TY  - JOUR
AU  - Milutinović, Milan M.
AU  - Čanović, Petar P.
AU  - Stevanović, Dragana D.
AU  - Masnikosa, Romana
AU  - Vraneš, Milan
AU  - Tot, Aleksandar
AU  - Zarić, Milan M.
AU  - Marković-Simović, Bojana
AU  - Misirkić-Marjanović, Maja
AU  - Vučićević, Ljubica
AU  - Savić, Maja
AU  - Jakovljević, Vladimir Lj.
AU  - Trajković, Vladimir S.
AU  - Volarević, Vladislav
AU  - Kanjevac, Tatjana
AU  - Rilak Simović, Ana
PY  - 2018
UR  - http://pubs.acs.org/doi/10.1021/acs.organomet.8b00604
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7967
AB  - The two new heterometallic Ru(II)-tpy/ferrocene complexes [Ru(tpy)Cl2(mtefc)] (1) and [Ru(tpy)Cl2(mtpfc)] (2) (where tpy = 2,2′:6′,2′′-terpyridine, mtefc = (2-(methylthio)ethyl)ferrocene, and mtpfc = (3-(methylthio)propyl)ferrocene) have been synthesized and then characterized through elemental analysis, followed by various spectroscopic (IR, UV-vis, 1D and 2D NMR) and mass spectrometric techniques (MALDI TOF and ESI Q-TOF MS). UV-vis and fluorescence spectroscopy and viscometry were employed to study the interactions of the complexes 1 and 2 with calf thymus DNA. Both 1 and 2 expelled ethidium bromide (EB) from the EB/DNA complex (Ksv = (1.5-1.8) × 104 M-1), which suggested that the complexes intercalated into the double helix of DNA. Both complexes strongly quenched the fluorescence of tryptophan residues in serum albumin through both static and dynamic quenching. Molecular docking confirmed the intercalative mode of complex interaction with DNA. The docking results implied that 1 and 2 interacted with hydrophobic residues of albumin, particularly with those lying in the proximity of Tyr 160. We here demonstrate the high cytotoxic potential of complexes 1 and 2 against the breast cancer cells that originated either from humans (MDA-MB-231) or from mice (4T1), with apoptosis being the main mechanism of complex-induced cell death. It is worth noting that both complexes promoted activation of innate and acquired antitumor immunity, which contributed to the reduced growth and progression of mammary carcinoma in vivo. Copyright © 2018 American Chemical Society.
T2  - Organometallics
T1  - Newly Synthesized Heteronuclear Ruthenium(II)/Ferrocene Complexes Suppress the Growth of Mammary Carcinoma in 4T1-Treated BALB/c Mice by Promoting Activation of Antitumor Immunity
VL  - 37
IS  - 22
SP  - 4250
EP  - 4266
DO  - 10.1021/acs.organomet.8b00604
ER  - 

@article{
author = "Milutinović, Milan M. and Čanović, Petar P. and Stevanović, Dragana D. and Masnikosa, Romana and Vraneš, Milan and Tot, Aleksandar and Zarić, Milan M. and Marković-Simović, Bojana and Misirkić-Marjanović, Maja and Vučićević, Ljubica and Savić, Maja and Jakovljević, Vladimir Lj. and Trajković, Vladimir S. and Volarević, Vladislav and Kanjevac, Tatjana and Rilak Simović, Ana",
year = "2018",
abstract = "The two new heterometallic Ru(II)-tpy/ferrocene complexes [Ru(tpy)Cl2(mtefc)] (1) and [Ru(tpy)Cl2(mtpfc)] (2) (where tpy = 2,2′:6′,2′′-terpyridine, mtefc = (2-(methylthio)ethyl)ferrocene, and mtpfc = (3-(methylthio)propyl)ferrocene) have been synthesized and then characterized through elemental analysis, followed by various spectroscopic (IR, UV-vis, 1D and 2D NMR) and mass spectrometric techniques (MALDI TOF and ESI Q-TOF MS). UV-vis and fluorescence spectroscopy and viscometry were employed to study the interactions of the complexes 1 and 2 with calf thymus DNA. Both 1 and 2 expelled ethidium bromide (EB) from the EB/DNA complex (Ksv = (1.5-1.8) × 104 M-1), which suggested that the complexes intercalated into the double helix of DNA. Both complexes strongly quenched the fluorescence of tryptophan residues in serum albumin through both static and dynamic quenching. Molecular docking confirmed the intercalative mode of complex interaction with DNA. The docking results implied that 1 and 2 interacted with hydrophobic residues of albumin, particularly with those lying in the proximity of Tyr 160. We here demonstrate the high cytotoxic potential of complexes 1 and 2 against the breast cancer cells that originated either from humans (MDA-MB-231) or from mice (4T1), with apoptosis being the main mechanism of complex-induced cell death. It is worth noting that both complexes promoted activation of innate and acquired antitumor immunity, which contributed to the reduced growth and progression of mammary carcinoma in vivo. Copyright © 2018 American Chemical Society.",
journal = "Organometallics",
title = "Newly Synthesized Heteronuclear Ruthenium(II)/Ferrocene Complexes Suppress the Growth of Mammary Carcinoma in 4T1-Treated BALB/c Mice by Promoting Activation of Antitumor Immunity",
volume = "37",
number = "22",
pages = "4250-4266",
doi = "10.1021/acs.organomet.8b00604"
}

Milutinović, M. M., Čanović, P. P., Stevanović, D. D., Masnikosa, R., Vraneš, M., Tot, A., Zarić, M. M., Marković-Simović, B., Misirkić-Marjanović, M., Vučićević, L., Savić, M., Jakovljević, V. Lj., Trajković, V. S., Volarević, V., Kanjevac, T.,& Rilak Simović, A.. (2018). Newly Synthesized Heteronuclear Ruthenium(II)/Ferrocene Complexes Suppress the Growth of Mammary Carcinoma in 4T1-Treated BALB/c Mice by Promoting Activation of Antitumor Immunity. in Organometallics, 37(22), 4250-4266.
https://doi.org/10.1021/acs.organomet.8b00604

Milutinović MM, Čanović PP, Stevanović DD, Masnikosa R, Vraneš M, Tot A, Zarić MM, Marković-Simović B, Misirkić-Marjanović M, Vučićević L, Savić M, Jakovljević VL, Trajković VS, Volarević V, Kanjevac T, Rilak Simović A. Newly Synthesized Heteronuclear Ruthenium(II)/Ferrocene Complexes Suppress the Growth of Mammary Carcinoma in 4T1-Treated BALB/c Mice by Promoting Activation of Antitumor Immunity. in Organometallics. 2018;37(22):4250-4266.
doi:10.1021/acs.organomet.8b00604 .

Milutinović, Milan M., Čanović, Petar P., Stevanović, Dragana D., Masnikosa, Romana, Vraneš, Milan, Tot, Aleksandar, Zarić, Milan M., Marković-Simović, Bojana, Misirkić-Marjanović, Maja, Vučićević, Ljubica, Savić, Maja, Jakovljević, Vladimir Lj., Trajković, Vladimir S., Volarević, Vladislav, Kanjevac, Tatjana, Rilak Simović, Ana, "Newly Synthesized Heteronuclear Ruthenium(II)/Ferrocene Complexes Suppress the Growth of Mammary Carcinoma in 4T1-Treated BALB/c Mice by Promoting Activation of Antitumor Immunity" in Organometallics, 37, no. 22 (2018):4250-4266,
https://doi.org/10.1021/acs.organomet.8b00604 . .

TY  - JOUR
AU  - Sudar, Emina
AU  - Jovanović, Aleksandra
AU  - Misirkić-Marjanović, Maja
AU  - Vučićević, Ljubica
AU  - Janjetović, Kristina D.
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/832
AB  - The aim of this study was to examine the effects of ghrelin on regulation of cardiac inducible nitric oxide synthase (iNOS) activity/expression in high fat (HF), obese rats. For this study, male Wistar rats fed with HF diet (30 % fat) for 4 weeks were injected every 24 h for 5 days intracerebroventriculary (ICV) with ghrelin (0.3 nmol/5 mu l) or with an equal volume of phosphate buffered saline (PBS). Control rats were ICV injected with an equal volume of PBS. Glucose, insulin and nitric oxide (NO) concentrations were measured in serum, while arginase activity and citrulline concentrations were measured in heart lysate. Protein iNOS and regulatory subunit of nuclear factor-kappa B (NF kappa B-p65), phosphorylation of enzymes protein kinase B (Akt) at Ser(473), and extracellular signal-regulated kinases 1/2 (ERK1/2) at Tyr(202)/Tyr(204) were determined in heart lysate by Western blot. For gene expression of iNOS qRT-PCR was used. Results show significantly (p LT 0.01) higher serum NO production in ghrelin treated HF rats compared with HF rats. Ghrelin significantly reduced citrulline concentration (p LT 0.05) and arginase activity (p LT 0.01) in HF rats. In ghrelin treated HF rats, gene and protein expression of iNOS and NF kappa B-p65 levels were significantly (p LT 0.05) increased compared with HF rats. Increased phosphorylation of Akt (p LT 0.01) and decreased (p LT 0.05) ERK1/2 phosphorylation were detected in HF ghrelin treated rats compared with HF rats hearts. Results from this study indicate that exogenous ghrelin induces expression and activity of cardiac iNOS via Akt phosphorylation followed by NF kappa B activation in HF rats.
PB  - Georg Thieme Verlag KG
T2  - Experimental and Clinical Endocrinology and Diabetes
T1  - Effects of Intracerebroventricularly (ICV) Injected Ghrelin on Cardiac Inducible Nitric Oxide Synthase Activity/Expression in Obese Rats
VL  - 123
IS  - 10
SP  - 581
EP  - 588
DO  - 10.1055/s-0035-1559758
ER  - 

@article{
author = "Sudar, Emina and Jovanović, Aleksandra and Misirkić-Marjanović, Maja and Vučićević, Ljubica and Janjetović, Kristina D. and Isenović, Esma R.",
year = "2015",
abstract = "The aim of this study was to examine the effects of ghrelin on regulation of cardiac inducible nitric oxide synthase (iNOS) activity/expression in high fat (HF), obese rats. For this study, male Wistar rats fed with HF diet (30 % fat) for 4 weeks were injected every 24 h for 5 days intracerebroventriculary (ICV) with ghrelin (0.3 nmol/5 mu l) or with an equal volume of phosphate buffered saline (PBS). Control rats were ICV injected with an equal volume of PBS. Glucose, insulin and nitric oxide (NO) concentrations were measured in serum, while arginase activity and citrulline concentrations were measured in heart lysate. Protein iNOS and regulatory subunit of nuclear factor-kappa B (NF kappa B-p65), phosphorylation of enzymes protein kinase B (Akt) at Ser(473), and extracellular signal-regulated kinases 1/2 (ERK1/2) at Tyr(202)/Tyr(204) were determined in heart lysate by Western blot. For gene expression of iNOS qRT-PCR was used. Results show significantly (p LT 0.01) higher serum NO production in ghrelin treated HF rats compared with HF rats. Ghrelin significantly reduced citrulline concentration (p LT 0.05) and arginase activity (p LT 0.01) in HF rats. In ghrelin treated HF rats, gene and protein expression of iNOS and NF kappa B-p65 levels were significantly (p LT 0.05) increased compared with HF rats. Increased phosphorylation of Akt (p LT 0.01) and decreased (p LT 0.05) ERK1/2 phosphorylation were detected in HF ghrelin treated rats compared with HF rats hearts. Results from this study indicate that exogenous ghrelin induces expression and activity of cardiac iNOS via Akt phosphorylation followed by NF kappa B activation in HF rats.",
publisher = "Georg Thieme Verlag KG",
journal = "Experimental and Clinical Endocrinology and Diabetes",
title = "Effects of Intracerebroventricularly (ICV) Injected Ghrelin on Cardiac Inducible Nitric Oxide Synthase Activity/Expression in Obese Rats",
volume = "123",
number = "10",
pages = "581-588",
doi = "10.1055/s-0035-1559758"
}

Sudar, E., Jovanović, A., Misirkić-Marjanović, M., Vučićević, L., Janjetović, K. D.,& Isenović, E. R.. (2015). Effects of Intracerebroventricularly (ICV) Injected Ghrelin on Cardiac Inducible Nitric Oxide Synthase Activity/Expression in Obese Rats. in Experimental and Clinical Endocrinology and Diabetes
Georg Thieme Verlag KG., 123(10), 581-588.
https://doi.org/10.1055/s-0035-1559758

Sudar E, Jovanović A, Misirkić-Marjanović M, Vučićević L, Janjetović KD, Isenović ER. Effects of Intracerebroventricularly (ICV) Injected Ghrelin on Cardiac Inducible Nitric Oxide Synthase Activity/Expression in Obese Rats. in Experimental and Clinical Endocrinology and Diabetes. 2015;123(10):581-588.
doi:10.1055/s-0035-1559758 .

Sudar, Emina, Jovanović, Aleksandra, Misirkić-Marjanović, Maja, Vučićević, Ljubica, Janjetović, Kristina D., Isenović, Esma R., "Effects of Intracerebroventricularly (ICV) Injected Ghrelin on Cardiac Inducible Nitric Oxide Synthase Activity/Expression in Obese Rats" in Experimental and Clinical Endocrinology and Diabetes, 123, no. 10 (2015):581-588,
https://doi.org/10.1055/s-0035-1559758 . .

TY  - JOUR
AU  - Volarevic, Vladislav
AU  - Paunović, Verica G.
AU  - Marković, Zoran M.
AU  - Marković-Simović, Bojana
AU  - Misirkić-Marjanović, Maja
AU  - Todorović-Marković, Biljana
AU  - Bojic, Sanja
AU  - Vucicevic, Ljubica
AU  - Jovanović, Svetlana P.
AU  - Arsenijević, Nebojša N.
AU  - Holclajtner-Antunović, Ivanka D.
AU  - Milosavljević, Momir
AU  - Dramićanin, Miroslav
AU  - Kravić-Stevović, Tamara K.
AU  - Ćirić, Darko
AU  - Lukić, Miodrag L.
AU  - Trajković, Vladimir S.
PY  - 2014
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/324
AB  - We investigated the effect of large (40 nm) graphene quantum dots (GQDs) in concanavalin A (Con A; 12 mg/kg i.v.)-induced mouse hepatitis, a T cell-mediated liver injury resembling fulminant hepatitis in humans. Intravenously injected GQDs (50 mg/kg) accumulated in liver and reduced Con A-mediated liver damage, as demonstrated by histopathological analysis and a decrease in liver lipid peroxidation and serum levels of liver transaminases. The cleavage of apoptotic markers caspase-3/PARP and mRNA levels of proapoptotic mediators Puma, Noxa, Bax, Bak1, Bim, Apaf1, and p21, as well as LC3-I conversion to autophagosome-associated LC3-II and expression of autophagy-related (Atg) genes Atg4b, Atg7, Atg12, and beclin-1, were attenuated by GQDs, indicating a decrease in both apoptosis and autophagy in the liver tissue. This was associated with the reduced liver infiltration of immune cells, particularly the T cells producing proinflammatory cytokine IFN-?, and a decrease in IFN-gamma serum levels. In the spleen of GQD-exposed mice, mRNA expression of IFN-? and its transcription factor T-bet was reduced, while that of the IL-33 ligand ST2 was increased. The hepatoprotective effect of GQDs was less pronounced in ST2-deficient mice, indicating that it might depend on ST2 upregulation. In vitro, GQDs inhibited splenocyte IFN-gamma production, reduced the activation of extracellular signal-regulated kinase in macrophage and T cell lines, inhibited macrophage production of the free radical nitric oxide, and reduced its cytotoxicity toward hepatocyte cell line HepG2. Therefore, GQDs alleviate immune-mediated fulminant hepatitis by interfering with T cell and macrophage activation and possibly by exerting a direct hepatoprotective effect.
T2  - ACS Nano
T1  - Large Graphene Quantum Dots Alleviate Immune-Mediated Liver Damage
VL  - 8
IS  - 12
SP  - 12098
EP  - 12109
DO  - 10.1021/nn502466z
ER  - 

@article{
author = "Volarevic, Vladislav and Paunović, Verica G. and Marković, Zoran M. and Marković-Simović, Bojana and Misirkić-Marjanović, Maja and Todorović-Marković, Biljana and Bojic, Sanja and Vucicevic, Ljubica and Jovanović, Svetlana P. and Arsenijević, Nebojša N. and Holclajtner-Antunović, Ivanka D. and Milosavljević, Momir and Dramićanin, Miroslav and Kravić-Stevović, Tamara K. and Ćirić, Darko and Lukić, Miodrag L. and Trajković, Vladimir S.",
year = "2014",
abstract = "We investigated the effect of large (40 nm) graphene quantum dots (GQDs) in concanavalin A (Con A; 12 mg/kg i.v.)-induced mouse hepatitis, a T cell-mediated liver injury resembling fulminant hepatitis in humans. Intravenously injected GQDs (50 mg/kg) accumulated in liver and reduced Con A-mediated liver damage, as demonstrated by histopathological analysis and a decrease in liver lipid peroxidation and serum levels of liver transaminases. The cleavage of apoptotic markers caspase-3/PARP and mRNA levels of proapoptotic mediators Puma, Noxa, Bax, Bak1, Bim, Apaf1, and p21, as well as LC3-I conversion to autophagosome-associated LC3-II and expression of autophagy-related (Atg) genes Atg4b, Atg7, Atg12, and beclin-1, were attenuated by GQDs, indicating a decrease in both apoptosis and autophagy in the liver tissue. This was associated with the reduced liver infiltration of immune cells, particularly the T cells producing proinflammatory cytokine IFN-?, and a decrease in IFN-gamma serum levels. In the spleen of GQD-exposed mice, mRNA expression of IFN-? and its transcription factor T-bet was reduced, while that of the IL-33 ligand ST2 was increased. The hepatoprotective effect of GQDs was less pronounced in ST2-deficient mice, indicating that it might depend on ST2 upregulation. In vitro, GQDs inhibited splenocyte IFN-gamma production, reduced the activation of extracellular signal-regulated kinase in macrophage and T cell lines, inhibited macrophage production of the free radical nitric oxide, and reduced its cytotoxicity toward hepatocyte cell line HepG2. Therefore, GQDs alleviate immune-mediated fulminant hepatitis by interfering with T cell and macrophage activation and possibly by exerting a direct hepatoprotective effect.",
journal = "ACS Nano",
title = "Large Graphene Quantum Dots Alleviate Immune-Mediated Liver Damage",
volume = "8",
number = "12",
pages = "12098-12109",
doi = "10.1021/nn502466z"
}

Volarevic, V., Paunović, V. G., Marković, Z. M., Marković-Simović, B., Misirkić-Marjanović, M., Todorović-Marković, B., Bojic, S., Vucicevic, L., Jovanović, S. P., Arsenijević, N. N., Holclajtner-Antunović, I. D., Milosavljević, M., Dramićanin, M., Kravić-Stevović, T. K., Ćirić, D., Lukić, M. L.,& Trajković, V. S.. (2014). Large Graphene Quantum Dots Alleviate Immune-Mediated Liver Damage. in ACS Nano, 8(12), 12098-12109.
https://doi.org/10.1021/nn502466z

Volarevic V, Paunović VG, Marković ZM, Marković-Simović B, Misirkić-Marjanović M, Todorović-Marković B, Bojic S, Vucicevic L, Jovanović SP, Arsenijević NN, Holclajtner-Antunović ID, Milosavljević M, Dramićanin M, Kravić-Stevović TK, Ćirić D, Lukić ML, Trajković VS. Large Graphene Quantum Dots Alleviate Immune-Mediated Liver Damage. in ACS Nano. 2014;8(12):12098-12109.
doi:10.1021/nn502466z .

Volarevic, Vladislav, Paunović, Verica G., Marković, Zoran M., Marković-Simović, Bojana, Misirkić-Marjanović, Maja, Todorović-Marković, Biljana, Bojic, Sanja, Vucicevic, Ljubica, Jovanović, Svetlana P., Arsenijević, Nebojša N., Holclajtner-Antunović, Ivanka D., Milosavljević, Momir, Dramićanin, Miroslav, Kravić-Stevović, Tamara K., Ćirić, Darko, Lukić, Miodrag L., Trajković, Vladimir S., "Large Graphene Quantum Dots Alleviate Immune-Mediated Liver Damage" in ACS Nano, 8, no. 12 (2014):12098-12109,
https://doi.org/10.1021/nn502466z . .

TY  - JOUR
AU  - Stevanović, Darko
AU  - Starčević, Vesna
AU  - Vilimanovich, Urosh
AU  - Nešić, Dejan
AU  - Vucicevic, Ljubica
AU  - Misirkić, Maja
AU  - Janjetović, Kristina D.
AU  - Savić, Emina
AU  - Popadic, Dusan
AU  - Sudar, Emina
AU  - Micic, Dragan
AU  - Šumarac-Dumanović, Mirjana
AU  - Trajković, Vladimir S.
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4590
AB  - We investigated the effects of centrally administered orexigenic hormone ghrelin on energy imbalance-induced inflammation. Rats were subjected for four weeks to three different dietary regimes: normal (standard food), high-fat (standard food with 30% lard) or food-restricted (70%, 50%, 40% and 40% of the expected food intake in 1st, 2nd, 3rd and 4th week, respectively). Compared to normal-weight controls, starved, but not obese rats had significantly higher levels of proinflammatory cytokines (TNF, IL-1 beta, IFN-gamma) in the blood. When compared to normally fed animals, the hearts of starved and obese animals expressed higher levels of mRNAs encoding proinflammatory mediators (TNF, IL-1 beta, IL-6, IFN-gamma, IL-17, IL-12, iNOS), while mRNA levels of the anti-inflammatory TGF-beta remained unchanged. Intracerebroventricular (ICV) injection of ghrelin (1 mu g/day) for five consecutive days significantly reduced TNF, IL-1 beta and IFN-gamma levels in the blood of starved rats, as well as TNF, IL-17 and IL-12p40 mRNA expression in the hearts of obese rats. Conversely, ICV ghrelin increased the levels of 1FN-gamma, IL-17,1L-12p35 and IL-12p40 mRNA in the heart tissue of food-restricted animals. This was associated with an increase of immunosuppressive ACTH/corticosterone production in starved animals and a decrease of the immunostimulatory adipokine leptin both in food-restricted and high-fat groups. Ghrelin activated the energy sensor AMP-activated protein kinase (AMPK) in the hypothalamus and inhibited extracellular signal-regulated kinase (ERK) in the hearts of obese, but not starved rats. Therefore, central ghrelin may play a complex role in energy imbalance-induced inflammation by modulating HPA axis, leptin and AMPK/ERK signaling pathways. (C) 2011 Elsevier Inc. All rights reserved.
T2  - Brain Behavior and Immunity
T1  - Immunomodulatory actions of central ghrelin in diet-induced energy imbalance
VL  - 26
IS  - 1
SP  - 150
EP  - 158
DO  - 10.1016/j.bbi.2011.08.009
ER  - 

@article{
author = "Stevanović, Darko and Starčević, Vesna and Vilimanovich, Urosh and Nešić, Dejan and Vucicevic, Ljubica and Misirkić, Maja and Janjetović, Kristina D. and Savić, Emina and Popadic, Dusan and Sudar, Emina and Micic, Dragan and Šumarac-Dumanović, Mirjana and Trajković, Vladimir S.",
year = "2012",
abstract = "We investigated the effects of centrally administered orexigenic hormone ghrelin on energy imbalance-induced inflammation. Rats were subjected for four weeks to three different dietary regimes: normal (standard food), high-fat (standard food with 30% lard) or food-restricted (70%, 50%, 40% and 40% of the expected food intake in 1st, 2nd, 3rd and 4th week, respectively). Compared to normal-weight controls, starved, but not obese rats had significantly higher levels of proinflammatory cytokines (TNF, IL-1 beta, IFN-gamma) in the blood. When compared to normally fed animals, the hearts of starved and obese animals expressed higher levels of mRNAs encoding proinflammatory mediators (TNF, IL-1 beta, IL-6, IFN-gamma, IL-17, IL-12, iNOS), while mRNA levels of the anti-inflammatory TGF-beta remained unchanged. Intracerebroventricular (ICV) injection of ghrelin (1 mu g/day) for five consecutive days significantly reduced TNF, IL-1 beta and IFN-gamma levels in the blood of starved rats, as well as TNF, IL-17 and IL-12p40 mRNA expression in the hearts of obese rats. Conversely, ICV ghrelin increased the levels of 1FN-gamma, IL-17,1L-12p35 and IL-12p40 mRNA in the heart tissue of food-restricted animals. This was associated with an increase of immunosuppressive ACTH/corticosterone production in starved animals and a decrease of the immunostimulatory adipokine leptin both in food-restricted and high-fat groups. Ghrelin activated the energy sensor AMP-activated protein kinase (AMPK) in the hypothalamus and inhibited extracellular signal-regulated kinase (ERK) in the hearts of obese, but not starved rats. Therefore, central ghrelin may play a complex role in energy imbalance-induced inflammation by modulating HPA axis, leptin and AMPK/ERK signaling pathways. (C) 2011 Elsevier Inc. All rights reserved.",
journal = "Brain Behavior and Immunity",
title = "Immunomodulatory actions of central ghrelin in diet-induced energy imbalance",
volume = "26",
number = "1",
pages = "150-158",
doi = "10.1016/j.bbi.2011.08.009"
}

Stevanović, D., Starčević, V., Vilimanovich, U., Nešić, D., Vucicevic, L., Misirkić, M., Janjetović, K. D., Savić, E., Popadic, D., Sudar, E., Micic, D., Šumarac-Dumanović, M.,& Trajković, V. S.. (2012). Immunomodulatory actions of central ghrelin in diet-induced energy imbalance. in Brain Behavior and Immunity, 26(1), 150-158.
https://doi.org/10.1016/j.bbi.2011.08.009

Stevanović D, Starčević V, Vilimanovich U, Nešić D, Vucicevic L, Misirkić M, Janjetović KD, Savić E, Popadic D, Sudar E, Micic D, Šumarac-Dumanović M, Trajković VS. Immunomodulatory actions of central ghrelin in diet-induced energy imbalance. in Brain Behavior and Immunity. 2012;26(1):150-158.
doi:10.1016/j.bbi.2011.08.009 .

Stevanović, Darko, Starčević, Vesna, Vilimanovich, Urosh, Nešić, Dejan, Vucicevic, Ljubica, Misirkić, Maja, Janjetović, Kristina D., Savić, Emina, Popadic, Dusan, Sudar, Emina, Micic, Dragan, Šumarac-Dumanović, Mirjana, Trajković, Vladimir S., "Immunomodulatory actions of central ghrelin in diet-induced energy imbalance" in Brain Behavior and Immunity, 26, no. 1 (2012):150-158,
https://doi.org/10.1016/j.bbi.2011.08.009 . .

TY  - JOUR
AU  - Janjetović, Kristina D.
AU  - Vucicevic, Ljubica
AU  - Misirkić, Maja
AU  - Vilimanovich, Urosh
AU  - Tovilovic, Gordana
AU  - Zogovic, Nevena
AU  - Nikolić, Zoran M.
AU  - Jovanović, Svetlana P.
AU  - Bumbaširević, Vladimir Ž.
AU  - Trajković, Vladimir S.
AU  - Harhaji-Trajković, Ljubica M.
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4205
AB  - Metformin is an antidiabetic drug with anticancer properties, which mainly acts through induction of AMP-activated protein kinase (AMPK). In the present study we investigated the influence of metformin on the in vitro anticancer activity of the well-known chemotherapeutic agent cisplatin. Cell viability was determined by MTT and LDH release assay, oxidative stress and apoptosis (caspase activation, DNA fragmentation, and phosphatidylserine exposure) were assessed by flow cytometry, while activation of AMPK and Akt was analyzed by immunoblotting. Although metformin reduced the number of tumour cells when applied alone, it surprisingly antagonized the cytotoxicity of cisplatin towards U251 human glioma, C6 rat glioma, SHSY5Y human neuroblastoma, L929 mouse fibrosarcoma and HL-60 human leukemia cell lines. Only in B16 mouse melanoma cells metformin augmented the cytotoxicity of cisplatin. In U251 glioma cells metformin suppressed cisplatin-induced apoptotic cell death through inhibition of oxidative stress and caspase activation. The observed cytoprotection was apparently AMPK-independent, as metformin did not further increase cisplatin-induced AMPK activation in U251 cells and other pharmacological AMPK activators failed to block cisplatin-mediated apoptosis. On the other hand, metformin induced Akt activation in cisplatin-treated cells and Akt inhibitor 10-DEBC hydrochloride or phosphoinositide 3-kinase/Akt inhibitor LY294002 abolished metformin-mediated antioxidant and antiapoptotic effects. In conclusion, the antidiabetic drug metformin reduces cisplatin in vitro anticancer activity through AMPK-independent upregulation of Akt survival pathway. These data warrant caution when considering metformin for treatment of diabetic cancer patients receiving cisplatin or as a potential adjuvant in cisplatin-based chemotherapeutic regimens. (c) 2010 Published by Elsevier B.V.
T2  - European Journal of Pharmacology
T1  - Metformin reduces cisplatin-mediated apoptotic death of cancer cells through AMPK-independent activation of Akt
VL  - 651
IS  - 1-3
SP  - 41
EP  - 50
DO  - 10.1016/j.ejphar.2010.11.005
ER  - 

@article{
author = "Janjetović, Kristina D. and Vucicevic, Ljubica and Misirkić, Maja and Vilimanovich, Urosh and Tovilovic, Gordana and Zogovic, Nevena and Nikolić, Zoran M. and Jovanović, Svetlana P. and Bumbaširević, Vladimir Ž. and Trajković, Vladimir S. and Harhaji-Trajković, Ljubica M.",
year = "2011",
abstract = "Metformin is an antidiabetic drug with anticancer properties, which mainly acts through induction of AMP-activated protein kinase (AMPK). In the present study we investigated the influence of metformin on the in vitro anticancer activity of the well-known chemotherapeutic agent cisplatin. Cell viability was determined by MTT and LDH release assay, oxidative stress and apoptosis (caspase activation, DNA fragmentation, and phosphatidylserine exposure) were assessed by flow cytometry, while activation of AMPK and Akt was analyzed by immunoblotting. Although metformin reduced the number of tumour cells when applied alone, it surprisingly antagonized the cytotoxicity of cisplatin towards U251 human glioma, C6 rat glioma, SHSY5Y human neuroblastoma, L929 mouse fibrosarcoma and HL-60 human leukemia cell lines. Only in B16 mouse melanoma cells metformin augmented the cytotoxicity of cisplatin. In U251 glioma cells metformin suppressed cisplatin-induced apoptotic cell death through inhibition of oxidative stress and caspase activation. The observed cytoprotection was apparently AMPK-independent, as metformin did not further increase cisplatin-induced AMPK activation in U251 cells and other pharmacological AMPK activators failed to block cisplatin-mediated apoptosis. On the other hand, metformin induced Akt activation in cisplatin-treated cells and Akt inhibitor 10-DEBC hydrochloride or phosphoinositide 3-kinase/Akt inhibitor LY294002 abolished metformin-mediated antioxidant and antiapoptotic effects. In conclusion, the antidiabetic drug metformin reduces cisplatin in vitro anticancer activity through AMPK-independent upregulation of Akt survival pathway. These data warrant caution when considering metformin for treatment of diabetic cancer patients receiving cisplatin or as a potential adjuvant in cisplatin-based chemotherapeutic regimens. (c) 2010 Published by Elsevier B.V.",
journal = "European Journal of Pharmacology",
title = "Metformin reduces cisplatin-mediated apoptotic death of cancer cells through AMPK-independent activation of Akt",
volume = "651",
number = "1-3",
pages = "41-50",
doi = "10.1016/j.ejphar.2010.11.005"
}

Janjetović, K. D., Vucicevic, L., Misirkić, M., Vilimanovich, U., Tovilovic, G., Zogovic, N., Nikolić, Z. M., Jovanović, S. P., Bumbaširević, V. Ž., Trajković, V. S.,& Harhaji-Trajković, L. M.. (2011). Metformin reduces cisplatin-mediated apoptotic death of cancer cells through AMPK-independent activation of Akt. in European Journal of Pharmacology, 651(1-3), 41-50.
https://doi.org/10.1016/j.ejphar.2010.11.005

Janjetović KD, Vucicevic L, Misirkić M, Vilimanovich U, Tovilovic G, Zogovic N, Nikolić ZM, Jovanović SP, Bumbaširević VŽ, Trajković VS, Harhaji-Trajković LM. Metformin reduces cisplatin-mediated apoptotic death of cancer cells through AMPK-independent activation of Akt. in European Journal of Pharmacology. 2011;651(1-3):41-50.
doi:10.1016/j.ejphar.2010.11.005 .

Janjetović, Kristina D., Vucicevic, Ljubica, Misirkić, Maja, Vilimanovich, Urosh, Tovilovic, Gordana, Zogovic, Nevena, Nikolić, Zoran M., Jovanović, Svetlana P., Bumbaširević, Vladimir Ž., Trajković, Vladimir S., Harhaji-Trajković, Ljubica M., "Metformin reduces cisplatin-mediated apoptotic death of cancer cells through AMPK-independent activation of Akt" in European Journal of Pharmacology, 651, no. 1-3 (2011):41-50,
https://doi.org/10.1016/j.ejphar.2010.11.005 . .

TY  - JOUR
AU  - Sudar, Emina
AU  - Dobutović, Branislava
AU  - Soskić, Sanja S.
AU  - Mandušić, Vesna
AU  - Žakula, Zorica
AU  - Misirkić, Maja
AU  - Vucicevic, Ljubica
AU  - Janjetović, Kristina D.
AU  - Trajković, Vladimir S.
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4317
AB  - The purpose of this study was to examine the effects of ghrelin on protein kinase B (Akt) and mitogen-activated protein kinase p42/44 (ERK1/2) activation as well as ghrelin effects on inducible nitric oxide (NO) synthase (iNOS; for gene Nos2) activity/expression in rat hearts. Male Wistar rats were treated with ghrelin (0.3 nmol/5 mu l) or an equal volume of phosphate-buffered saline, injected every 24 h into the lateral cerebral ventricle for 5 days and 2 h after the last treatment the animals were sacrificed. Serum NO, l-arginine (l-Arg), and arginase activity were measured spectrophotometrically. For phosphorylation of Akt, ERK1/2, and iNOS protein expression, Western blot method was used. The expression of Nos2 mRNA was measured by the quantitative real-time polymerase chain reaction (qRT-PCR). Treatment with ghrelin significantly increased NO production in serum by 1.4-fold compared with control. The concentration of l-Arg was significantly higher in ghrelin-treated rats than in control while arginase activity was significantly lower in ghrelin-treated than in control hearts. Ghrelin treatment increased phosphorylation of Akt by 1.9-fold and ERK1/2 by 1.6-fold and increased iNOS expression by 2.5-fold compared with control. In addition, ghrelin treatment increased Nos2 gene expression by 2.2-fold as determined by qRT-PCR. These results indicate that ghrelin regulation of iNOS expression/activity is mediated via Akt/ERK1/2 signaling pathway. These results may be relevant to understanding molecular mechanisms underlying direct cardiovascular actions of ghrelin.
T2  - Journal of Physiology and Biochemistry
T1  - Regulation of inducible nitric oxide synthase activity/expression in rat hearts from ghrelin-treated rats
VL  - 67
IS  - 2
SP  - 195
EP  - 204
DO  - 10.1007/s13105-010-0063-1
ER  - 

@article{
author = "Sudar, Emina and Dobutović, Branislava and Soskić, Sanja S. and Mandušić, Vesna and Žakula, Zorica and Misirkić, Maja and Vucicevic, Ljubica and Janjetović, Kristina D. and Trajković, Vladimir S. and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2011",
abstract = "The purpose of this study was to examine the effects of ghrelin on protein kinase B (Akt) and mitogen-activated protein kinase p42/44 (ERK1/2) activation as well as ghrelin effects on inducible nitric oxide (NO) synthase (iNOS; for gene Nos2) activity/expression in rat hearts. Male Wistar rats were treated with ghrelin (0.3 nmol/5 mu l) or an equal volume of phosphate-buffered saline, injected every 24 h into the lateral cerebral ventricle for 5 days and 2 h after the last treatment the animals were sacrificed. Serum NO, l-arginine (l-Arg), and arginase activity were measured spectrophotometrically. For phosphorylation of Akt, ERK1/2, and iNOS protein expression, Western blot method was used. The expression of Nos2 mRNA was measured by the quantitative real-time polymerase chain reaction (qRT-PCR). Treatment with ghrelin significantly increased NO production in serum by 1.4-fold compared with control. The concentration of l-Arg was significantly higher in ghrelin-treated rats than in control while arginase activity was significantly lower in ghrelin-treated than in control hearts. Ghrelin treatment increased phosphorylation of Akt by 1.9-fold and ERK1/2 by 1.6-fold and increased iNOS expression by 2.5-fold compared with control. In addition, ghrelin treatment increased Nos2 gene expression by 2.2-fold as determined by qRT-PCR. These results indicate that ghrelin regulation of iNOS expression/activity is mediated via Akt/ERK1/2 signaling pathway. These results may be relevant to understanding molecular mechanisms underlying direct cardiovascular actions of ghrelin.",
journal = "Journal of Physiology and Biochemistry",
title = "Regulation of inducible nitric oxide synthase activity/expression in rat hearts from ghrelin-treated rats",
volume = "67",
number = "2",
pages = "195-204",
doi = "10.1007/s13105-010-0063-1"
}

Sudar, E., Dobutović, B., Soskić, S. S., Mandušić, V., Žakula, Z., Misirkić, M., Vucicevic, L., Janjetović, K. D., Trajković, V. S., Mikhailidis, D. P.,& Isenović, E. R.. (2011). Regulation of inducible nitric oxide synthase activity/expression in rat hearts from ghrelin-treated rats. in Journal of Physiology and Biochemistry, 67(2), 195-204.
https://doi.org/10.1007/s13105-010-0063-1

Sudar E, Dobutović B, Soskić SS, Mandušić V, Žakula Z, Misirkić M, Vucicevic L, Janjetović KD, Trajković VS, Mikhailidis DP, Isenović ER. Regulation of inducible nitric oxide synthase activity/expression in rat hearts from ghrelin-treated rats. in Journal of Physiology and Biochemistry. 2011;67(2):195-204.
doi:10.1007/s13105-010-0063-1 .

Sudar, Emina, Dobutović, Branislava, Soskić, Sanja S., Mandušić, Vesna, Žakula, Zorica, Misirkić, Maja, Vucicevic, Ljubica, Janjetović, Kristina D., Trajković, Vladimir S., Mikhailidis, Dimitri P., Isenović, Esma R., "Regulation of inducible nitric oxide synthase activity/expression in rat hearts from ghrelin-treated rats" in Journal of Physiology and Biochemistry, 67, no. 2 (2011):195-204,
https://doi.org/10.1007/s13105-010-0063-1 . .

TY  - JOUR
AU  - Vucicevic, Ljubica
AU  - Misirkić, Maja
AU  - Janjetović, Kristina D.
AU  - Vilimanovich, Urosh
AU  - Sudar, Emina
AU  - Isenović, Esma R.
AU  - Prica, Marko
AU  - Harhaji-Trajković, Ljubica M.
AU  - Kravić-Stevović, Tamara K.
AU  - Bumbaširević, Vladimir Ž.
AU  - Trajković, Vladimir S.
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4180
AB  - In the present study, we report that compound C, an inhibitor of a key intracellular energy sensor AMP-activated protein kinase (AMPK), can induce autophagy in cancer cells. The induction of autophagy in U251 human glioma cell line was demonstrated by acridine orange staining of intracellular acidic vesicles, Beclin 1 induction, p62 decrease and conversion of LC3-I to autophagosome-associated LC3-II in the presence of proteolysis inhibitors. The presence of autophagosome-like vesicles was confirmed by transmission electron microscopy. Compound C-mediated inhibition of AMPK and raptor in U251 cells was associated with paradoxical decrease in phosphorylation of AMPK/raptor-repressed mTOR, a major negative regulator of autophagy, and its downstream target p70S6K. The phosphorylation of an mTOR activator Akt and the PI3K-activating kinase Src was also impaired in compound C-treated cells. The siRNA-mediated AMPK silencing did not reduce the activity of the Akt/mTOR/p70S6K pathway and AMPK activators metformin and AICAR failed to block compound C-induced autophagy. Autophagy inhibitors bafilomycin and chloroquine significantly increased the cytotoxicity of compound C towards U251 cells, as confirmed by increase in lactate dehydrogenase release, DNA fragmentation and caspase-3 activation. Similar effects of compound C were also observed in C6 rat glioma, L929 mouse fibrosarcoma and B16 mouse melanoma cell lines. Since compound C has previously been reported to suppress AMPK-dependent autophagy in different cell types, our findings suggest that the effects of compound C on autophagy might be dose-, cell type- and/or context-dependent. By demonstrating the ability of compound C to induce autophagic response in cancer cells via AMPK inhibition-independent downregulation of Akt/mTOR pathway, our results warrant caution when using compound C to inhibit AMPK-dependent cellular responses, but also support further exploration of compound C and related molecules as potential anticancer agents.
T2  - Autophagy
T1  - Compound C induces protective autophagy in cancer cells through AMPK inhibition-independent blockade of Akt/mTOR pathway
VL  - 7
IS  - 1
SP  - 40
EP  - 50
DO  - 10.4161/auto.7.1.13883
ER  - 

@article{
author = "Vucicevic, Ljubica and Misirkić, Maja and Janjetović, Kristina D. and Vilimanovich, Urosh and Sudar, Emina and Isenović, Esma R. and Prica, Marko and Harhaji-Trajković, Ljubica M. and Kravić-Stevović, Tamara K. and Bumbaširević, Vladimir Ž. and Trajković, Vladimir S.",
year = "2011",
abstract = "In the present study, we report that compound C, an inhibitor of a key intracellular energy sensor AMP-activated protein kinase (AMPK), can induce autophagy in cancer cells. The induction of autophagy in U251 human glioma cell line was demonstrated by acridine orange staining of intracellular acidic vesicles, Beclin 1 induction, p62 decrease and conversion of LC3-I to autophagosome-associated LC3-II in the presence of proteolysis inhibitors. The presence of autophagosome-like vesicles was confirmed by transmission electron microscopy. Compound C-mediated inhibition of AMPK and raptor in U251 cells was associated with paradoxical decrease in phosphorylation of AMPK/raptor-repressed mTOR, a major negative regulator of autophagy, and its downstream target p70S6K. The phosphorylation of an mTOR activator Akt and the PI3K-activating kinase Src was also impaired in compound C-treated cells. The siRNA-mediated AMPK silencing did not reduce the activity of the Akt/mTOR/p70S6K pathway and AMPK activators metformin and AICAR failed to block compound C-induced autophagy. Autophagy inhibitors bafilomycin and chloroquine significantly increased the cytotoxicity of compound C towards U251 cells, as confirmed by increase in lactate dehydrogenase release, DNA fragmentation and caspase-3 activation. Similar effects of compound C were also observed in C6 rat glioma, L929 mouse fibrosarcoma and B16 mouse melanoma cell lines. Since compound C has previously been reported to suppress AMPK-dependent autophagy in different cell types, our findings suggest that the effects of compound C on autophagy might be dose-, cell type- and/or context-dependent. By demonstrating the ability of compound C to induce autophagic response in cancer cells via AMPK inhibition-independent downregulation of Akt/mTOR pathway, our results warrant caution when using compound C to inhibit AMPK-dependent cellular responses, but also support further exploration of compound C and related molecules as potential anticancer agents.",
journal = "Autophagy",
title = "Compound C induces protective autophagy in cancer cells through AMPK inhibition-independent blockade of Akt/mTOR pathway",
volume = "7",
number = "1",
pages = "40-50",
doi = "10.4161/auto.7.1.13883"
}

Vucicevic, L., Misirkić, M., Janjetović, K. D., Vilimanovich, U., Sudar, E., Isenović, E. R., Prica, M., Harhaji-Trajković, L. M., Kravić-Stevović, T. K., Bumbaširević, V. Ž.,& Trajković, V. S.. (2011). Compound C induces protective autophagy in cancer cells through AMPK inhibition-independent blockade of Akt/mTOR pathway. in Autophagy, 7(1), 40-50.
https://doi.org/10.4161/auto.7.1.13883

Vucicevic L, Misirkić M, Janjetović KD, Vilimanovich U, Sudar E, Isenović ER, Prica M, Harhaji-Trajković LM, Kravić-Stevović TK, Bumbaširević VŽ, Trajković VS. Compound C induces protective autophagy in cancer cells through AMPK inhibition-independent blockade of Akt/mTOR pathway. in Autophagy. 2011;7(1):40-50.
doi:10.4161/auto.7.1.13883 .

Vucicevic, Ljubica, Misirkić, Maja, Janjetović, Kristina D., Vilimanovich, Urosh, Sudar, Emina, Isenović, Esma R., Prica, Marko, Harhaji-Trajković, Ljubica M., Kravić-Stevović, Tamara K., Bumbaširević, Vladimir Ž., Trajković, Vladimir S., "Compound C induces protective autophagy in cancer cells through AMPK inhibition-independent blockade of Akt/mTOR pathway" in Autophagy, 7, no. 1 (2011):40-50,
https://doi.org/10.4161/auto.7.1.13883 . .

TY  - JOUR
AU  - Trpković, Andreja
AU  - Todorović-Marković, Biljana
AU  - Kleut, Duška
AU  - Misirkić, Maja
AU  - Janjetović, Kristina D.
AU  - Vucicevic, Ljubica
AU  - Pantovic, Aleksandar
AU  - Jovanović, Svetlana P.
AU  - Dramićanin, Miroslav
AU  - Marković, Zoran M.
AU  - Trajković, Vladimir S.
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4093
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
VL  - 21
IS  - 37
DO  - 10.1088/0957-4484/21/37/375102
ER  - 

@article{
author = "Trpković, Andreja and Todorović-Marković, Biljana and Kleut, Duška and Misirkić, Maja and Janjetović, Kristina D. and Vucicevic, Ljubica and Pantovic, Aleksandar and Jovanović, Svetlana P. and Dramićanin, Miroslav and Marković, Zoran M. 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",
volume = "21",
number = "37",
doi = "10.1088/0957-4484/21/37/375102"
}

Trpković, A., Todorović-Marković, B., Kleut, D., Misirkić, M., Janjetović, K. D., Vucicevic, L., Pantovic, A., Jovanović, S. P., Dramićanin, M., Marković, Z. M.,& Trajković, V. S.. (2010). Oxidative stress-mediated hemolytic activity of solvent exchange-prepared fullerene (C-60) nanoparticles. in Nanotechnology, 21(37).
https://doi.org/10.1088/0957-4484/21/37/375102

Trpković A, Todorović-Marković B, Kleut D, Misirkić M, Janjetović KD, Vucicevic L, Pantovic A, Jovanović SP, Dramićanin M, Marković ZM, Trajković VS. Oxidative stress-mediated hemolytic activity of solvent exchange-prepared fullerene (C-60) nanoparticles. in Nanotechnology. 2010;21(37).
doi:10.1088/0957-4484/21/37/375102 .

Trpković, Andreja, Todorović-Marković, Biljana, Kleut, Duška, Misirkić, Maja, Janjetović, Kristina D., Vucicevic, Ljubica, Pantovic, Aleksandar, Jovanović, Svetlana P., Dramićanin, Miroslav, Marković, Zoran M., Trajković, Vladimir S., "Oxidative stress-mediated hemolytic activity of solvent exchange-prepared fullerene (C-60) nanoparticles" in Nanotechnology, 21, no. 37 (2010),
https://doi.org/10.1088/0957-4484/21/37/375102 . .

TY  - JOUR
AU  - Vucicevic, Ljubica
AU  - Misirkić, Maja
AU  - Janjetović, Kristina D.
AU  - Harhaji-Trajković, Ljubica M.
AU  - Prica, Marko
AU  - Stevanović, Darko
AU  - Isenović, Esma R.
AU  - Sudar, Emina
AU  - Šumarac-Dumanović, Mirjana
AU  - Micic, Dragan
AU  - Trajković, Vladimir S.
PY  - 2009
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/3690
AB  - We investigated the effect of compound C, a well-known inhibitor of the intracellular energy sensor AMP-activated protein kinase (AMPK), on proliferation and viability of human U251 and rat C6 glioma cell lines. Compound C caused G(2)/M cell cycle block, accompanied by apoptotic glioma cell death characterized by caspase activation, phosphatidylserine exposure and DNA fragmentation. The mechanisms underlying the pro-apoptotic action of compound C involved induction of oxidative stress and downregulation of antiapoptotic molecule Bcl-2, while no alteration of pro-apoptotic Bax was observed. Compound C diminished AMPK phosphorylation and enzymatic activity, resulting in reduced phosphorylation of its target acetyl CoA carboxylase. AMPK activators metformin and AICAR partly prevented the cell cycle block, oxidative stress and apoptosis induced by compound C. The small interfering RNA (siRNA) targeting of human AMPK mimicked compound C-induced G(2)/M cell cycle arrest, but failed to induce oxidative stress and apoptosis in U251 glioma cells. In conclusion, our data indicate that AMPK inhibition is required, but not sufficient for compound C-mediated apoptotic death of glioma cells. (c) 2009 Elsevier Inc. All rights reserved.
T2  - Biochemical Pharmacology
T1  - AMP-activated protein kinase-dependent and -independent mechanisms underlying in vitro antiglioma action of compound C
VL  - 77
IS  - 11
SP  - 1684
EP  - 1693
DO  - 10.1016/j.bcp.2009.03.005
ER  - 

@article{
author = "Vucicevic, Ljubica and Misirkić, Maja and Janjetović, Kristina D. and Harhaji-Trajković, Ljubica M. and Prica, Marko and Stevanović, Darko and Isenović, Esma R. and Sudar, Emina and Šumarac-Dumanović, Mirjana and Micic, Dragan and Trajković, Vladimir S.",
year = "2009",
abstract = "We investigated the effect of compound C, a well-known inhibitor of the intracellular energy sensor AMP-activated protein kinase (AMPK), on proliferation and viability of human U251 and rat C6 glioma cell lines. Compound C caused G(2)/M cell cycle block, accompanied by apoptotic glioma cell death characterized by caspase activation, phosphatidylserine exposure and DNA fragmentation. The mechanisms underlying the pro-apoptotic action of compound C involved induction of oxidative stress and downregulation of antiapoptotic molecule Bcl-2, while no alteration of pro-apoptotic Bax was observed. Compound C diminished AMPK phosphorylation and enzymatic activity, resulting in reduced phosphorylation of its target acetyl CoA carboxylase. AMPK activators metformin and AICAR partly prevented the cell cycle block, oxidative stress and apoptosis induced by compound C. The small interfering RNA (siRNA) targeting of human AMPK mimicked compound C-induced G(2)/M cell cycle arrest, but failed to induce oxidative stress and apoptosis in U251 glioma cells. In conclusion, our data indicate that AMPK inhibition is required, but not sufficient for compound C-mediated apoptotic death of glioma cells. (c) 2009 Elsevier Inc. All rights reserved.",
journal = "Biochemical Pharmacology",
title = "AMP-activated protein kinase-dependent and -independent mechanisms underlying in vitro antiglioma action of compound C",
volume = "77",
number = "11",
pages = "1684-1693",
doi = "10.1016/j.bcp.2009.03.005"
}

Vucicevic, L., Misirkić, M., Janjetović, K. D., Harhaji-Trajković, L. M., Prica, M., Stevanović, D., Isenović, E. R., Sudar, E., Šumarac-Dumanović, M., Micic, D.,& Trajković, V. S.. (2009). AMP-activated protein kinase-dependent and -independent mechanisms underlying in vitro antiglioma action of compound C. in Biochemical Pharmacology, 77(11), 1684-1693.
https://doi.org/10.1016/j.bcp.2009.03.005

Vucicevic L, Misirkić M, Janjetović KD, Harhaji-Trajković LM, Prica M, Stevanović D, Isenović ER, Sudar E, Šumarac-Dumanović M, Micic D, Trajković VS. AMP-activated protein kinase-dependent and -independent mechanisms underlying in vitro antiglioma action of compound C. in Biochemical Pharmacology. 2009;77(11):1684-1693.
doi:10.1016/j.bcp.2009.03.005 .

Vucicevic, Ljubica, Misirkić, Maja, Janjetović, Kristina D., Harhaji-Trajković, Ljubica M., Prica, Marko, Stevanović, Darko, Isenović, Esma R., Sudar, Emina, Šumarac-Dumanović, Mirjana, Micic, Dragan, Trajković, Vladimir S., "AMP-activated protein kinase-dependent and -independent mechanisms underlying in vitro antiglioma action of compound C" in Biochemical Pharmacology, 77, no. 11 (2009):1684-1693,
https://doi.org/10.1016/j.bcp.2009.03.005 . .

TY  - JOUR
AU  - Misirkić, Maja S.
AU  - Todorović-Marković, Biljana
AU  - Vucicevic, Ljubica M.
AU  - Janjetović, Kristina D.
AU  - Jokanović, Vukoman R.
AU  - Dramićanin, Miroslav
AU  - Marković, Zoran M.
AU  - Trajković, Vladimir S.
PY  - 2009
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/3659
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
VL  - 30
IS  - 12
SP  - 2319
EP  - 2328
DO  - 10.1016/j.biomaterials.2009.01.023
ER  - 

@article{
author = "Misirkić, Maja S. and Todorović-Marković, Biljana and Vucicevic, Ljubica M. and Janjetović, Kristina D. and Jokanović, Vukoman R. and Dramićanin, Miroslav 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",
volume = "30",
number = "12",
pages = "2319-2328",
doi = "10.1016/j.biomaterials.2009.01.023"
}

Misirkić, M. S., Todorović-Marković, B., Vucicevic, L. M., Janjetović, K. D., Jokanović, V. R., Dramićanin, M., 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), 2319-2328.
https://doi.org/10.1016/j.biomaterials.2009.01.023

Misirkić MS, Todorović-Marković B, Vucicevic LM, Janjetović KD, Jokanović VR, Dramićanin M, 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):2319-2328.
doi:10.1016/j.biomaterials.2009.01.023 .

Misirkić, Maja S., Todorović-Marković, Biljana, Vucicevic, Ljubica M., Janjetović, Kristina D., Jokanović, Vukoman R., Dramićanin, Miroslav, 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):2319-2328,
https://doi.org/10.1016/j.biomaterials.2009.01.023 . .

TY  - JOUR
AU  - Zogovic, Nevena S.
AU  - Nikolić, Nadežda S.
AU  - Vranješ-Đurić, Sanja
AU  - Harhaji, Ljubica M.
AU  - Vucicevic, Ljubica M.
AU  - Janjetović, Kristina D.
AU  - Misirkić, Maja S.
AU  - Todorović-Marković, Biljana
AU  - Marković, Zoran M.
AU  - Milonjić, Slobodan K.
AU  - Trajković, Vladimir S.
PY  - 2009
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/3830
AB  - In the present study, we compared the effects of nanocrystalline fullerene suspension (nanoC(60)) on tumour cell growth in vitro and in vivo. NanoC(60) suspension was prepared by solvent exchange using tetrahydrofuran to dissolve C-60. In vitro, nanoC(60) caused oxidative stress, mitochondrial depolarization and caspase activation, leading to apoptotic and necrotic death in mouse B16 melanoma cells. Bio-distribution studies demonstrated that intraperitoneally injected radiolabeled (I-125) nanoC(60) readily accumulated in the tumour tissue of mice subcutaneously inoculated with B16 cells. However, intraperitoneal administration of nanoC(60) over the course of two weeks starting from melanoma cell implantation not only failed to reduce, but significantly augmented turnout growth. The tumour-promoting effect of nanoC(60) was accompanied by a significant increase in splenocyte production of the immunoregulatory free radical nitric oxide (NO), as well as by a reduction in splenocyte proliferative responses to T- and B-cell mitogens ConcanavalinA and bacterial lipopolysaccharide, respectively. A negative correlation between NO production and splenocyte proliferation indicated a possible role of NO in reducing the proliferation of splenocytes from nanoC(60)-injected mice. These data demonstrate that nanoC(60), in contrast to its potent anticancer activity in vitro, can potentiate tumour growth in vivo, possibly by causing NO-dependent suppression of anticancer immune response. (C) 2009 Elsevier Ltd. All rights reserved.
T2  - Biomaterials
T1  - Opposite effects of nanocrystalline fullerene (C-60) on tumour cell growth in vitro and in vivo and a possible role of immunosupression in the cancer-promoting activity of C-60
VL  - 30
IS  - 36
SP  - 6940
EP  - 6946
DO  - 10.1016/j.biomaterials.2009.09.007
ER  - 

@article{
author = "Zogovic, Nevena S. and Nikolić, Nadežda S. and Vranješ-Đurić, Sanja and Harhaji, Ljubica M. and Vucicevic, Ljubica M. and Janjetović, Kristina D. and Misirkić, Maja S. and Todorović-Marković, Biljana and Marković, Zoran M. and Milonjić, Slobodan K. and Trajković, Vladimir S.",
year = "2009",
abstract = "In the present study, we compared the effects of nanocrystalline fullerene suspension (nanoC(60)) on tumour cell growth in vitro and in vivo. NanoC(60) suspension was prepared by solvent exchange using tetrahydrofuran to dissolve C-60. In vitro, nanoC(60) caused oxidative stress, mitochondrial depolarization and caspase activation, leading to apoptotic and necrotic death in mouse B16 melanoma cells. Bio-distribution studies demonstrated that intraperitoneally injected radiolabeled (I-125) nanoC(60) readily accumulated in the tumour tissue of mice subcutaneously inoculated with B16 cells. However, intraperitoneal administration of nanoC(60) over the course of two weeks starting from melanoma cell implantation not only failed to reduce, but significantly augmented turnout growth. The tumour-promoting effect of nanoC(60) was accompanied by a significant increase in splenocyte production of the immunoregulatory free radical nitric oxide (NO), as well as by a reduction in splenocyte proliferative responses to T- and B-cell mitogens ConcanavalinA and bacterial lipopolysaccharide, respectively. A negative correlation between NO production and splenocyte proliferation indicated a possible role of NO in reducing the proliferation of splenocytes from nanoC(60)-injected mice. These data demonstrate that nanoC(60), in contrast to its potent anticancer activity in vitro, can potentiate tumour growth in vivo, possibly by causing NO-dependent suppression of anticancer immune response. (C) 2009 Elsevier Ltd. All rights reserved.",
journal = "Biomaterials",
title = "Opposite effects of nanocrystalline fullerene (C-60) on tumour cell growth in vitro and in vivo and a possible role of immunosupression in the cancer-promoting activity of C-60",
volume = "30",
number = "36",
pages = "6940-6946",
doi = "10.1016/j.biomaterials.2009.09.007"
}

Zogovic, N. S., Nikolić, N. S., Vranješ-Đurić, S., Harhaji, L. M., Vucicevic, L. M., Janjetović, K. D., Misirkić, M. S., Todorović-Marković, B., Marković, Z. M., Milonjić, S. K.,& Trajković, V. S.. (2009). Opposite effects of nanocrystalline fullerene (C-60) on tumour cell growth in vitro and in vivo and a possible role of immunosupression in the cancer-promoting activity of C-60. in Biomaterials, 30(36), 6940-6946.
https://doi.org/10.1016/j.biomaterials.2009.09.007

Zogovic NS, Nikolić NS, Vranješ-Đurić S, Harhaji LM, Vucicevic LM, Janjetović KD, Misirkić MS, Todorović-Marković B, Marković ZM, Milonjić SK, Trajković VS. Opposite effects of nanocrystalline fullerene (C-60) on tumour cell growth in vitro and in vivo and a possible role of immunosupression in the cancer-promoting activity of C-60. in Biomaterials. 2009;30(36):6940-6946.
doi:10.1016/j.biomaterials.2009.09.007 .

Zogovic, Nevena S., Nikolić, Nadežda S., Vranješ-Đurić, Sanja, Harhaji, Ljubica M., Vucicevic, Ljubica M., Janjetović, Kristina D., Misirkić, Maja S., Todorović-Marković, Biljana, Marković, Zoran M., Milonjić, Slobodan K., Trajković, Vladimir S., "Opposite effects of nanocrystalline fullerene (C-60) on tumour cell growth in vitro and in vivo and a possible role of immunosupression in the cancer-promoting activity of C-60" in Biomaterials, 30, no. 36 (2009):6940-6946,
https://doi.org/10.1016/j.biomaterials.2009.09.007 . .

TY  - JOUR
AU  - Harhaji, Ljubica M.
AU  - Isaković, Aleksandra J.
AU  - Vucicevic, Ljubica
AU  - Janjetović, Kristina D.
AU  - Misirkić, Maja
AU  - Marković, Zoran M.
AU  - Todorović-Marković, Biljana
AU  - Nikolić, Nadežda S.
AU  - Vranješ-Đurić, Sanja
AU  - Nikolić, Zoran M.
AU  - Trajković, Vladimir S.
PY  - 2008
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/3445
AB  - Purpose. The fullerene (C-60/C-70 mixture-C-60/70) nanocrystalline suspension prepared by solvent exchange method using tetrahydrofyran (THF/nC(60/70)) and polyhydroxylated C-60/70 [C-60/70(OH)(n)] were compared for their ability to modulate cytotoxicity of the proinflammatory cytokine tumor necrosis factor (TNT). Materials and Methods. TNF-induced cytotoxicity was assessed in L929 fibrosarcoma cells by crystal violet assay. The type of cell death (apoptosis/necrosis), production of reactive oxygen species, mitochondrial depolarization and caspase activation were determined by flow cytometry using the appropriate reporter dyes. Results. THF/nC(60/70) augmented, while C-60/70(OH)(n) reduced the cytotoxicity of TNF. The numbers of cells undergoing apoptosis/necrosis, as well as of those displaying the activation of apoptosis-inducing enzymes of caspase family, were respectively increased or reduced by THF/nC(60/70) or C-60/70(OH)(n). The antioxidant N-acetylcysteine and mitochondrial permeability transition inhibitor cyclosporin A each partly blocked the cytotoxic action of TNF, indicating the involvement of oxidative stress and mitochondrial dysfunction in the TNF cytotoxicity. Accordingly, THF/nC(60/70) or C-60/70(OH)(n) potentiated or suppressed, respectively, TNF-triggered oxidative stress and mitochondrial depolarization. Conclusion. The ability of different fullerene preparations to modulate TNF-induced oxidative stress and subsequent cell death suggests their potential value in the TNF-based cancer therapy or prevention of TNF-dependent tissue damage.
T2  - Pharmaceutical Research
T1  - Modulation of tumor necrosis factor-mediated cell death by fullerenes
VL  - 25
IS  - 6
SP  - 1365
EP  - 1376
DO  - 10.1007/s11095-007-9486-y
ER  - 

@article{
author = "Harhaji, Ljubica M. and Isaković, Aleksandra J. and Vucicevic, Ljubica and Janjetović, Kristina D. and Misirkić, Maja and Marković, Zoran M. and Todorović-Marković, Biljana and Nikolić, Nadežda S. and Vranješ-Đurić, Sanja and Nikolić, Zoran M. and Trajković, Vladimir S.",
year = "2008",
abstract = "Purpose. The fullerene (C-60/C-70 mixture-C-60/70) nanocrystalline suspension prepared by solvent exchange method using tetrahydrofyran (THF/nC(60/70)) and polyhydroxylated C-60/70 [C-60/70(OH)(n)] were compared for their ability to modulate cytotoxicity of the proinflammatory cytokine tumor necrosis factor (TNT). Materials and Methods. TNF-induced cytotoxicity was assessed in L929 fibrosarcoma cells by crystal violet assay. The type of cell death (apoptosis/necrosis), production of reactive oxygen species, mitochondrial depolarization and caspase activation were determined by flow cytometry using the appropriate reporter dyes. Results. THF/nC(60/70) augmented, while C-60/70(OH)(n) reduced the cytotoxicity of TNF. The numbers of cells undergoing apoptosis/necrosis, as well as of those displaying the activation of apoptosis-inducing enzymes of caspase family, were respectively increased or reduced by THF/nC(60/70) or C-60/70(OH)(n). The antioxidant N-acetylcysteine and mitochondrial permeability transition inhibitor cyclosporin A each partly blocked the cytotoxic action of TNF, indicating the involvement of oxidative stress and mitochondrial dysfunction in the TNF cytotoxicity. Accordingly, THF/nC(60/70) or C-60/70(OH)(n) potentiated or suppressed, respectively, TNF-triggered oxidative stress and mitochondrial depolarization. Conclusion. The ability of different fullerene preparations to modulate TNF-induced oxidative stress and subsequent cell death suggests their potential value in the TNF-based cancer therapy or prevention of TNF-dependent tissue damage.",
journal = "Pharmaceutical Research",
title = "Modulation of tumor necrosis factor-mediated cell death by fullerenes",
volume = "25",
number = "6",
pages = "1365-1376",
doi = "10.1007/s11095-007-9486-y"
}

Harhaji, L. M., Isaković, A. J., Vucicevic, L., Janjetović, K. D., Misirkić, M., Marković, Z. M., Todorović-Marković, B., Nikolić, N. S., Vranješ-Đurić, S., Nikolić, Z. M.,& Trajković, V. S.. (2008). Modulation of tumor necrosis factor-mediated cell death by fullerenes. in Pharmaceutical Research, 25(6), 1365-1376.
https://doi.org/10.1007/s11095-007-9486-y

Harhaji LM, Isaković AJ, Vucicevic L, Janjetović KD, Misirkić M, Marković ZM, Todorović-Marković B, Nikolić NS, Vranješ-Đurić S, Nikolić ZM, Trajković VS. Modulation of tumor necrosis factor-mediated cell death by fullerenes. in Pharmaceutical Research. 2008;25(6):1365-1376.
doi:10.1007/s11095-007-9486-y .

Harhaji, Ljubica M., Isaković, Aleksandra J., Vucicevic, Ljubica, Janjetović, Kristina D., Misirkić, Maja, Marković, Zoran M., Todorović-Marković, Biljana, Nikolić, Nadežda S., Vranješ-Đurić, Sanja, Nikolić, Zoran M., Trajković, Vladimir S., "Modulation of tumor necrosis factor-mediated cell death by fullerenes" in Pharmaceutical Research, 25, no. 6 (2008):1365-1376,
https://doi.org/10.1007/s11095-007-9486-y . .

TY  - JOUR
AU  - Marković, Zoran M.
AU  - Todorović-Marković, Biljana
AU  - Kleut, Duška
AU  - Nikolić, Nadežda S.
AU  - Vranješ-Đurić, Sanja
AU  - Misirkić, Maja
AU  - Vucicevic, Ljubica
AU  - Janjetović, Kristina D.
AU  - Isaković, Aleksandra J.
AU  - Harhaji, Ljubica M.
AU  - Babić-Stojić, Branka S.
AU  - Dramićanin, Miroslav
AU  - Trajković, Vladimir S.
PY  - 2007
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/3322
AB  - Because of the ability to induce cell death in certain conditions, the fullerenes (C-60) are potential anticancer and toxic agents. The colloidal suspension of crystalline C-60 (nano-C-60, nC(60)) is extremely toxic, but the mechanisms of its cytotoxicity are not completely understood. By combining experimental analysis and mathematical modelling, we investigate the requirements for the reactive oxygen species (ROS)-mediated cytotoxicity of different nC(60) suspensions, prepared by solvent exchange method in tetrahydrofuran (THF/nC(60)) and ethanol (EtOH/nC(60)), or by extended mixing in water (aqu/nC(60)). With regard to their capacity to generate ROS and cause mitochondrial depolarization followed by necrotic cell death, the nC(60) suspensions are ranked in the following order: THF/nC(60) GT EtOH/nC(60) GT aqu/nC(60). Mathematical modelling of singlet oxygen (O-1(2)) generation indicates that the O-1(2)-quenching power (THF/nC(60) LT EtOH/nC(60) LT aqU/nC(60)) of the solvent intercalated in the fullerene crystals determines their ability to produce ROS and cause cell damage. These data could. have important implications for toxicology and biomedical application of colloidal fullerenes. (C) 2007 Elsevier Ltd. All rights reserved.
T2  - Biomaterials
T1  - The mechanism of cell-damaging reactive oxygen generation by colloidal fullerenes
VL  - 28
IS  - 36
SP  - 5437
EP  - 5448
DO  - 10.1016/j.biomaterials.2007.09.002
ER  - 

@article{
author = "Marković, Zoran M. and Todorović-Marković, Biljana and Kleut, Duška and Nikolić, Nadežda S. and Vranješ-Đurić, Sanja and Misirkić, Maja and Vucicevic, Ljubica and Janjetović, Kristina D. and Isaković, Aleksandra J. and Harhaji, Ljubica M. and Babić-Stojić, Branka S. and Dramićanin, Miroslav and Trajković, Vladimir S.",
year = "2007",
abstract = "Because of the ability to induce cell death in certain conditions, the fullerenes (C-60) are potential anticancer and toxic agents. The colloidal suspension of crystalline C-60 (nano-C-60, nC(60)) is extremely toxic, but the mechanisms of its cytotoxicity are not completely understood. By combining experimental analysis and mathematical modelling, we investigate the requirements for the reactive oxygen species (ROS)-mediated cytotoxicity of different nC(60) suspensions, prepared by solvent exchange method in tetrahydrofuran (THF/nC(60)) and ethanol (EtOH/nC(60)), or by extended mixing in water (aqu/nC(60)). With regard to their capacity to generate ROS and cause mitochondrial depolarization followed by necrotic cell death, the nC(60) suspensions are ranked in the following order: THF/nC(60) GT EtOH/nC(60) GT aqu/nC(60). Mathematical modelling of singlet oxygen (O-1(2)) generation indicates that the O-1(2)-quenching power (THF/nC(60) LT EtOH/nC(60) LT aqU/nC(60)) of the solvent intercalated in the fullerene crystals determines their ability to produce ROS and cause cell damage. These data could. have important implications for toxicology and biomedical application of colloidal fullerenes. (C) 2007 Elsevier Ltd. All rights reserved.",
journal = "Biomaterials",
title = "The mechanism of cell-damaging reactive oxygen generation by colloidal fullerenes",
volume = "28",
number = "36",
pages = "5437-5448",
doi = "10.1016/j.biomaterials.2007.09.002"
}

Marković, Z. M., Todorović-Marković, B., Kleut, D., Nikolić, N. S., Vranješ-Đurić, S., Misirkić, M., Vucicevic, L., Janjetović, K. D., Isaković, A. J., Harhaji, L. M., Babić-Stojić, B. S., Dramićanin, M.,& Trajković, V. S.. (2007). The mechanism of cell-damaging reactive oxygen generation by colloidal fullerenes. in Biomaterials, 28(36), 5437-5448.
https://doi.org/10.1016/j.biomaterials.2007.09.002

Marković ZM, Todorović-Marković B, Kleut D, Nikolić NS, Vranješ-Đurić S, Misirkić M, Vucicevic L, Janjetović KD, Isaković AJ, Harhaji LM, Babić-Stojić BS, Dramićanin M, Trajković VS. The mechanism of cell-damaging reactive oxygen generation by colloidal fullerenes. in Biomaterials. 2007;28(36):5437-5448.
doi:10.1016/j.biomaterials.2007.09.002 .

Marković, Zoran M., Todorović-Marković, Biljana, Kleut, Duška, Nikolić, Nadežda S., Vranješ-Đurić, Sanja, Misirkić, Maja, Vucicevic, Ljubica, Janjetović, Kristina D., Isaković, Aleksandra J., Harhaji, Ljubica M., Babić-Stojić, Branka S., Dramićanin, Miroslav, Trajković, Vladimir S., "The mechanism of cell-damaging reactive oxygen generation by colloidal fullerenes" in Biomaterials, 28, no. 36 (2007):5437-5448,
https://doi.org/10.1016/j.biomaterials.2007.09.002 . .