Todorović-Marković, Biljana M

Link to this page

Authority KeyName Variants
4c70a028-707d-49f2-aafb-8d67d1c4817f
  • Todorović-Marković, Biljana M (2)
  • Todorović-Marković, Biljana (1)
  • Todorović-Marković, Biljana M. (1)
Projects

Author's Bibliography

Graphene quantum dots as autophagy-inducing photodynamic agents

Marković, Zoran M.; Ristić, Biljana Z.; Arsikin, Katarina M.; Klisić, Đorđe G.; Harhaji-Trajković, Ljubica; Todorović-Marković, Biljana M.; Kepić, Dejan P.; Kravić-Stevović, Tamara K.; Jovanović, Svetlana P.; Milenković, Marina M.; Milivojević, Dusan D.; Bumbaširević, Vladimir Z.; Dramićanin, Miroslav D.; Trajković, Vladimir S.

(Elsevier BV, 2012)

TY  - JOUR
AU  - Marković, Zoran M.
AU  - Ristić, Biljana Z.
AU  - Arsikin, Katarina M.
AU  - Klisić, Đorđe G.
AU  - Harhaji-Trajković, Ljubica
AU  - Todorović-Marković, Biljana M.
AU  - Kepić, Dejan P.
AU  - Kravić-Stevović, Tamara K.
AU  - Jovanović, Svetlana P.
AU  - Milenković, Marina M.
AU  - Milivojević, Dusan D.
AU  - Bumbaširević, Vladimir Z.
AU  - Dramićanin, Miroslav D.
AU  - Trajković, Vladimir S.
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3587
AB  - The excellent photoluminescent properties of graphene quantum dots (GQD) makes them suitable candidates for biomedical applications, but their cytotoxicity has not been extensively studied. Here we show that electrochemically produced GQD irradiated with blue light (470. nm, 1. W) generate reactive oxygen species, including singlet oxygen, and kill U251 human glioma cells by causing oxidative stress. The cell death induced by photoexcited GQD displayed morphological and/or biochemical characteristics of both apoptosis (phosphatidylserine externalization, caspase activation, DNA fragmentation) and autophagy (formation of autophagic vesicles, LC3-I/LC3-II conversion, degradation of autophagic target p62). Moreover, a genetic inactivation of autophagy-essential LC3B protein partly abrogated the photodynamic cytotoxicity of GQD. These data indicate potential usefulness of GQD in photodynamic therapy, but also raise concerns about their possible toxicity.
PB  - Elsevier BV
T2  - Biomaterials
T1  - Graphene quantum dots as autophagy-inducing photodynamic agents
IS  - 29
VL  - 33
DO  - 10.1016/j.biomaterials.2012.06.060
SP  - 7084
EP  - 7092
ER  - 
@article{
author = "Marković, Zoran M. and Ristić, Biljana Z. and Arsikin, Katarina M. and Klisić, Đorđe G. and Harhaji-Trajković, Ljubica and Todorović-Marković, Biljana M. and Kepić, Dejan P. and Kravić-Stevović, Tamara K. and Jovanović, Svetlana P. and Milenković, Marina M. and Milivojević, Dusan D. and Bumbaširević, Vladimir Z. and Dramićanin, Miroslav D. and Trajković, Vladimir S.",
year = "2012",
abstract = "The excellent photoluminescent properties of graphene quantum dots (GQD) makes them suitable candidates for biomedical applications, but their cytotoxicity has not been extensively studied. Here we show that electrochemically produced GQD irradiated with blue light (470. nm, 1. W) generate reactive oxygen species, including singlet oxygen, and kill U251 human glioma cells by causing oxidative stress. The cell death induced by photoexcited GQD displayed morphological and/or biochemical characteristics of both apoptosis (phosphatidylserine externalization, caspase activation, DNA fragmentation) and autophagy (formation of autophagic vesicles, LC3-I/LC3-II conversion, degradation of autophagic target p62). Moreover, a genetic inactivation of autophagy-essential LC3B protein partly abrogated the photodynamic cytotoxicity of GQD. These data indicate potential usefulness of GQD in photodynamic therapy, but also raise concerns about their possible toxicity.",
publisher = "Elsevier BV",
journal = "Biomaterials",
title = "Graphene quantum dots as autophagy-inducing photodynamic agents",
number = "29",
volume = "33",
doi = "10.1016/j.biomaterials.2012.06.060",
pages = "7084-7092"
}
Marković, Z. M., Ristić, B. Z., Arsikin, K. M., Klisić, Đ. G., Harhaji-Trajković, L., Todorović-Marković, B. M., Kepić, D. P., Kravić-Stevović, T. K., Jovanović, S. P., Milenković, M. M., Milivojević, D. D., Bumbaširević, V. Z., Dramićanin, M. D.,& Trajković, V. S.. (2012). Graphene quantum dots as autophagy-inducing photodynamic agents. in Biomaterials
Elsevier BV., 33(29), 7084-7092.
https://doi.org/10.1016/j.biomaterials.2012.06.060
Marković ZM, Ristić BZ, Arsikin KM, Klisić ĐG, Harhaji-Trajković L, Todorović-Marković BM, Kepić DP, Kravić-Stevović TK, Jovanović SP, Milenković MM, Milivojević DD, Bumbaširević VZ, Dramićanin MD, Trajković VS. Graphene quantum dots as autophagy-inducing photodynamic agents. in Biomaterials. 2012;33(29):7084-7092.
doi:10.1016/j.biomaterials.2012.06.060 .
Marković, Zoran M., Ristić, Biljana Z., Arsikin, Katarina M., Klisić, Đorđe G., Harhaji-Trajković, Ljubica, Todorović-Marković, Biljana M., Kepić, Dejan P., Kravić-Stevović, Tamara K., Jovanović, Svetlana P., Milenković, Marina M., Milivojević, Dusan D., Bumbaširević, Vladimir Z., Dramićanin, Miroslav D., Trajković, Vladimir S., "Graphene quantum dots as autophagy-inducing photodynamic agents" in Biomaterials, 33, no. 29 (2012):7084-7092,
https://doi.org/10.1016/j.biomaterials.2012.06.060 . .
4
375
284
380

Oxidative stress-mediated hemolytic activity of solvent exchange-prepared fullerene (C-60) nanoparticles

Trpković, Andreja; Todorović-Marković, Biljana M; Kleut, Duska N; Misirkić Marjanović, Maja; Janjetović, Kristina; Vučićević, Ljubica; Pantović, Aleksandar C; Jovanović, Svetlana P; Dramicanin, Miroslav D; Marković, Zoran J; Trajković, Vladimir S

(2010)

TY  - JOUR
AU  - Trpković, Andreja
AU  - Todorović-Marković, Biljana M
AU  - Kleut, Duska N
AU  - Misirkić Marjanović, Maja
AU  - Janjetović, Kristina
AU  - Vučićević, Ljubica
AU  - Pantović, Aleksandar C
AU  - Jovanović, Svetlana P
AU  - Dramicanin, Miroslav D
AU  - Marković, Zoran J
AU  - Trajković, Vladimir S
PY  - 2010
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1140
AB  - The present study investigated the hemolytic properties of fullerene (C-60) nanoparticles prepared by solvent exchange using tetrahydrofuran (nC(60)THF), or by mechanochemically assisted complexation with macrocyclic oligosaccharide gamma-cyclodextrin (nC(60)CDX) or the copolymer ethylene vinyl acetate-ethylene vinyl versatate (nC(60)EVA-EVV). The spectrophotometrical analysis of hemoglobin release revealed that only nC(60)THF, but not nC(60)CDX or nC(60)EVA-EVV, was able to cause lysis of human erythrocytes in a dose-and time-dependent manner. Atomic force microscopy revealed that nC(60)THF-mediated hemolysis was preceded by erythrocyte shrinkage and increase in cell surface roughness. A flow cytometric analysis confirmed a decrease in erythrocyte size and demonstrated a significant increase in reactive oxygen species production in red blood cells exposed to nC(60)THF. The nC(60)THF-triggered hemolytic activity was efficiently reduced by the antioxidants N-acetylcysteine and butylated hydroxyanisole, as well as by serum albumin, the most abundant protein in human blood plasma. These data indicate that nC(60)THF can cause serum albumin-preventable hemolysis through oxidative stress-mediated damage of the erythrocyte membrane.
T2  - Nanotechnology
T1  - Oxidative stress-mediated hemolytic activity of solvent exchange-prepared fullerene (C-60) nanoparticles
IS  - 37
VL  - 21
SP  - 601
EP  - na
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1140
ER  - 
@article{
author = "Trpković, Andreja and Todorović-Marković, Biljana M and Kleut, Duska N and Misirkić Marjanović, Maja and Janjetović, Kristina and Vučićević, Ljubica and Pantović, Aleksandar C and Jovanović, Svetlana P and Dramicanin, Miroslav D and Marković, Zoran J and Trajković, Vladimir S",
year = "2010",
abstract = "The present study investigated the hemolytic properties of fullerene (C-60) nanoparticles prepared by solvent exchange using tetrahydrofuran (nC(60)THF), or by mechanochemically assisted complexation with macrocyclic oligosaccharide gamma-cyclodextrin (nC(60)CDX) or the copolymer ethylene vinyl acetate-ethylene vinyl versatate (nC(60)EVA-EVV). The spectrophotometrical analysis of hemoglobin release revealed that only nC(60)THF, but not nC(60)CDX or nC(60)EVA-EVV, was able to cause lysis of human erythrocytes in a dose-and time-dependent manner. Atomic force microscopy revealed that nC(60)THF-mediated hemolysis was preceded by erythrocyte shrinkage and increase in cell surface roughness. A flow cytometric analysis confirmed a decrease in erythrocyte size and demonstrated a significant increase in reactive oxygen species production in red blood cells exposed to nC(60)THF. The nC(60)THF-triggered hemolytic activity was efficiently reduced by the antioxidants N-acetylcysteine and butylated hydroxyanisole, as well as by serum albumin, the most abundant protein in human blood plasma. These data indicate that nC(60)THF can cause serum albumin-preventable hemolysis through oxidative stress-mediated damage of the erythrocyte membrane.",
journal = "Nanotechnology",
title = "Oxidative stress-mediated hemolytic activity of solvent exchange-prepared fullerene (C-60) nanoparticles",
number = "37",
volume = "21",
pages = "601-na",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1140"
}
Trpković, A., Todorović-Marković, B. M., Kleut, D. N., Misirkić Marjanović, M., Janjetović, K., Vučićević, L., Pantović, A. C., Jovanović, S. P., Dramicanin, M. D., Marković, Z. J.,& Trajković, V. S.. (2010). Oxidative stress-mediated hemolytic activity of solvent exchange-prepared fullerene (C-60) nanoparticles. in Nanotechnology, 21(37), 601-na.
https://hdl.handle.net/21.15107/rcub_ibiss_1140
Trpković A, Todorović-Marković BM, Kleut DN, Misirkić Marjanović M, Janjetović K, Vučićević L, Pantović AC, Jovanović SP, Dramicanin MD, Marković ZJ, Trajković VS. Oxidative stress-mediated hemolytic activity of solvent exchange-prepared fullerene (C-60) nanoparticles. in Nanotechnology. 2010;21(37):601-na.
https://hdl.handle.net/21.15107/rcub_ibiss_1140 .
Trpković, Andreja, Todorović-Marković, Biljana M, Kleut, Duska N, Misirkić Marjanović, Maja, Janjetović, Kristina, Vučićević, Ljubica, Pantović, Aleksandar C, Jovanović, Svetlana P, Dramicanin, Miroslav D, Marković, Zoran J, Trajković, Vladimir S, "Oxidative stress-mediated hemolytic activity of solvent exchange-prepared fullerene (C-60) nanoparticles" in Nanotechnology, 21, no. 37 (2010):601-na,
https://hdl.handle.net/21.15107/rcub_ibiss_1140 .

The protection of cells from nitric oxide-mediated apoptotic death by mechanochemically synthesized fullerene (C-60) nanoparticles

Misirkić Marjanović, Maja; Todorović-Marković, Biljana M; Vučićević, Ljubica; Janjetović, Kristina; Jokanović, Vukoman R; Dramicanin, Miroslav D; Marković, Zoran M; Trajković, Vladimir S

(2009)

TY  - JOUR
AU  - Misirkić Marjanović, Maja
AU  - Todorović-Marković, Biljana M
AU  - Vučićević, Ljubica
AU  - Janjetović, Kristina
AU  - Jokanović, Vukoman R
AU  - Dramicanin, Miroslav D
AU  - Marković, Zoran M
AU  - Trajković, Vladimir S
PY  - 2009
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1456
AB  - The influence of fullerene (C-60) nanoparticles on the cytotoxicity of a highly reactive free radical nitric oxide (NO) was investigated. Fullerene nanoparticles were prepared by mechanochemically assisted complexation with anionic surfactant sodium dodecyl sulfate, macrocyclic oligosaccharide gamma-cyclodextrin or the copolymer ethylene vinyl acetate-ethylene vinyl versatate. C-60 nanoparticles were characterized by UV-vis and atomic force microscopy. While readily internalized by mouse L929 fibroblasts, C-60 nanoparticles were not cytotoxic. Moreover, they partially protected L929 cells from the cytotoxic effect of NO-releasing compounds sodium nitroprusside (SNP), S-nitroso-N-acetylpenicillamine (SNAP), S-nitrosoglutathione (GSNO) and 3-morpholino-sydnonimine (SIN-1). C-60 nanoparticles reduced SNP-induced apoptotic cell death by preventing mitochondrial depolarization, caspase activation, cell membrane phosphatidylserine exposure and DNA fragmentation. The protective action of C-60 nanoparticles was not exerted via direct interaction with NO, but through neutralization of mitochondria-produced superoxide radical in NO-treated cells, as demonstrated by using different redox-sensitive reporter fluorochromes. These data suggest that C-60 complexes with appropriate host molecules might be plausible candidates for preventing NO-mediated cell injury in inflammatory/autoimmune disorders. (C) 2009 Elsevier Ltd. All rights reserved.
T2  - Biomaterials
T1  - The protection of cells from nitric oxide-mediated apoptotic death by mechanochemically synthesized fullerene (C-60) nanoparticles
IS  - 12
VL  - 30
EP  - 2328
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1456
ER  - 
@article{
author = "Misirkić Marjanović, Maja and Todorović-Marković, Biljana M and Vučićević, Ljubica and Janjetović, Kristina and Jokanović, Vukoman R and Dramicanin, Miroslav D and Marković, Zoran M and Trajković, Vladimir S",
year = "2009",
abstract = "The influence of fullerene (C-60) nanoparticles on the cytotoxicity of a highly reactive free radical nitric oxide (NO) was investigated. Fullerene nanoparticles were prepared by mechanochemically assisted complexation with anionic surfactant sodium dodecyl sulfate, macrocyclic oligosaccharide gamma-cyclodextrin or the copolymer ethylene vinyl acetate-ethylene vinyl versatate. C-60 nanoparticles were characterized by UV-vis and atomic force microscopy. While readily internalized by mouse L929 fibroblasts, C-60 nanoparticles were not cytotoxic. Moreover, they partially protected L929 cells from the cytotoxic effect of NO-releasing compounds sodium nitroprusside (SNP), S-nitroso-N-acetylpenicillamine (SNAP), S-nitrosoglutathione (GSNO) and 3-morpholino-sydnonimine (SIN-1). C-60 nanoparticles reduced SNP-induced apoptotic cell death by preventing mitochondrial depolarization, caspase activation, cell membrane phosphatidylserine exposure and DNA fragmentation. The protective action of C-60 nanoparticles was not exerted via direct interaction with NO, but through neutralization of mitochondria-produced superoxide radical in NO-treated cells, as demonstrated by using different redox-sensitive reporter fluorochromes. These data suggest that C-60 complexes with appropriate host molecules might be plausible candidates for preventing NO-mediated cell injury in inflammatory/autoimmune disorders. (C) 2009 Elsevier Ltd. All rights reserved.",
journal = "Biomaterials",
title = "The protection of cells from nitric oxide-mediated apoptotic death by mechanochemically synthesized fullerene (C-60) nanoparticles",
number = "12",
volume = "30",
pages = "2328",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1456"
}
Misirkić Marjanović, M., Todorović-Marković, B. M., Vučićević, L., Janjetović, K., Jokanović, V. R., Dramicanin, M. D., Marković, Z. M.,& Trajković, V. S.. (2009). The protection of cells from nitric oxide-mediated apoptotic death by mechanochemically synthesized fullerene (C-60) nanoparticles. in Biomaterials, 30(12).
https://hdl.handle.net/21.15107/rcub_ibiss_1456
Misirkić Marjanović M, Todorović-Marković BM, Vučićević L, Janjetović K, Jokanović VR, Dramicanin MD, Marković ZM, Trajković VS. The protection of cells from nitric oxide-mediated apoptotic death by mechanochemically synthesized fullerene (C-60) nanoparticles. in Biomaterials. 2009;30(12):null-2328.
https://hdl.handle.net/21.15107/rcub_ibiss_1456 .
Misirkić Marjanović, Maja, Todorović-Marković, Biljana M, Vučićević, Ljubica, Janjetović, Kristina, Jokanović, Vukoman R, Dramicanin, Miroslav D, Marković, Zoran M, Trajković, Vladimir S, "The protection of cells from nitric oxide-mediated apoptotic death by mechanochemically synthesized fullerene (C-60) nanoparticles" in Biomaterials, 30, no. 12 (2009),
https://hdl.handle.net/21.15107/rcub_ibiss_1456 .

Distinct Cytotoxic Mechanisms of Pristine versus Hydroxylated Fullerene

Isaković, Aleksandra; Marković, Zoran; Todorović-Marković, Biljana; Nikolić, Nadežda; Vranješ-Đurić, Sanja; Mirković, Marija; Dramićanin, Miroslav; Harhaji-Trajković, Ljubica; Zogović, Nevena; Nikolić, Zoran; Trajković, Vladimir

(Oxford University Press (OUP), 2006)

TY  - JOUR
AU  - Isaković, Aleksandra
AU  - Marković, Zoran
AU  - Todorović-Marković, Biljana
AU  - Nikolić, Nadežda
AU  - Vranješ-Đurić, Sanja
AU  - Mirković, Marija
AU  - Dramićanin, Miroslav
AU  - Harhaji-Trajković, Ljubica
AU  - Zogović, Nevena
AU  - Nikolić, Zoran
AU  - Trajković, Vladimir
PY  - 2006
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3589
AB  - The mechanisms underlying the cytotoxic action of pure fullerene suspension (nano-C 60 ) and water-soluble polyhydroxylated fullerene [C 60 (OH) n ] were investigated. Crystal violet assay for cell viability demonstrated that nano-C 60 was at least three orders of magnitude more toxic than C 60 (OH) n to mouse L929 fibrosarcoma, rat C6 glioma, and U251 human glioma cell lines. Flow cytometry analysis of cells stained with propidium iodide (PI), PI/annexin V-fluorescein isothiocyanate, or the redox-sensitive dye dihydrorhodamine revealed that nano-C 60 caused rapid (observable after few hours), reactive oxygen species (ROS)-associated necrosis characterized by cell membrane damage without DNA fragmentation. In contrast, C 60 (OH) n caused delayed, ROS-independent cell death with characteristics of apoptosis, including DNA fragmentation and loss of cell membrane asymmetry in the absence of increased permeability. Accordingly, the antioxidant N-acetylcysteine protected the cell lines from nano-C 60 toxicity, but not C 60 (OH) n toxicity, while the pan-caspase inhibitor z-VAD-fmk blocked C 60 (OH) n -induced apoptosis, but not nano-C 60 -mediated necrosis. Finally, C 60 (OH) n antagomozed, while nano-C 60 synergized with, the cytotoxic action of oxidative stress-inducing agents hydrogen peroxide and peroxynitrite donor 3-morpholinosydnonimine. Therefore, unlike polyhydroxylated C 60 that exerts mainly antioxidant/cytoprotective and only mild ROS-independent pro-apoptotic activity, pure crystalline C 60 seems to be endowed with strong pro-oxidant capacity responsible for the rapid necrotic cell death.
PB  - Oxford University Press (OUP)
T2  - Toxicological Sciences
T1  - Distinct Cytotoxic Mechanisms of Pristine versus Hydroxylated Fullerene
IS  - 1
VL  - 91
DO  - 10.1093/toxsci/kfj127
SP  - 173
EP  - 183
ER  - 
@article{
author = "Isaković, Aleksandra and Marković, Zoran and Todorović-Marković, Biljana and Nikolić, Nadežda and Vranješ-Đurić, Sanja and Mirković, Marija and Dramićanin, Miroslav and Harhaji-Trajković, Ljubica and Zogović, Nevena and Nikolić, Zoran and Trajković, Vladimir",
year = "2006",
abstract = "The mechanisms underlying the cytotoxic action of pure fullerene suspension (nano-C 60 ) and water-soluble polyhydroxylated fullerene [C 60 (OH) n ] were investigated. Crystal violet assay for cell viability demonstrated that nano-C 60 was at least three orders of magnitude more toxic than C 60 (OH) n to mouse L929 fibrosarcoma, rat C6 glioma, and U251 human glioma cell lines. Flow cytometry analysis of cells stained with propidium iodide (PI), PI/annexin V-fluorescein isothiocyanate, or the redox-sensitive dye dihydrorhodamine revealed that nano-C 60 caused rapid (observable after few hours), reactive oxygen species (ROS)-associated necrosis characterized by cell membrane damage without DNA fragmentation. In contrast, C 60 (OH) n caused delayed, ROS-independent cell death with characteristics of apoptosis, including DNA fragmentation and loss of cell membrane asymmetry in the absence of increased permeability. Accordingly, the antioxidant N-acetylcysteine protected the cell lines from nano-C 60 toxicity, but not C 60 (OH) n toxicity, while the pan-caspase inhibitor z-VAD-fmk blocked C 60 (OH) n -induced apoptosis, but not nano-C 60 -mediated necrosis. Finally, C 60 (OH) n antagomozed, while nano-C 60 synergized with, the cytotoxic action of oxidative stress-inducing agents hydrogen peroxide and peroxynitrite donor 3-morpholinosydnonimine. Therefore, unlike polyhydroxylated C 60 that exerts mainly antioxidant/cytoprotective and only mild ROS-independent pro-apoptotic activity, pure crystalline C 60 seems to be endowed with strong pro-oxidant capacity responsible for the rapid necrotic cell death.",
publisher = "Oxford University Press (OUP)",
journal = "Toxicological Sciences",
title = "Distinct Cytotoxic Mechanisms of Pristine versus Hydroxylated Fullerene",
number = "1",
volume = "91",
doi = "10.1093/toxsci/kfj127",
pages = "173-183"
}
Isaković, A., Marković, Z., Todorović-Marković, B., Nikolić, N., Vranješ-Đurić, S., Mirković, M., Dramićanin, M., Harhaji-Trajković, L., Zogović, N., Nikolić, Z.,& Trajković, V.. (2006). Distinct Cytotoxic Mechanisms of Pristine versus Hydroxylated Fullerene. in Toxicological Sciences
Oxford University Press (OUP)., 91(1), 173-183.
https://doi.org/10.1093/toxsci/kfj127
Isaković A, Marković Z, Todorović-Marković B, Nikolić N, Vranješ-Đurić S, Mirković M, Dramićanin M, Harhaji-Trajković L, Zogović N, Nikolić Z, Trajković V. Distinct Cytotoxic Mechanisms of Pristine versus Hydroxylated Fullerene. in Toxicological Sciences. 2006;91(1):173-183.
doi:10.1093/toxsci/kfj127 .
Isaković, Aleksandra, Marković, Zoran, Todorović-Marković, Biljana, Nikolić, Nadežda, Vranješ-Đurić, Sanja, Mirković, Marija, Dramićanin, Miroslav, Harhaji-Trajković, Ljubica, Zogović, Nevena, Nikolić, Zoran, Trajković, Vladimir, "Distinct Cytotoxic Mechanisms of Pristine versus Hydroxylated Fullerene" in Toxicological Sciences, 91, no. 1 (2006):173-183,
https://doi.org/10.1093/toxsci/kfj127 . .
1
262
224
274