and
ERK signal pathways. Conclusion: These findings indicate that level of DNA damage in
diabetic liver depends on the extent of oxidative stress, antioxidant activity and balance
between JNK and Akt/ERK signal pathways activation.
PB  - Karger Publishers
T2  - Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
T1  - Activation Level of JNK and Akt/ERK Signaling Pathways Determinates Extent of DNA Damage in the Liver of Diabetic Rats
IS  - 3
VL  - 30
DO  - 10.1159/000341452
SP  - 723
EP  - 734
ER  - 

@article{
author = "Martinović, Vesna and Grigorov, Ilijana and Bogojević, Desanka and Petrović, Anja and Jovanović Stojanov, Sofija and Ilić, Mirka and Ivanović-Matić, Svetlana",
year = "2012",
abstract = "Aims: Diabetes-related oxidative stress conditions lead to progressive tissue damage and
disfunctionality. Mechanisms underlying liver pathophysiology during diabetes are not
fully understood. The aim of this study was to find relationship between diabetes-related
DNA damage in the rat liver and activities of prosurvival signaling pathways. Methods:
Diabetes, induced by single intraperitoneal injection of streptozotocin, was analyzed two
(development stage) and eight weeks after treatment (stable diabetes). Extent of DNA
damage, analysed by commet assay, was corelated with oxidative status (plasma level of
ROS, liver antioxidant capacity) and activity/abundance of kinases (Akt, p38, ERK1,
JNK, JAK) and transcription factors NF-kB p65 and STAT3. Results: Significant DNA
damage in development stage is accompanied by elevated plasma levels of O2
- and H2O2,
decreased activities of CAT, MnSOD, and GST in the liver and increased activation of
proapoptotic JNK signal pathway. Lower DNA damage in stable diabetes, is
accompanied by elevated plasma level of O2
-, restored antioxidative liver enzyme
activity, decreased activation of JNK and increased activation of prosurvival Akt and
ERK signal pathways. Conclusion: These findings indicate that level of DNA damage in
diabetic liver depends on the extent of oxidative stress, antioxidant activity and balance
between JNK and Akt/ERK signal pathways activation.",
publisher = "Karger Publishers",
journal = "Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology",
title = "Activation Level of JNK and Akt/ERK Signaling Pathways Determinates Extent of DNA Damage in the Liver of Diabetic Rats",
number = "3",
volume = "30",
doi = "10.1159/000341452",
pages = "723-734"
}

Martinović, V., Grigorov, I., Bogojević, D., Petrović, A., Jovanović Stojanov, S., Ilić, M.,& Ivanović-Matić, S.. (2012). Activation Level of JNK and Akt/ERK Signaling Pathways Determinates Extent of DNA Damage in the Liver of Diabetic Rats. in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
Karger Publishers., 30(3), 723-734.
https://doi.org/10.1159/000341452

Martinović V, Grigorov I, Bogojević D, Petrović A, Jovanović Stojanov S, Ilić M, Ivanović-Matić S. Activation Level of JNK and Akt/ERK Signaling Pathways Determinates Extent of DNA Damage in the Liver of Diabetic Rats. in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology. 2012;30(3):723-734.
doi:10.1159/000341452 .

Martinović, Vesna, Grigorov, Ilijana, Bogojević, Desanka, Petrović, Anja, Jovanović Stojanov, Sofija, Ilić, Mirka, Ivanović-Matić, Svetlana, "Activation Level of JNK and Akt/ERK Signaling Pathways Determinates Extent of DNA Damage in the Liver of Diabetic Rats" in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 30, no. 3 (2012):723-734,
https://doi.org/10.1159/000341452 . .

TY  - JOUR
AU  - Martinović, Vesna
AU  - Grigorov, Ilijana
AU  - Bogojević, Desanka
AU  - Petrović, Anja
AU  - Jovanović Stojanov, Sofija
AU  - Ilić, Mirka
AU  - Ivanović Matić, Svetlana
PY  - 2012
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/4865
AB  - Aims: Diabetes-related oxidative stress conditions lead to progressive tissue damage and disfunctionality. Mechanisms underlying liver pathophysiology during diabetes are not fully understood. The aim of this study was to find relationship between diabetes-related DNA damage in the rat liver and activities of prosurvival signaling pathways.

Methods: Effect of diabetes was analyzed two (development stage) and eight weeks (stable diabetes) after single intraperitoneal injection of streptozotocin. Extent of DNA damage, analysed by comet assay, was corelated with oxidative status (plasma level of ROS, liver antioxidant capacity) and activity/abundance of kinases (Akt, p38, ERK1, JNK, JAK) and transcription factors NF-κB p65 and STAT3.

Results: Significant DNA damage in development stage is accompanied by elevated plasma levels of O(2)(-) and H(2)O(2), decreased activities of CAT, MnSOD, and GST in the liver and increased activation of proapoptotic JNK signal pathway. Lower DNA damage in stable diabetes, is accompanied by elevated plasma level of O(2)(-), restored antioxidative liver enzyme activity, decreased activation of JNK and increased activation of prosurvival Akt and ERK signal pathways.

Conclusion: These findings indicate that level of DNA damage in diabetic liver depends on the extent of oxidative stress, antioxidant activity and balance between JNK and Akt/ERK signal pathways activation .
PB  - Basel: Krager
T2  - Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
T1  - Activation Level of JNK and Akt/ERK Signaling Pathways Determinates Extent of DNA Damage in the Liver of Diabetic Rats
IS  - 3
VL  - 30
DO  - 10.1159/000341452
SP  - 732
EP  - 734
ER  - 

@article{
author = "Martinović, Vesna and Grigorov, Ilijana and Bogojević, Desanka and Petrović, Anja and Jovanović Stojanov, Sofija and Ilić, Mirka and Ivanović Matić, Svetlana",
year = "2012",
abstract = "Aims: Diabetes-related oxidative stress conditions lead to progressive tissue damage and disfunctionality. Mechanisms underlying liver pathophysiology during diabetes are not fully understood. The aim of this study was to find relationship between diabetes-related DNA damage in the rat liver and activities of prosurvival signaling pathways.

Methods: Effect of diabetes was analyzed two (development stage) and eight weeks (stable diabetes) after single intraperitoneal injection of streptozotocin. Extent of DNA damage, analysed by comet assay, was corelated with oxidative status (plasma level of ROS, liver antioxidant capacity) and activity/abundance of kinases (Akt, p38, ERK1, JNK, JAK) and transcription factors NF-κB p65 and STAT3.

Results: Significant DNA damage in development stage is accompanied by elevated plasma levels of O(2)(-) and H(2)O(2), decreased activities of CAT, MnSOD, and GST in the liver and increased activation of proapoptotic JNK signal pathway. Lower DNA damage in stable diabetes, is accompanied by elevated plasma level of O(2)(-), restored antioxidative liver enzyme activity, decreased activation of JNK and increased activation of prosurvival Akt and ERK signal pathways.

Conclusion: These findings indicate that level of DNA damage in diabetic liver depends on the extent of oxidative stress, antioxidant activity and balance between JNK and Akt/ERK signal pathways activation .",
publisher = "Basel: Krager",
journal = "Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology",
title = "Activation Level of JNK and Akt/ERK Signaling Pathways Determinates Extent of DNA Damage in the Liver of Diabetic Rats",
number = "3",
volume = "30",
doi = "10.1159/000341452",
pages = "732-734"
}

Martinović, V., Grigorov, I., Bogojević, D., Petrović, A., Jovanović Stojanov, S., Ilić, M.,& Ivanović Matić, S.. (2012). Activation Level of JNK and Akt/ERK Signaling Pathways Determinates Extent of DNA Damage in the Liver of Diabetic Rats. in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
Basel: Krager., 30(3), 732-734.
https://doi.org/10.1159/000341452

Martinović V, Grigorov I, Bogojević D, Petrović A, Jovanović Stojanov S, Ilić M, Ivanović Matić S. Activation Level of JNK and Akt/ERK Signaling Pathways Determinates Extent of DNA Damage in the Liver of Diabetic Rats. in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology. 2012;30(3):732-734.
doi:10.1159/000341452 .

Martinović, Vesna, Grigorov, Ilijana, Bogojević, Desanka, Petrović, Anja, Jovanović Stojanov, Sofija, Ilić, Mirka, Ivanović Matić, Svetlana, "Activation Level of JNK and Akt/ERK Signaling Pathways Determinates Extent of DNA Damage in the Liver of Diabetic Rats" in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 30, no. 3 (2012):732-734,
https://doi.org/10.1159/000341452 . .

TY  - JOUR
AU  - Uskoković, Aleksandra
AU  - Dinić, Svetlana
AU  - Mihailović, Mirjana
AU  - Grdović, Nevena
AU  - Arambašić Jovanović, Jelena
AU  - Vidaković, Melita
AU  - Bogojević, Desanka
AU  - Ivanović Matić, Svetlana
AU  - Martinović, Vesna
AU  - Petrović, Miodrag
AU  - Poznanović, Goran
AU  - Grigorov, Ilijana
PY  - 2012
UR  - http://link.springer.com/10.1007/s11033-011-0722-5
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3199
AB  - Haptoglobin is a constitutively expressed protein which is predominantly synthesized in the liver. During the acute-phase (AP) response haptoglobin is upregulated along with other AP proteins. Its upregulation during the AP response is mediated by cis-trans interactions between the hormone-responsive element (HRE) residing in the haptoglobin gene and inducible transcription factors STAT3 and C/EBP beta. In male rats that have been subjected to chronic 50% dietary restriction (DR), the basal haptoglobin serum level is decreased. The aim of this study was to characterize the trans-acting factor(s) responsible for the reduction of haptoglobin expression in male rats subjected to 50% DR for 6 weeks. Protein-DNA interactions between C/EBP and STAT families of transcription factors and the HRE region of the haptoglobin gene were examined in livers of male rats subjected to DR, as well as during the AP response that was induced by turpentine administration. In DR rats, we observed associations between the HRE and C/EBPalpha/beta, STAT5b and NF-kappaB p50, and the absence of interactions between STAT3 and NF-kB p65. Subsequent induction of the AP response in DR rats by turpentine administration elicited a normal, almost 2-fold increase in the serum haptoglobin level that was accompanied by HRE-binding of C/EBPbeta, STAT3/5b and NF-kB p65/p50, and the establishment of interaction between STAT3 and NF-kappaB p65. These results suggest that STAT3 and NF-kappaB p65 crosstalk plays a central role while C/EBPbeta acquires an accessory role in establishing the level of haptoglobin gene expression in male rats exposed to DR and AP stimuli.
PB  - Springer Nature
T2  - Molecular Biology Reports
T1  - STAT3/NF-κB interactions determine the level of haptoglobin expression in male rats exposed to dietary restriction and/or acute phase stimuli
IS  - 1
VL  - 39
DO  - 10.1007/s11033-011-0722-5
SP  - 167
EP  - 176
ER  - 

@article{
author = "Uskoković, Aleksandra and Dinić, Svetlana and Mihailović, Mirjana and Grdović, Nevena and Arambašić Jovanović, Jelena and Vidaković, Melita and Bogojević, Desanka and Ivanović Matić, Svetlana and Martinović, Vesna and Petrović, Miodrag and Poznanović, Goran and Grigorov, Ilijana",
year = "2012",
abstract = "Haptoglobin is a constitutively expressed protein which is predominantly synthesized in the liver. During the acute-phase (AP) response haptoglobin is upregulated along with other AP proteins. Its upregulation during the AP response is mediated by cis-trans interactions between the hormone-responsive element (HRE) residing in the haptoglobin gene and inducible transcription factors STAT3 and C/EBP beta. In male rats that have been subjected to chronic 50% dietary restriction (DR), the basal haptoglobin serum level is decreased. The aim of this study was to characterize the trans-acting factor(s) responsible for the reduction of haptoglobin expression in male rats subjected to 50% DR for 6 weeks. Protein-DNA interactions between C/EBP and STAT families of transcription factors and the HRE region of the haptoglobin gene were examined in livers of male rats subjected to DR, as well as during the AP response that was induced by turpentine administration. In DR rats, we observed associations between the HRE and C/EBPalpha/beta, STAT5b and NF-kappaB p50, and the absence of interactions between STAT3 and NF-kB p65. Subsequent induction of the AP response in DR rats by turpentine administration elicited a normal, almost 2-fold increase in the serum haptoglobin level that was accompanied by HRE-binding of C/EBPbeta, STAT3/5b and NF-kB p65/p50, and the establishment of interaction between STAT3 and NF-kappaB p65. These results suggest that STAT3 and NF-kappaB p65 crosstalk plays a central role while C/EBPbeta acquires an accessory role in establishing the level of haptoglobin gene expression in male rats exposed to DR and AP stimuli.",
publisher = "Springer Nature",
journal = "Molecular Biology Reports",
title = "STAT3/NF-κB interactions determine the level of haptoglobin expression in male rats exposed to dietary restriction and/or acute phase stimuli",
number = "1",
volume = "39",
doi = "10.1007/s11033-011-0722-5",
pages = "167-176"
}

Uskoković, A., Dinić, S., Mihailović, M., Grdović, N., Arambašić Jovanović, J., Vidaković, M., Bogojević, D., Ivanović Matić, S., Martinović, V., Petrović, M., Poznanović, G.,& Grigorov, I.. (2012). STAT3/NF-κB interactions determine the level of haptoglobin expression in male rats exposed to dietary restriction and/or acute phase stimuli. in Molecular Biology Reports
Springer Nature., 39(1), 167-176.
https://doi.org/10.1007/s11033-011-0722-5

Uskoković A, Dinić S, Mihailović M, Grdović N, Arambašić Jovanović J, Vidaković M, Bogojević D, Ivanović Matić S, Martinović V, Petrović M, Poznanović G, Grigorov I. STAT3/NF-κB interactions determine the level of haptoglobin expression in male rats exposed to dietary restriction and/or acute phase stimuli. in Molecular Biology Reports. 2012;39(1):167-176.
doi:10.1007/s11033-011-0722-5 .

Uskoković, Aleksandra, Dinić, Svetlana, Mihailović, Mirjana, Grdović, Nevena, Arambašić Jovanović, Jelena, Vidaković, Melita, Bogojević, Desanka, Ivanović Matić, Svetlana, Martinović, Vesna, Petrović, Miodrag, Poznanović, Goran, Grigorov, Ilijana, "STAT3/NF-κB interactions determine the level of haptoglobin expression in male rats exposed to dietary restriction and/or acute phase stimuli" in Molecular Biology Reports, 39, no. 1 (2012):167-176,
https://doi.org/10.1007/s11033-011-0722-5 . .

TY  - JOUR
AU  - Milošević, Verica
AU  - Ajdžanović, Vladimir
AU  - Bogojević, Desanka
AU  - Jarić, Ivana
AU  - Ivanović Matić, Svetlana
AU  - Martinović, Vesna
AU  - Grigorov, Ilijana
PY  - 2011
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1266
AB  - In peripubertal female rats, we have previously found that 50% food restriction (FR) increases plasma IL-6, haptoglobin and both alanine transaminase (ALT) and alkaline phosphatase (AST) aminotransferases, indicating the existence of an inflammatory response. To study whether such FR influences the hypothalamic-pituitary-adrenal (HPA) axis, we examined by immunohistochemistry the morphofunctional features of pituitary adrenocorticotropic (ACTH) cells. In FR rats the volume and volume density of ACTH cells as well as plasma ACTH levels were increased by 17.6%, 12.5% and 13.4%, respectively, in comparison with controls (p < 0.05). We concluded that chronic FR is a systemic stressor in young females, capable to stimulate the HPA axis, probably as a result of IL-6 action.
T2  - General Physiology and Biophysics
T1  - The effect of chronic food restriction on immunopositive ACTH cells in peripubertal female rats
IS  - 3
VL  - 30
EP  - 324
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1266
ER  - 

@article{
author = "Milošević, Verica and Ajdžanović, Vladimir and Bogojević, Desanka and Jarić, Ivana and Ivanović Matić, Svetlana and Martinović, Vesna and Grigorov, Ilijana",
year = "2011",
abstract = "In peripubertal female rats, we have previously found that 50% food restriction (FR) increases plasma IL-6, haptoglobin and both alanine transaminase (ALT) and alkaline phosphatase (AST) aminotransferases, indicating the existence of an inflammatory response. To study whether such FR influences the hypothalamic-pituitary-adrenal (HPA) axis, we examined by immunohistochemistry the morphofunctional features of pituitary adrenocorticotropic (ACTH) cells. In FR rats the volume and volume density of ACTH cells as well as plasma ACTH levels were increased by 17.6%, 12.5% and 13.4%, respectively, in comparison with controls (p < 0.05). We concluded that chronic FR is a systemic stressor in young females, capable to stimulate the HPA axis, probably as a result of IL-6 action.",
journal = "General Physiology and Biophysics",
title = "The effect of chronic food restriction on immunopositive ACTH cells in peripubertal female rats",
number = "3",
volume = "30",
pages = "324",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1266"
}

Milošević, V., Ajdžanović, V., Bogojević, D., Jarić, I., Ivanović Matić, S., Martinović, V.,& Grigorov, I.. (2011). The effect of chronic food restriction on immunopositive ACTH cells in peripubertal female rats. in General Physiology and Biophysics, 30(3).
https://hdl.handle.net/21.15107/rcub_ibiss_1266

Milošević V, Ajdžanović V, Bogojević D, Jarić I, Ivanović Matić S, Martinović V, Grigorov I. The effect of chronic food restriction on immunopositive ACTH cells in peripubertal female rats. in General Physiology and Biophysics. 2011;30(3):null-324.
https://hdl.handle.net/21.15107/rcub_ibiss_1266 .

Milošević, Verica, Ajdžanović, Vladimir, Bogojević, Desanka, Jarić, Ivana, Ivanović Matić, Svetlana, Martinović, Vesna, Grigorov, Ilijana, "The effect of chronic food restriction on immunopositive ACTH cells in peripubertal female rats" in General Physiology and Biophysics, 30, no. 3 (2011),
https://hdl.handle.net/21.15107/rcub_ibiss_1266 .

TY  - JOUR
AU  - Arambašić Jovanović, Jelena
AU  - Poznanović, Goran
AU  - Ivanović-Matić, Svetlana
AU  - Bogojević, Desanka
AU  - Mihailović, Mirjana
AU  - Uskoković, Aleksandra
AU  - Grigorov, Ilijana
PY  - 2010
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6148
AB  - Upregulation of haptoglobin (Hp) expression in the rat during the acute phase (AP) response is the result of synergistic effects of IL-6–, IL-1β–, and corticosterone-activated signaling pathways. IL-6 signaling terminates in cis–trans interactions of the Hp gene hormone-responsive element (HRE) with transcription factors STAT3 and C/EBPβ. The aim of this study was to examine the unresolved molecular mechanism of glucocorticoid action. A 3-fold rise in serum corticosterone at 2 and 4 h of the AP response induced by turpentine administration preceded a 2.3-fold increase in the rate of Hp gene transcription at 12 h that was accompanied by a 4.8-fold increase in glucocorticoid receptor (GR), the appearance of an 86-kDa STAT3 isoform and 3.9-, 1.9-, and 1.7-fold increased amounts of 91-kDa STAT3, 35- and 42-kDa C/EBPβ isoforms in the nucleus. These events resulted in 4.6- and 2.5-fold increased Hp levels in the liver and serum at 24 h. HRE affinity chromatography and immunoblot analysis revealed that maximal occupancy of the HRE with GR, STAT3, and C/EBPβ at 12 h correlated with increased transcriptional activity of the Hp gene. Coimmunoprecipitation experiments showed that activated GR established de novo interaction with STAT3 isoforms while GR–C/EBPβ interactions observed during basal transcription increased during the AP response. Computer analysis of the HRE disclosed two potential GR-binding sites: one overlapping STAT3, another adjacent to a C/EBPβ-binding site. This finding and the experimental results suggest that activated GR through direct interactions with STAT3 and C/EBPβ, participates in Hp gene upregulation as a transcriptional coactivator.
PB  - Wiley
T2  - IUBMB Life
T1  - Association of the glucocorticoid receptor with STAT3, C/EBPβ, and the hormone-responsive element within the rat haptoglobin gene promoter during the acute phase response
IS  - 3
VL  - 62
DO  - 10.1002/iub.313
SP  - 227
EP  - 236
ER  - 

@article{
author = "Arambašić Jovanović, Jelena and Poznanović, Goran and Ivanović-Matić, Svetlana and Bogojević, Desanka and Mihailović, Mirjana and Uskoković, Aleksandra and Grigorov, Ilijana",
year = "2010",
abstract = "Upregulation of haptoglobin (Hp) expression in the rat during the acute phase (AP) response is the result of synergistic effects of IL-6–, IL-1β–, and corticosterone-activated signaling pathways. IL-6 signaling terminates in cis–trans interactions of the Hp gene hormone-responsive element (HRE) with transcription factors STAT3 and C/EBPβ. The aim of this study was to examine the unresolved molecular mechanism of glucocorticoid action. A 3-fold rise in serum corticosterone at 2 and 4 h of the AP response induced by turpentine administration preceded a 2.3-fold increase in the rate of Hp gene transcription at 12 h that was accompanied by a 4.8-fold increase in glucocorticoid receptor (GR), the appearance of an 86-kDa STAT3 isoform and 3.9-, 1.9-, and 1.7-fold increased amounts of 91-kDa STAT3, 35- and 42-kDa C/EBPβ isoforms in the nucleus. These events resulted in 4.6- and 2.5-fold increased Hp levels in the liver and serum at 24 h. HRE affinity chromatography and immunoblot analysis revealed that maximal occupancy of the HRE with GR, STAT3, and C/EBPβ at 12 h correlated with increased transcriptional activity of the Hp gene. Coimmunoprecipitation experiments showed that activated GR established de novo interaction with STAT3 isoforms while GR–C/EBPβ interactions observed during basal transcription increased during the AP response. Computer analysis of the HRE disclosed two potential GR-binding sites: one overlapping STAT3, another adjacent to a C/EBPβ-binding site. This finding and the experimental results suggest that activated GR through direct interactions with STAT3 and C/EBPβ, participates in Hp gene upregulation as a transcriptional coactivator.",
publisher = "Wiley",
journal = "IUBMB Life",
title = "Association of the glucocorticoid receptor with STAT3, C/EBPβ, and the hormone-responsive element within the rat haptoglobin gene promoter during the acute phase response",
number = "3",
volume = "62",
doi = "10.1002/iub.313",
pages = "227-236"
}

Arambašić Jovanović, J., Poznanović, G., Ivanović-Matić, S., Bogojević, D., Mihailović, M., Uskoković, A.,& Grigorov, I.. (2010). Association of the glucocorticoid receptor with STAT3, C/EBPβ, and the hormone-responsive element within the rat haptoglobin gene promoter during the acute phase response. in IUBMB Life
Wiley., 62(3), 227-236.
https://doi.org/10.1002/iub.313

Arambašić Jovanović J, Poznanović G, Ivanović-Matić S, Bogojević D, Mihailović M, Uskoković A, Grigorov I. Association of the glucocorticoid receptor with STAT3, C/EBPβ, and the hormone-responsive element within the rat haptoglobin gene promoter during the acute phase response. in IUBMB Life. 2010;62(3):227-236.
doi:10.1002/iub.313 .

Arambašić Jovanović, Jelena, Poznanović, Goran, Ivanović-Matić, Svetlana, Bogojević, Desanka, Mihailović, Mirjana, Uskoković, Aleksandra, Grigorov, Ilijana, "Association of the glucocorticoid receptor with STAT3, C/EBPβ, and the hormone-responsive element within the rat haptoglobin gene promoter during the acute phase response" in IUBMB Life, 62, no. 3 (2010):227-236,
https://doi.org/10.1002/iub.313 . .

TY  - CONF
AU  - Milošević, Verica
AU  - Ajdžanović, Vladimir
AU  - Trifunović, Svetlana
AU  - Bogojević, Desanka
AU  - Ivanović-Matić, Svetlana
AU  - Martinović, Vesna
AU  - Grigorov, Ilijana
PY  - 2010
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6100
AB  - Dietary restriction (DR) in female rats pre­ sumably activates the stress (hypothalamo-pituitary­ adrenal) system. It's well known that various pituitary cell types are involved in the reaction to stress, i.e. adrenocorticotropic hormone (ACTH), prolactin and growth hormone cells. The aim of this study was to examine the effects of DR on the immunohistomor­ phometric features of pituitary ACTH cells and blood levels of ACTH. Peripubertal (38 days old) female Wistar rats were housed one per cage, under standard environmental conditions (12 h light/dark cycle, 22  ±
2  °C)  with  food  and  water  ad libitum. ·Experimental
females were fed with 50% of the total amount of food consumed by the controls, during 6 weeks. The ACTH cells were stained using the peroxidase-antiperoxidase immunohistochemical procedure and stereological analyses were conducted. The blood ACTH was measured by radioimmunoassay (ACTH-IMMULITE kit).   In   the   experimental   group   body   weight was (p<0.05) decreased by 48.8%, while the relative pituitary weight was (p<0.05) increased by 76 .9% in comparison   with   corresponding   parameters   ir1 controls . The volume of ACTH cells, as well as their volume density was significantly increased (p< 0.05 ) in the experimental group, by 17 .6% and 1 2.5% respectively. The blood ACTH level was increased (p<0.05) in experimental group by  13.4% .  Our findings show that the DR in peripubertal female rats stimulates the stress system, which was confirmed by increased morphofunctional parameters of ACTH ce lls .
.
PB  - Belgrade: Society of Medical Biochemists of Serbia
C3  - 17th Congress of Medical Biochemistry and Laboratory Medicine, with international participations, 6th EFCC Symposium for Balkan Region; 2010 Oct 5-9; Belgrade, Serbia.
T1  - Dietary restriction affectsS ACTH Cells of peripubertal female rats
SP  - 454
EP  - 455
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_6100
ER  - 

@conference{
author = "Milošević, Verica and Ajdžanović, Vladimir and Trifunović, Svetlana and Bogojević, Desanka and Ivanović-Matić, Svetlana and Martinović, Vesna and Grigorov, Ilijana",
year = "2010",
abstract = "Dietary restriction (DR) in female rats pre­ sumably activates the stress (hypothalamo-pituitary­ adrenal) system. It's well known that various pituitary cell types are involved in the reaction to stress, i.e. adrenocorticotropic hormone (ACTH), prolactin and growth hormone cells. The aim of this study was to examine the effects of DR on the immunohistomor­ phometric features of pituitary ACTH cells and blood levels of ACTH. Peripubertal (38 days old) female Wistar rats were housed one per cage, under standard environmental conditions (12 h light/dark cycle, 22  ±
2  °C)  with  food  and  water  ad libitum. ·Experimental
females were fed with 50% of the total amount of food consumed by the controls, during 6 weeks. The ACTH cells were stained using the peroxidase-antiperoxidase immunohistochemical procedure and stereological analyses were conducted. The blood ACTH was measured by radioimmunoassay (ACTH-IMMULITE kit).   In   the   experimental   group   body   weight was (p<0.05) decreased by 48.8%, while the relative pituitary weight was (p<0.05) increased by 76 .9% in comparison   with   corresponding   parameters   ir1 controls . The volume of ACTH cells, as well as their volume density was significantly increased (p< 0.05 ) in the experimental group, by 17 .6% and 1 2.5% respectively. The blood ACTH level was increased (p<0.05) in experimental group by  13.4% .  Our findings show that the DR in peripubertal female rats stimulates the stress system, which was confirmed by increased morphofunctional parameters of ACTH ce lls .
.",
publisher = "Belgrade: Society of Medical Biochemists of Serbia",
journal = "17th Congress of Medical Biochemistry and Laboratory Medicine, with international participations, 6th EFCC Symposium for Balkan Region; 2010 Oct 5-9; Belgrade, Serbia.",
title = "Dietary restriction affectsS ACTH Cells of peripubertal female rats",
pages = "454-455",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_6100"
}

Milošević, V., Ajdžanović, V., Trifunović, S., Bogojević, D., Ivanović-Matić, S., Martinović, V.,& Grigorov, I.. (2010). Dietary restriction affectsS ACTH Cells of peripubertal female rats. in 17th Congress of Medical Biochemistry and Laboratory Medicine, with international participations, 6th EFCC Symposium for Balkan Region; 2010 Oct 5-9; Belgrade, Serbia.
Belgrade: Society of Medical Biochemists of Serbia., 454-455.
https://hdl.handle.net/21.15107/rcub_ibiss_6100

Milošević V, Ajdžanović V, Trifunović S, Bogojević D, Ivanović-Matić S, Martinović V, Grigorov I. Dietary restriction affectsS ACTH Cells of peripubertal female rats. in 17th Congress of Medical Biochemistry and Laboratory Medicine, with international participations, 6th EFCC Symposium for Balkan Region; 2010 Oct 5-9; Belgrade, Serbia.. 2010;:454-455.
https://hdl.handle.net/21.15107/rcub_ibiss_6100 .

Milošević, Verica, Ajdžanović, Vladimir, Trifunović, Svetlana, Bogojević, Desanka, Ivanović-Matić, Svetlana, Martinović, Vesna, Grigorov, Ilijana, "Dietary restriction affectsS ACTH Cells of peripubertal female rats" in 17th Congress of Medical Biochemistry and Laboratory Medicine, with international participations, 6th EFCC Symposium for Balkan Region; 2010 Oct 5-9; Belgrade, Serbia. (2010):454-455,
https://hdl.handle.net/21.15107/rcub_ibiss_6100 .

TY  - JOUR
AU  - Mihailović, Mirjana
AU  - Grdović, Nevena
AU  - Dinić, Svetlana
AU  - Uskoković, Aleksandra
AU  - Vidaković, Melita
AU  - Grigorov, Ilijana
AU  - Bogojević, Desanka
AU  - Ivanović Matić, Svetlana
AU  - Petrović, Miodrag
AU  - Labus-Blagojević, Svetlana
AU  - Martinović, Vesna
AU  - Arambašić Jovanović, Jelena
AU  - Poznanović, Goran
PY  - 2010
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1342
AB  - Background and Purpose CYP1A is one of the most sensitive biomarkers in fish of exposure to polycyclic aromatic hydrocarbons (PAHs) and polychlorinated biphenyls (PCBs) These compounds induce a dose-dependent transcriptional induction of the CYP1A gene that results in increased protein concentrations The aim of this study was the detection of changes in CYP1A protein levels as a result of the exposure of fish to PAHs and PCBs at the mouth of the river Bojana in the spring Materials and Methods The PAH and PCB contents in seawater and sediment were determined by gas chromatography CYP1A induction was examined in the hepatopancreas of Red mullet (Mullus barbatus), European hake (Merluccius merluccius) and Tub gurnard (Trigla lucerna) by immunoblot analysis Results and Conclusions Chemical analyses of seawater and sediment revealed the presence of several PAHs and PCBs CYP1A was detected in the hepatic microsomal fraction in all examined fish species as an adaptive response to the presence of pollutants The reported changes at the molecular level represent an early-warning signal that reflected the biological response of fish to elevated toxin concentrations in the environment
PB  - Zagreb: Hrvatsko prirodoslovno društvo
T2  - Periodicum Biologorum
T1  - CYP1A expression in the hepatopancreas of Mullus barbatus, Merluccius merluccius and Trigla lucerna at the mouth of the river Bojana
IS  - 2
VL  - 112
SP  - 167
EP  - 171
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1342
ER  - 

@article{
author = "Mihailović, Mirjana and Grdović, Nevena and Dinić, Svetlana and Uskoković, Aleksandra and Vidaković, Melita and Grigorov, Ilijana and Bogojević, Desanka and Ivanović Matić, Svetlana and Petrović, Miodrag and Labus-Blagojević, Svetlana and Martinović, Vesna and Arambašić Jovanović, Jelena and Poznanović, Goran",
year = "2010",
abstract = "Background and Purpose CYP1A is one of the most sensitive biomarkers in fish of exposure to polycyclic aromatic hydrocarbons (PAHs) and polychlorinated biphenyls (PCBs) These compounds induce a dose-dependent transcriptional induction of the CYP1A gene that results in increased protein concentrations The aim of this study was the detection of changes in CYP1A protein levels as a result of the exposure of fish to PAHs and PCBs at the mouth of the river Bojana in the spring Materials and Methods The PAH and PCB contents in seawater and sediment were determined by gas chromatography CYP1A induction was examined in the hepatopancreas of Red mullet (Mullus barbatus), European hake (Merluccius merluccius) and Tub gurnard (Trigla lucerna) by immunoblot analysis Results and Conclusions Chemical analyses of seawater and sediment revealed the presence of several PAHs and PCBs CYP1A was detected in the hepatic microsomal fraction in all examined fish species as an adaptive response to the presence of pollutants The reported changes at the molecular level represent an early-warning signal that reflected the biological response of fish to elevated toxin concentrations in the environment",
publisher = "Zagreb: Hrvatsko prirodoslovno društvo",
journal = "Periodicum Biologorum",
title = "CYP1A expression in the hepatopancreas of Mullus barbatus, Merluccius merluccius and Trigla lucerna at the mouth of the river Bojana",
number = "2",
volume = "112",
pages = "167-171",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1342"
}

Mihailović, M., Grdović, N., Dinić, S., Uskoković, A., Vidaković, M., Grigorov, I., Bogojević, D., Ivanović Matić, S., Petrović, M., Labus-Blagojević, S., Martinović, V., Arambašić Jovanović, J.,& Poznanović, G.. (2010). CYP1A expression in the hepatopancreas of Mullus barbatus, Merluccius merluccius and Trigla lucerna at the mouth of the river Bojana. in Periodicum Biologorum
Zagreb: Hrvatsko prirodoslovno društvo., 112(2), 167-171.
https://hdl.handle.net/21.15107/rcub_ibiss_1342

Mihailović M, Grdović N, Dinić S, Uskoković A, Vidaković M, Grigorov I, Bogojević D, Ivanović Matić S, Petrović M, Labus-Blagojević S, Martinović V, Arambašić Jovanović J, Poznanović G. CYP1A expression in the hepatopancreas of Mullus barbatus, Merluccius merluccius and Trigla lucerna at the mouth of the river Bojana. in Periodicum Biologorum. 2010;112(2):167-171.
https://hdl.handle.net/21.15107/rcub_ibiss_1342 .

Mihailović, Mirjana, Grdović, Nevena, Dinić, Svetlana, Uskoković, Aleksandra, Vidaković, Melita, Grigorov, Ilijana, Bogojević, Desanka, Ivanović Matić, Svetlana, Petrović, Miodrag, Labus-Blagojević, Svetlana, Martinović, Vesna, Arambašić Jovanović, Jelena, Poznanović, Goran, "CYP1A expression in the hepatopancreas of Mullus barbatus, Merluccius merluccius and Trigla lucerna at the mouth of the river Bojana" in Periodicum Biologorum, 112, no. 2 (2010):167-171,
https://hdl.handle.net/21.15107/rcub_ibiss_1342 .

TY  - JOUR
AU  - Mihailović, Mirjana
AU  - Petrović, Miodrag
AU  - Grdović, Nevena
AU  - Dinić, Svetlana
AU  - Uskoković, Aleksandra
AU  - Vidaković, Melita
AU  - Grigorov, Ilijana
AU  - Bogojević, Desanka
AU  - Ivanović Matić, Svetlana
AU  - Martinović, Vesna
AU  - Arambašić Jovanović, Jelena
AU  - Joksimović, Danijela
AU  - Labus-Blagojević, Svetlana
AU  - Poznanović, Goran
PY  - 2010
PY  - 2010
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/561
AB  - The enzyme CYP1A is an established biomarker of fish exposure to polycyclic aromatic hydrocarbons (PAHs) and polychlorinated biphenyls (PCBs). The metallothioneins (MT), a family of Cys-rich proteins, bind a wide range of metals and participate in their metabolism. The aim of the study was to examine the correlation between CYP1A and MT expression in commercially important fish species Mullus barbatus and Merluccius merluccius and contaminants (PAHs, PCBs, toxic metals) in seawater and sediment from three localities with different level of contamination in the Adriatic Sea in winter, i.e., Platamuni, Valdanos and the port of Bar. The relative concentration of CYP1A was the highest in both fish species from Bar. Increased concentrations of PCBs in the seawater were observed only in Bar. A species-specific higher increase in the protein concentration of CYP1A was observed in Mullus barbatus compared to Merluccius merluccius. The levels of MT were the highest in Merluccius merluccius from Bar and in Mullus barbatus from Valdanos. The induction of MT correlated with the elevated concentrations of Cu and Pb determined by chemical analysis of the seawater from Bar and Valdanos, respectively. According to the chemical analysis of the seawater and the biological response of the fish, the Platamuni locality exhibited the lowest level of contamination.
AB  - CYP1A predstavlja dobro okarakterisan biomarker kod riba pri izlaganju policikličnim aromatičnim ugljovodonicima (PAH) i policikličnim bifeholima (PCB). Metalotioneini (MT) pretstavljaju familiju proteina koji vezuju metale i učestvuju u njihovoj metabolizmu, transportu i regulaciji. Cilj ovog rada je bio da se ispitaju korelacije između promena u nivou CYP1A i MT u hepatopankreasu dve komercijalno važne ribe: Mullus barbatus (trlja) i Merluccius merluccius (oslić) i kontaminanatata: PAH, PCB i toksičnih metala) na tri lokaliteta u Jadrnskom moru (Platamuni, Valdanos i luka Bar) u zimu. CYP1A je u najvećem stepenu indukovan na lokalitetu Bar u obe ispitivane vrste, što je u korelaciji sa prisustvom povećane količine PCB u morskoj vodi u Baru. Nivo MT je najveći kod oslića izlovljenog u Baru, a kod trlje u Valdanosu. To je u korelaciji sa izmerenim povećanim koncentracijama bakra u Baru, a olova u Valdanosu. Na osnovu izučavanih parametara, Platamuni su lokalitet sa najmanjim stepenom kontaminacije.
PB  - Belgrade: Serbian Chemical Society
T2  - Journal of the Serbian Chemical Society
T1  - Ekspresija CYPLA i metalotioneina u hepatopankreasu oslića i trlje iz Jadranskog mora
T1  - CYP1A and metallothionein expression in the hepatopancreas of merluccius merluccius and mullus barbatus from the Adriatic sea
IS  - 8
VL  - 75
DO  - 10.2298/JSC091029083M
SP  - 1149
EP  - 1159
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_561
ER  - 

@article{
author = "Mihailović, Mirjana and Petrović, Miodrag and Grdović, Nevena and Dinić, Svetlana and Uskoković, Aleksandra and Vidaković, Melita and Grigorov, Ilijana and Bogojević, Desanka and Ivanović Matić, Svetlana and Martinović, Vesna and Arambašić Jovanović, Jelena and Joksimović, Danijela and Labus-Blagojević, Svetlana and Poznanović, Goran",
year = "2010, 2010",
abstract = "The enzyme CYP1A is an established biomarker of fish exposure to polycyclic aromatic hydrocarbons (PAHs) and polychlorinated biphenyls (PCBs). The metallothioneins (MT), a family of Cys-rich proteins, bind a wide range of metals and participate in their metabolism. The aim of the study was to examine the correlation between CYP1A and MT expression in commercially important fish species Mullus barbatus and Merluccius merluccius and contaminants (PAHs, PCBs, toxic metals) in seawater and sediment from three localities with different level of contamination in the Adriatic Sea in winter, i.e., Platamuni, Valdanos and the port of Bar. The relative concentration of CYP1A was the highest in both fish species from Bar. Increased concentrations of PCBs in the seawater were observed only in Bar. A species-specific higher increase in the protein concentration of CYP1A was observed in Mullus barbatus compared to Merluccius merluccius. The levels of MT were the highest in Merluccius merluccius from Bar and in Mullus barbatus from Valdanos. The induction of MT correlated with the elevated concentrations of Cu and Pb determined by chemical analysis of the seawater from Bar and Valdanos, respectively. According to the chemical analysis of the seawater and the biological response of the fish, the Platamuni locality exhibited the lowest level of contamination., CYP1A predstavlja dobro okarakterisan biomarker kod riba pri izlaganju policikličnim aromatičnim ugljovodonicima (PAH) i policikličnim bifeholima (PCB). Metalotioneini (MT) pretstavljaju familiju proteina koji vezuju metale i učestvuju u njihovoj metabolizmu, transportu i regulaciji. Cilj ovog rada je bio da se ispitaju korelacije između promena u nivou CYP1A i MT u hepatopankreasu dve komercijalno važne ribe: Mullus barbatus (trlja) i Merluccius merluccius (oslić) i kontaminanatata: PAH, PCB i toksičnih metala) na tri lokaliteta u Jadrnskom moru (Platamuni, Valdanos i luka Bar) u zimu. CYP1A je u najvećem stepenu indukovan na lokalitetu Bar u obe ispitivane vrste, što je u korelaciji sa prisustvom povećane količine PCB u morskoj vodi u Baru. Nivo MT je najveći kod oslića izlovljenog u Baru, a kod trlje u Valdanosu. To je u korelaciji sa izmerenim povećanim koncentracijama bakra u Baru, a olova u Valdanosu. Na osnovu izučavanih parametara, Platamuni su lokalitet sa najmanjim stepenom kontaminacije.",
publisher = "Belgrade: Serbian Chemical Society",
journal = "Journal of the Serbian Chemical Society",
title = "Ekspresija CYPLA i metalotioneina u hepatopankreasu oslića i trlje iz Jadranskog mora, CYP1A and metallothionein expression in the hepatopancreas of merluccius merluccius and mullus barbatus from the Adriatic sea",
number = "8",
volume = "75",
doi = "10.2298/JSC091029083M",
pages = "1149-1159",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_561"
}

Mihailović, M., Petrović, M., Grdović, N., Dinić, S., Uskoković, A., Vidaković, M., Grigorov, I., Bogojević, D., Ivanović Matić, S., Martinović, V., Arambašić Jovanović, J., Joksimović, D., Labus-Blagojević, S.,& Poznanović, G.. (2010). Ekspresija CYPLA i metalotioneina u hepatopankreasu oslića i trlje iz Jadranskog mora. in Journal of the Serbian Chemical Society
Belgrade: Serbian Chemical Society., 75(8), 1149-1159.
https://doi.org/10.2298/JSC091029083M
https://hdl.handle.net/21.15107/rcub_ibiss_561

Mihailović M, Petrović M, Grdović N, Dinić S, Uskoković A, Vidaković M, Grigorov I, Bogojević D, Ivanović Matić S, Martinović V, Arambašić Jovanović J, Joksimović D, Labus-Blagojević S, Poznanović G. Ekspresija CYPLA i metalotioneina u hepatopankreasu oslića i trlje iz Jadranskog mora. in Journal of the Serbian Chemical Society. 2010;75(8):1149-1159.
doi:10.2298/JSC091029083M
https://hdl.handle.net/21.15107/rcub_ibiss_561 .

Mihailović, Mirjana, Petrović, Miodrag, Grdović, Nevena, Dinić, Svetlana, Uskoković, Aleksandra, Vidaković, Melita, Grigorov, Ilijana, Bogojević, Desanka, Ivanović Matić, Svetlana, Martinović, Vesna, Arambašić Jovanović, Jelena, Joksimović, Danijela, Labus-Blagojević, Svetlana, Poznanović, Goran, "Ekspresija CYPLA i metalotioneina u hepatopankreasu oslića i trlje iz Jadranskog mora" in Journal of the Serbian Chemical Society, 75, no. 8 (2010):1149-1159,
https://doi.org/10.2298/JSC091029083M .,
https://hdl.handle.net/21.15107/rcub_ibiss_561 .