TY  - CHAP
AU  - Jelenković, Ankica
AU  - Jovanović, Marina D.
AU  - Petronijević, Nataša
AU  - Lepić, Toplica
PY  - 2016
UR  - https://www.novapublishers.com/catalog/product_info.php?products_id=59851&osCsid=8e6df2fe6f876c8f3f77799c9f9187b2
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2627
AB  - Numerous research studies have undoubtedly shown that aluminium is a very harmful substance which enters the human body externally from the environment. The aluminum intake usually happens unintentionally, due to the fact that people know little about its prevalence in water, factory-processed foods, medicines, cosmetics, etc. When accumulated in human organs, it can cause severe damage, and even lead to chronic neurodegenerative diseases, including Alzheimer‘s disease. The extent to which nitric oxide (NO) is involved in the basic mechanisms of aluminum neurotoxicity, like oxidative stress and the antioxidant defense, is intriguing scientific community. In this chapter are presented results of the intrahippocampal application of aluminum chloride and a pretreatment with Nω-nitro-L-arginine methyl ester (L-NAME), the non-selective inhibitor of nitric oxide synthase activities. It turned out that, in order to avoid erroneous conclusions about NO not being involved in aluminium-induced neurotoxicity, it was necessary to titrate the dose of L-NAME (1, 10 and 100 micrograms). Among the three doses applied prior to the application of aluminum, only the highest dose acted as an antioxidant in the four examined brain structures.
PB  - Nova Science Publishers
T2  - Aluminum Neurotoxicity: From Subtle Molecular Lesions to Neurological Diseases
T1  - The Protective and Dose-Dependent Effects of L-Name in Aluminium-Induced Neurotoxicity
SP  - 69
EP  - 90
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_2627
ER  - 

@inbook{
editor = "Jelenković, Ankica",
author = "Jelenković, Ankica and Jovanović, Marina D. and Petronijević, Nataša and Lepić, Toplica",
year = "2016",
abstract = "Numerous research studies have undoubtedly shown that aluminium is a very harmful substance which enters the human body externally from the environment. The aluminum intake usually happens unintentionally, due to the fact that people know little about its prevalence in water, factory-processed foods, medicines, cosmetics, etc. When accumulated in human organs, it can cause severe damage, and even lead to chronic neurodegenerative diseases, including Alzheimer‘s disease. The extent to which nitric oxide (NO) is involved in the basic mechanisms of aluminum neurotoxicity, like oxidative stress and the antioxidant defense, is intriguing scientific community. In this chapter are presented results of the intrahippocampal application of aluminum chloride and a pretreatment with Nω-nitro-L-arginine methyl ester (L-NAME), the non-selective inhibitor of nitric oxide synthase activities. It turned out that, in order to avoid erroneous conclusions about NO not being involved in aluminium-induced neurotoxicity, it was necessary to titrate the dose of L-NAME (1, 10 and 100 micrograms). Among the three doses applied prior to the application of aluminum, only the highest dose acted as an antioxidant in the four examined brain structures.",
publisher = "Nova Science Publishers",
journal = "Aluminum Neurotoxicity: From Subtle Molecular Lesions to Neurological Diseases",
booktitle = "The Protective and Dose-Dependent Effects of L-Name in Aluminium-Induced Neurotoxicity",
pages = "69-90",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_2627"
}

Jelenković, A., Jelenković, A., Jovanović, M. D., Petronijević, N.,& Lepić, T.. (2016). The Protective and Dose-Dependent Effects of L-Name in Aluminium-Induced Neurotoxicity. in Aluminum Neurotoxicity: From Subtle Molecular Lesions to Neurological Diseases
Nova Science Publishers., 69-90.
https://hdl.handle.net/21.15107/rcub_ibiss_2627

Jelenković A, Jelenković A, Jovanović MD, Petronijević N, Lepić T. The Protective and Dose-Dependent Effects of L-Name in Aluminium-Induced Neurotoxicity. in Aluminum Neurotoxicity: From Subtle Molecular Lesions to Neurological Diseases. 2016;:69-90.
https://hdl.handle.net/21.15107/rcub_ibiss_2627 .

Jelenković, Ankica, Jelenković, Ankica, Jovanović, Marina D., Petronijević, Nataša, Lepić, Toplica, "The Protective and Dose-Dependent Effects of L-Name in Aluminium-Induced Neurotoxicity" in Aluminum Neurotoxicity: From Subtle Molecular Lesions to Neurological Diseases (2016):69-90,
https://hdl.handle.net/21.15107/rcub_ibiss_2627 .

TY  - CHAP
AU  - Jelenković, Ankica
AU  - Jovanović, Marina D.
AU  - Petronijević, Nataša
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2567
UR  - https://www.novapublishers.com/catalog/product_info.php?products_id=54968
AB  - Diets have attracted great interest on the account of growing evidence of their beneficial effects on human health. Green tea has been used for a very long time as a folk remedy for a wide array of diseases. The well-known green tea beverage is made from a plant Camellia sinensis. The healthy properties of green tea are linked closely to its content of phenolic compounds, particularly to the (-)-epigallocatechin-3-gallate. It has been proposed that green tea may have a beneficial impact on a number of brain functions, as well as on neurodegenerative disorder prevention in humans and in various animal models, including Alzheimer's disease (AD). A large number of scientific studies have supported some of these assumptions. In the case of AD, aluminium may have an important role in the disease aetiology/pathogenesis/precipitation. However, aluminium has biological effects in the green tea plant, where it is a cofactor for polyphenol biosynthesis. Consequently, leaves of green tea accumulate and store large quantities of this element during the plant growth. Thus, it was intriguing whether the unilateral intrahippocampal application of green tea leaf extract (GTLE) and aluminium chloride would have any interaction, measured by the biochemical parameters in six brain structures: the forebrain cortex, striatum, basal forebrain, hippocampus, brain stem and cerebellum, of the adult male Wistar rats. It was found that GTLE given alone demonstrated biochemical effects not only in the ipsilateral hippocampus, but also spread into the five other examined structures at the same side, as well as into the identical brain structures on the contralateral hemisphere. In fact, there were no differences in the activity of superoxide dismutase, cytochrome c oxidase (COX) and acetylcholinesterase (AChE) between the right and the corresponding left brain structures. Moreover, the activity of COX and AChE were significantly higher when compared to the control group. Out of the three observed parameters, the content of reduced glutathione (GSH), superoxide anion and nitrites, aluminium itself demonstrated the strongest effects towards GSH, which was significantly reduced in all structures, compared to the control group. The changes were identical in the ipsi- and contralateral corresponding structures. Howewer, the application of GTLE just before aluminium prevented the reduction of GSH induced by aluminium, and significantly increased its content compared to the control group. Also, the content of superoxide anion was significantly reduced in most structures compared to the control, and to the aluminium-treated group as well. The obtained results of GTE in the aluminium-induced neurotoxicity are in accordance with the antioxidant effects of GTLE. Also, it is clear that GTE administered alone did not demonstrate neurotoxic effects as did the solution of aluminium chloride, but, on the contrary, showed the opposite, neuroprotective effects. To sum up, GTLE has proved to manifest strong antioxidant effects in the brain of healthy rats, and in the cases of neurotoxicity induced by aluminum, as well.
PB  - Nova Science Publishers, Inc., New York
T2  - Green tea and health: antioxidant properties, consumption and role in disease prevention
T1  - The protective effects of intrahippocampal application of green tea leaf extract on aluminium-induced brain toxicity
SP  - 33
EP  - 56
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_2567
ER  - 

@inbook{
editor = "Powell, Nicolas",
author = "Jelenković, Ankica and Jovanović, Marina D. and Petronijević, Nataša",
year = "2015",
abstract = "Diets have attracted great interest on the account of growing evidence of their beneficial effects on human health. Green tea has been used for a very long time as a folk remedy for a wide array of diseases. The well-known green tea beverage is made from a plant Camellia sinensis. The healthy properties of green tea are linked closely to its content of phenolic compounds, particularly to the (-)-epigallocatechin-3-gallate. It has been proposed that green tea may have a beneficial impact on a number of brain functions, as well as on neurodegenerative disorder prevention in humans and in various animal models, including Alzheimer's disease (AD). A large number of scientific studies have supported some of these assumptions. In the case of AD, aluminium may have an important role in the disease aetiology/pathogenesis/precipitation. However, aluminium has biological effects in the green tea plant, where it is a cofactor for polyphenol biosynthesis. Consequently, leaves of green tea accumulate and store large quantities of this element during the plant growth. Thus, it was intriguing whether the unilateral intrahippocampal application of green tea leaf extract (GTLE) and aluminium chloride would have any interaction, measured by the biochemical parameters in six brain structures: the forebrain cortex, striatum, basal forebrain, hippocampus, brain stem and cerebellum, of the adult male Wistar rats. It was found that GTLE given alone demonstrated biochemical effects not only in the ipsilateral hippocampus, but also spread into the five other examined structures at the same side, as well as into the identical brain structures on the contralateral hemisphere. In fact, there were no differences in the activity of superoxide dismutase, cytochrome c oxidase (COX) and acetylcholinesterase (AChE) between the right and the corresponding left brain structures. Moreover, the activity of COX and AChE were significantly higher when compared to the control group. Out of the three observed parameters, the content of reduced glutathione (GSH), superoxide anion and nitrites, aluminium itself demonstrated the strongest effects towards GSH, which was significantly reduced in all structures, compared to the control group. The changes were identical in the ipsi- and contralateral corresponding structures. Howewer, the application of GTLE just before aluminium prevented the reduction of GSH induced by aluminium, and significantly increased its content compared to the control group. Also, the content of superoxide anion was significantly reduced in most structures compared to the control, and to the aluminium-treated group as well. The obtained results of GTE in the aluminium-induced neurotoxicity are in accordance with the antioxidant effects of GTLE. Also, it is clear that GTE administered alone did not demonstrate neurotoxic effects as did the solution of aluminium chloride, but, on the contrary, showed the opposite, neuroprotective effects. To sum up, GTLE has proved to manifest strong antioxidant effects in the brain of healthy rats, and in the cases of neurotoxicity induced by aluminum, as well.",
publisher = "Nova Science Publishers, Inc., New York",
journal = "Green tea and health: antioxidant properties, consumption and role in disease prevention",
booktitle = "The protective effects of intrahippocampal application of green tea leaf extract on aluminium-induced brain toxicity",
pages = "33-56",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_2567"
}

Powell, N., Jelenković, A., Jovanović, M. D.,& Petronijević, N.. (2015). The protective effects of intrahippocampal application of green tea leaf extract on aluminium-induced brain toxicity. in Green tea and health: antioxidant properties, consumption and role in disease prevention
Nova Science Publishers, Inc., New York., 33-56.
https://hdl.handle.net/21.15107/rcub_ibiss_2567

Powell N, Jelenković A, Jovanović MD, Petronijević N. The protective effects of intrahippocampal application of green tea leaf extract on aluminium-induced brain toxicity. in Green tea and health: antioxidant properties, consumption and role in disease prevention. 2015;:33-56.
https://hdl.handle.net/21.15107/rcub_ibiss_2567 .

Powell, Nicolas, Jelenković, Ankica, Jovanović, Marina D., Petronijević, Nataša, "The protective effects of intrahippocampal application of green tea leaf extract on aluminium-induced brain toxicity" in Green tea and health: antioxidant properties, consumption and role in disease prevention (2015):33-56,
https://hdl.handle.net/21.15107/rcub_ibiss_2567 .

TY  - JOUR
AU  - Jelenković, Ankica V.
AU  - Jovanović, Marina D.
AU  - Bokonjić, Dubravko
AU  - Maksimović, Milan
AU  - Bošković, Bogdan
PY  - 2012
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/444
AB  - Background/Aim. Despite years of research in a number of experimental models the question whether nitric oxide (NO) and methylene blue (MB) have pro- or anticonvulsant effects remains to be fully resolved. Methods. In adult Wistar rats the influence of a nonselective inhibitor of nitric oxide synthase NG-nitro-L-arginine methyl ester (LNAME, 10µg) on clinical and biochemical effects of MB (10µg) given before the intraperitoneally administered chemical convulsant pentylenetetrazole (PTZ, 80 mg/kg) was examined. MB and L-NAME were applied intracerebroventricularly. PTZ application was followed by a 4- minute observation time, after which rats were sacrificed and elements of oxido-reductive balance were measured in a crude mitochondrial fraction of forebrain cortex, hippocampus and striatum. Results. Convulsive responses (forelimb dystonia - FLD, generalised clonic- and clonic-tonic convulsions - GCC and GCTC respectively) were observed in all rats received PTZ, together with significantly decreased lipid peroxidation in the forebrain cortex and striatum and increased superoxide dismutase activity in the hippocampus, in comparison to controls (saline treated). It was registered anticonvulsant effects of L-NAME pretreatment. However, these effects were insignificant. In the hippocampus of these animals there was decreased lipid peroxidation (p < 0.01, p < 0.05 vs saline-treated and PTZ-treated rats, respectively) and reverted PTZ-induced increase of superoxide dismutase activity. But MB individually pretreatment significantly decreased the incidence of CTCs and GCCs (FLD: p = 0.0513), prolonged the convulsive latent time for FLD, GCTCs and GCCs, in all the examined brain regions increased lipid peroxidation and decreased the level of superoxide anion. Administration of L-NAME 10 minutes before MB reverted all MB-evoked clinical and biochemical effects. Conclusion. Methylene blue applied individually before PTZ has strong anticonvulsant effects that were eliminated by L-NAME pretreatment. These effects and changed biochemical parameters in the brains of animals treated by L-NAME before MB in comparison to MBtreated group suggest involvement of NO in MB's effects in the animal model of PTZ-evoked convulsions.
AB  - Uvod/Cilj. I pored višegodišnjeg istraživanja na različitim eksperimentalnim modelima, nije potpuno odgovoreno na pitanje da li azot-oksid (NO) i metilen plavo (MP) deluju konvulzivno ili antikonvulzivno. Metode. Na odraslim pacovima Vistar soja ispitivan je uticaj NG-nitro-L-arginin metil estra (L-NAME, 10 µg), neselektivnog inhibitora azot oksid sintaze, na kliničke i biohemijske efekte metilen plavog (MP, 10 µg) datog intracerebroventrikularno pre hemijskog konvulziva pentilentetrazola (PTZ, 80 mg/kg), primenjenog intraperitonealno. Pacovi su posmatrani četiri minuta posle davanja PTZ-a, posle čega su žrtvovani i u neprečišćenoj mitohondrijskoj frakciji prednjeg mozga, hipokampusa i strijatuma određivani su parametri oksidoreduktivne ravnoteže. Rezultati. Posle primene PTZ-a, konvulzivni odgovor (distonija prednjih nogu - DPN, generalizovane klonične - GKK i generalizovane kloničnotonične konvulzije - GKTK) bio je ispoljen kod svih životinja, kao i statistički značajno sniženje lipidne peroksidacije u kori prednjeg mozga i strijatuma, i povećanje aktivnosti superoksid dizmutaze (SOD) u hipokampusu, u poređenju sa kontrolnom grupom (dobila fiziološki rastvor NaCl). Registrovani su antikonvulzivni efekti L-NAME koji nisu bili statistički značajni. U hipokampusu ovih životinja bila je snižena lipidna peroksidacija (p < 0,01 u poređenju sa kontrolnom grupom, p < 0,05 u poređenju sa životinjama koje su dobile PTZ), kao i aktivnost SOD u poređenju sa životinjama koje su dobile PTZ. Samo metilen plavo dovelo je do statistički značajnog smanjenja incidencije GKK I GKTK (DPN: p = 0,0513), produžilo je latentni period DPN, GKK i GKTK, a u svim ispitivanim strukturama mozga bila je povećana lipidna peroksidacija i smanjen nivo superoksidnog anjona. Svi klinički i biohemijski efekti izazvani primenom MP u potpunosti su odstranjeni primenom L-NAME 10 minuta pre davanja MP. Zaključak. Metilen plavo, dat samostalno pre PTZ, ispoljio je snažne antikonvulzivne efekte. Nestanak ovih efekata i izmenjeni biohemijski parametri u mozgovima pacova koji su pre MP dobili L-NAME, sugerišu da je NO uključen u efekte MP ispoljene na životinjskom modelu konvulzija izazvanih primenom PTZ-a.
T2  - Vojnosanitetski pregled
T1  - Uticaj NG-nitro-L-arginin metil estra na kliničke i biohemijske efekte metilen plavog kod konvulzija izazvanih pentilentetrazolom
T1  - Influence of NG-nitro-L-arginine methyl ester on clinical and biochemical effects of methylene blue in pentylenetetrazole-evoked convulsions
IS  - 6
VL  - 69
SP  - 481
EP  - 487
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_444
ER  - 

@article{
author = "Jelenković, Ankica V. and Jovanović, Marina D. and Bokonjić, Dubravko and Maksimović, Milan and Bošković, Bogdan",
year = "2012, 2012",
abstract = "Background/Aim. Despite years of research in a number of experimental models the question whether nitric oxide (NO) and methylene blue (MB) have pro- or anticonvulsant effects remains to be fully resolved. Methods. In adult Wistar rats the influence of a nonselective inhibitor of nitric oxide synthase NG-nitro-L-arginine methyl ester (LNAME, 10µg) on clinical and biochemical effects of MB (10µg) given before the intraperitoneally administered chemical convulsant pentylenetetrazole (PTZ, 80 mg/kg) was examined. MB and L-NAME were applied intracerebroventricularly. PTZ application was followed by a 4- minute observation time, after which rats were sacrificed and elements of oxido-reductive balance were measured in a crude mitochondrial fraction of forebrain cortex, hippocampus and striatum. Results. Convulsive responses (forelimb dystonia - FLD, generalised clonic- and clonic-tonic convulsions - GCC and GCTC respectively) were observed in all rats received PTZ, together with significantly decreased lipid peroxidation in the forebrain cortex and striatum and increased superoxide dismutase activity in the hippocampus, in comparison to controls (saline treated). It was registered anticonvulsant effects of L-NAME pretreatment. However, these effects were insignificant. In the hippocampus of these animals there was decreased lipid peroxidation (p < 0.01, p < 0.05 vs saline-treated and PTZ-treated rats, respectively) and reverted PTZ-induced increase of superoxide dismutase activity. But MB individually pretreatment significantly decreased the incidence of CTCs and GCCs (FLD: p = 0.0513), prolonged the convulsive latent time for FLD, GCTCs and GCCs, in all the examined brain regions increased lipid peroxidation and decreased the level of superoxide anion. Administration of L-NAME 10 minutes before MB reverted all MB-evoked clinical and biochemical effects. Conclusion. Methylene blue applied individually before PTZ has strong anticonvulsant effects that were eliminated by L-NAME pretreatment. These effects and changed biochemical parameters in the brains of animals treated by L-NAME before MB in comparison to MBtreated group suggest involvement of NO in MB's effects in the animal model of PTZ-evoked convulsions., Uvod/Cilj. I pored višegodišnjeg istraživanja na različitim eksperimentalnim modelima, nije potpuno odgovoreno na pitanje da li azot-oksid (NO) i metilen plavo (MP) deluju konvulzivno ili antikonvulzivno. Metode. Na odraslim pacovima Vistar soja ispitivan je uticaj NG-nitro-L-arginin metil estra (L-NAME, 10 µg), neselektivnog inhibitora azot oksid sintaze, na kliničke i biohemijske efekte metilen plavog (MP, 10 µg) datog intracerebroventrikularno pre hemijskog konvulziva pentilentetrazola (PTZ, 80 mg/kg), primenjenog intraperitonealno. Pacovi su posmatrani četiri minuta posle davanja PTZ-a, posle čega su žrtvovani i u neprečišćenoj mitohondrijskoj frakciji prednjeg mozga, hipokampusa i strijatuma određivani su parametri oksidoreduktivne ravnoteže. Rezultati. Posle primene PTZ-a, konvulzivni odgovor (distonija prednjih nogu - DPN, generalizovane klonične - GKK i generalizovane kloničnotonične konvulzije - GKTK) bio je ispoljen kod svih životinja, kao i statistički značajno sniženje lipidne peroksidacije u kori prednjeg mozga i strijatuma, i povećanje aktivnosti superoksid dizmutaze (SOD) u hipokampusu, u poređenju sa kontrolnom grupom (dobila fiziološki rastvor NaCl). Registrovani su antikonvulzivni efekti L-NAME koji nisu bili statistički značajni. U hipokampusu ovih životinja bila je snižena lipidna peroksidacija (p < 0,01 u poređenju sa kontrolnom grupom, p < 0,05 u poređenju sa životinjama koje su dobile PTZ), kao i aktivnost SOD u poređenju sa životinjama koje su dobile PTZ. Samo metilen plavo dovelo je do statistički značajnog smanjenja incidencije GKK I GKTK (DPN: p = 0,0513), produžilo je latentni period DPN, GKK i GKTK, a u svim ispitivanim strukturama mozga bila je povećana lipidna peroksidacija i smanjen nivo superoksidnog anjona. Svi klinički i biohemijski efekti izazvani primenom MP u potpunosti su odstranjeni primenom L-NAME 10 minuta pre davanja MP. Zaključak. Metilen plavo, dat samostalno pre PTZ, ispoljio je snažne antikonvulzivne efekte. Nestanak ovih efekata i izmenjeni biohemijski parametri u mozgovima pacova koji su pre MP dobili L-NAME, sugerišu da je NO uključen u efekte MP ispoljene na životinjskom modelu konvulzija izazvanih primenom PTZ-a.",
journal = "Vojnosanitetski pregled",
title = "Uticaj NG-nitro-L-arginin metil estra na kliničke i biohemijske efekte metilen plavog kod konvulzija izazvanih pentilentetrazolom, Influence of NG-nitro-L-arginine methyl ester on clinical and biochemical effects of methylene blue in pentylenetetrazole-evoked convulsions",
number = "6",
volume = "69",
pages = "481-487",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_444"
}

Jelenković, A. V., Jovanović, M. D., Bokonjić, D., Maksimović, M.,& Bošković, B.. (2012). Uticaj NG-nitro-L-arginin metil estra na kliničke i biohemijske efekte metilen plavog kod konvulzija izazvanih pentilentetrazolom. in Vojnosanitetski pregled, 69(6), 481-487.
https://hdl.handle.net/21.15107/rcub_ibiss_444

Jelenković AV, Jovanović MD, Bokonjić D, Maksimović M, Bošković B. Uticaj NG-nitro-L-arginin metil estra na kliničke i biohemijske efekte metilen plavog kod konvulzija izazvanih pentilentetrazolom. in Vojnosanitetski pregled. 2012;69(6):481-487.
https://hdl.handle.net/21.15107/rcub_ibiss_444 .

Jelenković, Ankica V., Jovanović, Marina D., Bokonjić, Dubravko, Maksimović, Milan, Bošković, Bogdan, "Uticaj NG-nitro-L-arginin metil estra na kliničke i biohemijske efekte metilen plavog kod konvulzija izazvanih pentilentetrazolom" in Vojnosanitetski pregled, 69, no. 6 (2012):481-487,
https://hdl.handle.net/21.15107/rcub_ibiss_444 .

TY  - JOUR
AU  - Jelenković, Ankica V.
AU  - Jovanović, Marina D.
AU  - Ninković, Milica
AU  - Maksimović, Milan
AU  - Bošković, Bogdan
PY  - 2003
PY  - 2003
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/465
AB  - Controversy about proconvulsant and anticonvulsant nitric oxide (NO) effects and the place of oxidative stress in convulsions, are still a matter of research. We investigated the interaction between 2-amino-5-phosphonovaleric acid (APV), a competitive N-methyl-D-aspartate (NMDA) receptor antagonist and Nw-nitro-L-arginine methyl ester (L-NAME), a nonselective nitric oxide synthase (NOS) antagonist, in pentylenetetrazole (PTZ)-induced convulsions. Pentylenetetrazole was applied to adult Wistar rats intraperitoneally (ip) in a single dose of 80 mg/kg, and L-NAME (10 µg/10 µl) or APV (20 µg/10 µl) intracerebroventricularly (icv), 30 and 10 minutes before PTZ, respectively. In the same manner, another group received both antagonists. Control animals were given 0.9% saline. Nw-nitro-L-arginine methyl ester exerted a weak anticonvulsant effect, preventing generalized clonic (GCC) and clonic-tonic convulsions (CTC) in 17% of cases. With APV protection against GCC and CTC was 100%, forelimb dystonia (FLD) was decreased in 33% of cases, and time to onset of all convulsive patterns was prolonged (p<0.05 to 0.01). All effects of APV, except in CTC, were reversed by L-NAME applied prior to APV. In APV-PTZ treated animals, superoxide anion content was increased in the forebrain cortex, striatum and hippocampus, without an overwhelmed antioxidative superoxide dismutase (SOD) defense system in the other treatments. When the APV-PTZ group was treated with L-NAME, both SOD activity and superoxide anion content were additionally decreased indicating that the NOS-NO system was involved in the metabolism of superoxide anions. It is suggested that clinical and biochemical effects of NO strongly depend upon the pretreatment and might lead to a wrong impression of NO contradictory activity.
AB  - Kontroverzni nalazi o prokonvulzivnim kao i antikonvulzivnim efektima azot oksida (NO) i značaju oksidativnog stresa u konvulzijama, i dalje su predmet istraživanja. U konvulzijama izazvanim primenom pentilentetrazola (PTZ) ispitivali smo interakciju između 2-amino-5-fosfovalerinske kiseline (APV) kompetitivnog antagoniste N-metil-D-aspartat (NMDA) receptora i Nw-nitro-L-arginin metil estra (L-NAME), neselektivnog antagoniste azot oksid sintaze (NOS). Odraslim pacovima Wistar soja, PTZ je ubrizgavan intraperitonealno (ip) u jednoj dozi od 80 mg/kg. Ostale supstance, L-NAME (10 µg/10 µl) i APV (20 µg/10 µl), primenjivale su se intracerebroventrikularno (icv), i to L-NAME 30, a APV 10 minuta pre PTZ. Po istom vremenskom principu, jedna grupa dobila je oba antagonista, a kontrolna fiziološki rastvor NaCl. Nw-nitro-L-arginin metil estar ispoljio je slabo antikonvulzivno dejstvo, smanjujući incidenciju generalizovanih kloničnih (GCC) i klonično-toničnih konvulzija (CTC) za 17%. Za razliku od L-NAME, APV je sprečila nastanak GCC i CTC kod svih životinja (100%), a incidencija klonusa prednjih nogu (FLD) smanjena je za 33%. Istovremeno primenom APV produženo je vreme od aplikacije PTZ do pojave svih konvulzivnih tipova (p<.05 do 0.01). Primenom L-NAME pre APV, umanjeni su efekti APV, pri čemu je došlo do povećanja incidencije FLD i GCC za 16% odnosno 50%. U kori prednjeg mozga, strijatumu i hipokampusu, životinja koje su dobile APV+PTZ, došlo do povećanja koncentracije superoksidnog anjona. Aktivnost superoksid dizmutaze ne prati ovaj skok. Njen dodatni pad u grupi tretiranoj sa L-NAME pre APV+PTZ, ukazuje da je sistem NOS-NO uključen u metabolizam superoksidnog anjona. Dobijeni rezultati ukazuju da klinički i biohemijski efekti NO u velikoj meri zavise od prethodno primenjenih supstanci i promena izazvanih njima, što može da doprinose sticanju pogrešnog utiska o kontradiktornim dejstvima NO.
T2  - Acta veterinaria
T1  - Azot oksid (NO) i antagonist NMDA receptora u konvulzijama izazvanim pentilenetetrazolom
T1  - Nitric oxide (NO) and an NMDA receptor antagonist in pentylenetetrazole-induced convulsions
IS  - 2-3
VL  - 53
SP  - 103
EP  - 112
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_465
ER  - 

@article{
author = "Jelenković, Ankica V. and Jovanović, Marina D. and Ninković, Milica and Maksimović, Milan and Bošković, Bogdan",
year = "2003, 2003",
abstract = "Controversy about proconvulsant and anticonvulsant nitric oxide (NO) effects and the place of oxidative stress in convulsions, are still a matter of research. We investigated the interaction between 2-amino-5-phosphonovaleric acid (APV), a competitive N-methyl-D-aspartate (NMDA) receptor antagonist and Nw-nitro-L-arginine methyl ester (L-NAME), a nonselective nitric oxide synthase (NOS) antagonist, in pentylenetetrazole (PTZ)-induced convulsions. Pentylenetetrazole was applied to adult Wistar rats intraperitoneally (ip) in a single dose of 80 mg/kg, and L-NAME (10 µg/10 µl) or APV (20 µg/10 µl) intracerebroventricularly (icv), 30 and 10 minutes before PTZ, respectively. In the same manner, another group received both antagonists. Control animals were given 0.9% saline. Nw-nitro-L-arginine methyl ester exerted a weak anticonvulsant effect, preventing generalized clonic (GCC) and clonic-tonic convulsions (CTC) in 17% of cases. With APV protection against GCC and CTC was 100%, forelimb dystonia (FLD) was decreased in 33% of cases, and time to onset of all convulsive patterns was prolonged (p<0.05 to 0.01). All effects of APV, except in CTC, were reversed by L-NAME applied prior to APV. In APV-PTZ treated animals, superoxide anion content was increased in the forebrain cortex, striatum and hippocampus, without an overwhelmed antioxidative superoxide dismutase (SOD) defense system in the other treatments. When the APV-PTZ group was treated with L-NAME, both SOD activity and superoxide anion content were additionally decreased indicating that the NOS-NO system was involved in the metabolism of superoxide anions. It is suggested that clinical and biochemical effects of NO strongly depend upon the pretreatment and might lead to a wrong impression of NO contradictory activity., Kontroverzni nalazi o prokonvulzivnim kao i antikonvulzivnim efektima azot oksida (NO) i značaju oksidativnog stresa u konvulzijama, i dalje su predmet istraživanja. U konvulzijama izazvanim primenom pentilentetrazola (PTZ) ispitivali smo interakciju između 2-amino-5-fosfovalerinske kiseline (APV) kompetitivnog antagoniste N-metil-D-aspartat (NMDA) receptora i Nw-nitro-L-arginin metil estra (L-NAME), neselektivnog antagoniste azot oksid sintaze (NOS). Odraslim pacovima Wistar soja, PTZ je ubrizgavan intraperitonealno (ip) u jednoj dozi od 80 mg/kg. Ostale supstance, L-NAME (10 µg/10 µl) i APV (20 µg/10 µl), primenjivale su se intracerebroventrikularno (icv), i to L-NAME 30, a APV 10 minuta pre PTZ. Po istom vremenskom principu, jedna grupa dobila je oba antagonista, a kontrolna fiziološki rastvor NaCl. Nw-nitro-L-arginin metil estar ispoljio je slabo antikonvulzivno dejstvo, smanjujući incidenciju generalizovanih kloničnih (GCC) i klonično-toničnih konvulzija (CTC) za 17%. Za razliku od L-NAME, APV je sprečila nastanak GCC i CTC kod svih životinja (100%), a incidencija klonusa prednjih nogu (FLD) smanjena je za 33%. Istovremeno primenom APV produženo je vreme od aplikacije PTZ do pojave svih konvulzivnih tipova (p<.05 do 0.01). Primenom L-NAME pre APV, umanjeni su efekti APV, pri čemu je došlo do povećanja incidencije FLD i GCC za 16% odnosno 50%. U kori prednjeg mozga, strijatumu i hipokampusu, životinja koje su dobile APV+PTZ, došlo do povećanja koncentracije superoksidnog anjona. Aktivnost superoksid dizmutaze ne prati ovaj skok. Njen dodatni pad u grupi tretiranoj sa L-NAME pre APV+PTZ, ukazuje da je sistem NOS-NO uključen u metabolizam superoksidnog anjona. Dobijeni rezultati ukazuju da klinički i biohemijski efekti NO u velikoj meri zavise od prethodno primenjenih supstanci i promena izazvanih njima, što može da doprinose sticanju pogrešnog utiska o kontradiktornim dejstvima NO.",
journal = "Acta veterinaria",
title = "Azot oksid (NO) i antagonist NMDA receptora u konvulzijama izazvanim pentilenetetrazolom, Nitric oxide (NO) and an NMDA receptor antagonist in pentylenetetrazole-induced convulsions",
number = "2-3",
volume = "53",
pages = "103-112",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_465"
}

Jelenković, A. V., Jovanović, M. D., Ninković, M., Maksimović, M.,& Bošković, B.. (2003). Azot oksid (NO) i antagonist NMDA receptora u konvulzijama izazvanim pentilenetetrazolom. in Acta veterinaria, 53(2-3), 103-112.
https://hdl.handle.net/21.15107/rcub_ibiss_465

Jelenković AV, Jovanović MD, Ninković M, Maksimović M, Bošković B. Azot oksid (NO) i antagonist NMDA receptora u konvulzijama izazvanim pentilenetetrazolom. in Acta veterinaria. 2003;53(2-3):103-112.
https://hdl.handle.net/21.15107/rcub_ibiss_465 .

Jelenković, Ankica V., Jovanović, Marina D., Ninković, Milica, Maksimović, Milan, Bošković, Bogdan, "Azot oksid (NO) i antagonist NMDA receptora u konvulzijama izazvanim pentilenetetrazolom" in Acta veterinaria, 53, no. 2-3 (2003):103-112,
https://hdl.handle.net/21.15107/rcub_ibiss_465 .

TY  - JOUR
AU  - Ninković, Milica
AU  - Jovanović, Marina D.
AU  - Maličević, Živorad
AU  - Jelenković, Ankica V.
AU  - Đukić, Mirjana
AU  - Vasiljević, Ivana D.
PY  - 2003
PY  - 2003
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/464
AB  - Quinolinic acid (QA) produces a pattern of selective cell loss in the striatum, that closely mimics that of Huntington's disease (HD). The aim of this study was to investigate the antioxidative status in the thalamus after intrastriatal application of QA and the influence of nerve growth factor (NGF) on such neurotoxicity. Wistar rats were treated intrastriatally (coordinates: 8.4A, 2.6L, 4.8V), using a stereotaxic instrument. The first group was treated with QA (150 nmol/l). The second group was treated with QA, followed by NGF (4.5 mg/kg b.w). The control group was treated with 0.9 % saline solution. Seven days after the treatment, we found decreased superoxide dismutase (SOD) activity in mitochondrial fractions of the striatum of both groups. In the thalamus, SOD activity showed no differences. The content of superoxide anion increased in the striatum of QA- treated animals. It was decreased in both structures in the group that was treated with QA and NGF. In the QA+ NGF-treated group, we found increased glutathione peroxidase (GSHPx) and GSH, compared to the group that was treated with QA only, but these values were lower than in the controls. Thus, NGF showed beneficial effects on the oxido-reduction status in the striatum, and also in the thalamus, a structure that is separated from but tightly connected with the striatum.
AB  - Hinolinska kiselina (HK) prouzrokuje takav selektivni gubitak ćelija u strijatumu, koji veoma dobro imitira onaj kod Huntingtonove bolesti. Cilj ovog istraživanja bio je da se ispita antioksidativni status u talamusu nakon aplikacije HK u strijatum i uticaj NGF na takvu neurotoksičnost. Wistar pacovi su tretirani intrastrijatno, pomoću stereotaksičnog instrumenta (koordinate: 8,4A, 2,6L, 4,8V). Prva grupa je bila tretirana HK (150 nmol/l). Druga grupa je bila tretirana HK, a nakon toga je dobila NGF (4.5 mg/ kg b.w). Kontrolna grupa je bila tretirana fiziološkim rastvorom. Sedam dana nakon tretmana, u mitohondrijskim frakcijama strijatuma, našli smo smanjenu aktivnost SOD u obema grupama. U talamusu, aktivnost SOD se nije promenila. Sadržaj superoksidnog anjona se povećao u strijatumu životinja koje su bile tretirane HK, a smanjio se u obema strukturama, u grupi koja je bila tretirana sa HK i NGF. U HK+ NGF-tretiranoj grupi, našli smo povećanu aktivnost GSHPx i GSH u odnosu na grupu koja je bila tretirana samo sa HK, ali su te vrednosti bile manje u odnosu na kontrolne. NGF je pokazao povoljne efekte na oksido-reduktivni status u strijatumu, ali takođe i u talamusu, strukturi koja je odvojena, ali veoma blisko povezana sa strijatumom.
T2  - Acta veterinaria
T1  - Efekat NGF na antioksidativnu odbranu u talamusu pacova nakon neurotoksičnog delovanja hinolinske kiseline
T1  - Antioxidative effect of nerve growth factor (NGF) in rat thalamus after quinolinic acid-induced neurotoxicity
IS  - 2-3
VL  - 53
SP  - 77
EP  - 86
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_464
ER  - 

@article{
author = "Ninković, Milica and Jovanović, Marina D. and Maličević, Živorad and Jelenković, Ankica V. and Đukić, Mirjana and Vasiljević, Ivana D.",
year = "2003, 2003",
abstract = "Quinolinic acid (QA) produces a pattern of selective cell loss in the striatum, that closely mimics that of Huntington's disease (HD). The aim of this study was to investigate the antioxidative status in the thalamus after intrastriatal application of QA and the influence of nerve growth factor (NGF) on such neurotoxicity. Wistar rats were treated intrastriatally (coordinates: 8.4A, 2.6L, 4.8V), using a stereotaxic instrument. The first group was treated with QA (150 nmol/l). The second group was treated with QA, followed by NGF (4.5 mg/kg b.w). The control group was treated with 0.9 % saline solution. Seven days after the treatment, we found decreased superoxide dismutase (SOD) activity in mitochondrial fractions of the striatum of both groups. In the thalamus, SOD activity showed no differences. The content of superoxide anion increased in the striatum of QA- treated animals. It was decreased in both structures in the group that was treated with QA and NGF. In the QA+ NGF-treated group, we found increased glutathione peroxidase (GSHPx) and GSH, compared to the group that was treated with QA only, but these values were lower than in the controls. Thus, NGF showed beneficial effects on the oxido-reduction status in the striatum, and also in the thalamus, a structure that is separated from but tightly connected with the striatum., Hinolinska kiselina (HK) prouzrokuje takav selektivni gubitak ćelija u strijatumu, koji veoma dobro imitira onaj kod Huntingtonove bolesti. Cilj ovog istraživanja bio je da se ispita antioksidativni status u talamusu nakon aplikacije HK u strijatum i uticaj NGF na takvu neurotoksičnost. Wistar pacovi su tretirani intrastrijatno, pomoću stereotaksičnog instrumenta (koordinate: 8,4A, 2,6L, 4,8V). Prva grupa je bila tretirana HK (150 nmol/l). Druga grupa je bila tretirana HK, a nakon toga je dobila NGF (4.5 mg/ kg b.w). Kontrolna grupa je bila tretirana fiziološkim rastvorom. Sedam dana nakon tretmana, u mitohondrijskim frakcijama strijatuma, našli smo smanjenu aktivnost SOD u obema grupama. U talamusu, aktivnost SOD se nije promenila. Sadržaj superoksidnog anjona se povećao u strijatumu životinja koje su bile tretirane HK, a smanjio se u obema strukturama, u grupi koja je bila tretirana sa HK i NGF. U HK+ NGF-tretiranoj grupi, našli smo povećanu aktivnost GSHPx i GSH u odnosu na grupu koja je bila tretirana samo sa HK, ali su te vrednosti bile manje u odnosu na kontrolne. NGF je pokazao povoljne efekte na oksido-reduktivni status u strijatumu, ali takođe i u talamusu, strukturi koja je odvojena, ali veoma blisko povezana sa strijatumom.",
journal = "Acta veterinaria",
title = "Efekat NGF na antioksidativnu odbranu u talamusu pacova nakon neurotoksičnog delovanja hinolinske kiseline, Antioxidative effect of nerve growth factor (NGF) in rat thalamus after quinolinic acid-induced neurotoxicity",
number = "2-3",
volume = "53",
pages = "77-86",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_464"
}

Ninković, M., Jovanović, M. D., Maličević, Ž., Jelenković, A. V., Đukić, M.,& Vasiljević, I. D.. (2003). Efekat NGF na antioksidativnu odbranu u talamusu pacova nakon neurotoksičnog delovanja hinolinske kiseline. in Acta veterinaria, 53(2-3), 77-86.
https://hdl.handle.net/21.15107/rcub_ibiss_464

Ninković M, Jovanović MD, Maličević Ž, Jelenković AV, Đukić M, Vasiljević ID. Efekat NGF na antioksidativnu odbranu u talamusu pacova nakon neurotoksičnog delovanja hinolinske kiseline. in Acta veterinaria. 2003;53(2-3):77-86.
https://hdl.handle.net/21.15107/rcub_ibiss_464 .

Ninković, Milica, Jovanović, Marina D., Maličević, Živorad, Jelenković, Ankica V., Đukić, Mirjana, Vasiljević, Ivana D., "Efekat NGF na antioksidativnu odbranu u talamusu pacova nakon neurotoksičnog delovanja hinolinske kiseline" in Acta veterinaria, 53, no. 2-3 (2003):77-86,
https://hdl.handle.net/21.15107/rcub_ibiss_464 .

TY  - JOUR
AU  - Jelenković, Ankica V.
AU  - Veskov, Rosica
AU  - Jovanović, Marina D.
AU  - Raičević, Ranko
AU  - Bokonjić, Dubravko
AU  - Pešić, Vesna
AU  - Bošković, Bogdan
PY  - 2002
PY  - 2002
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/400
T2  - Vojnosanitetski pregled
T1  - Bol i ekscitatorne aminokiseline
IS  - 1
VL  - 59
SP  - 49
EP  - 58
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_400
ER  - 

@article{
author = "Jelenković, Ankica V. and Veskov, Rosica and Jovanović, Marina D. and Raičević, Ranko and Bokonjić, Dubravko and Pešić, Vesna and Bošković, Bogdan",
year = "2002, 2002",
journal = "Vojnosanitetski pregled",
title = "Bol i ekscitatorne aminokiseline",
number = "1",
volume = "59",
pages = "49-58",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_400"
}

Jelenković, A. V., Veskov, R., Jovanović, M. D., Raičević, R., Bokonjić, D., Pešić, V.,& Bošković, B.. (2002). Bol i ekscitatorne aminokiseline. in Vojnosanitetski pregled, 59(1), 49-58.
https://hdl.handle.net/21.15107/rcub_ibiss_400

Jelenković AV, Veskov R, Jovanović MD, Raičević R, Bokonjić D, Pešić V, Bošković B. Bol i ekscitatorne aminokiseline. in Vojnosanitetski pregled. 2002;59(1):49-58.
https://hdl.handle.net/21.15107/rcub_ibiss_400 .

Jelenković, Ankica V., Veskov, Rosica, Jovanović, Marina D., Raičević, Ranko, Bokonjić, Dubravko, Pešić, Vesna, Bošković, Bogdan, "Bol i ekscitatorne aminokiseline" in Vojnosanitetski pregled, 59, no. 1 (2002):49-58,
https://hdl.handle.net/21.15107/rcub_ibiss_400 .