TY  - CONF
AU  - Đukić-Ćosić, Danijela
AU  - Vukomanović, Predrag
AU  - Bulat, Zorica
AU  - Ninković, Milica
AU  - Maličević, Živorad
AU  - Matović, Vesna
PY  - 2011
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/1471
PB  - Elsevier Ireland Ltd, Clare
C3  - Toxicology Letters
T1  - Background explanation of oxidative stress in kidney of mice induced by subacute cadmium intoxication
VL  - 205
IS  - Supplement
SP  - S187
EP  - S187
DO  - 10.1016/j.toxlet.2011.05.648
ER  - 

@conference{
author = "Đukić-Ćosić, Danijela and Vukomanović, Predrag and Bulat, Zorica and Ninković, Milica and Maličević, Živorad and Matović, Vesna",
year = "2011",
publisher = "Elsevier Ireland Ltd, Clare",
journal = "Toxicology Letters",
title = "Background explanation of oxidative stress in kidney of mice induced by subacute cadmium intoxication",
volume = "205",
number = "Supplement",
pages = "S187-S187",
doi = "10.1016/j.toxlet.2011.05.648"
}

Đukić-Ćosić, D., Vukomanović, P., Bulat, Z., Ninković, M., Maličević, Ž.,& Matović, V.. (2011). Background explanation of oxidative stress in kidney of mice induced by subacute cadmium intoxication. in Toxicology Letters
Elsevier Ireland Ltd, Clare., 205(Supplement), S187-S187.
https://doi.org/10.1016/j.toxlet.2011.05.648

Đukić-Ćosić D, Vukomanović P, Bulat Z, Ninković M, Maličević Ž, Matović V. Background explanation of oxidative stress in kidney of mice induced by subacute cadmium intoxication. in Toxicology Letters. 2011;205(Supplement):S187-S187.
doi:10.1016/j.toxlet.2011.05.648 .

Đukić-Ćosić, Danijela, Vukomanović, Predrag, Bulat, Zorica, Ninković, Milica, Maličević, Živorad, Matović, Vesna, "Background explanation of oxidative stress in kidney of mice induced by subacute cadmium intoxication" in Toxicology Letters, 205, no. Supplement (2011):S187-S187,
https://doi.org/10.1016/j.toxlet.2011.05.648 . .

TY  - CONF
AU  - Đukić-Ćosić, Danijela
AU  - Plamenac-Bulat, Zorica
AU  - Ninković, Milica
AU  - Maličević, Živorad
AU  - Matović, Vesna
PY  - 2009
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/1270
PB  - Elsevier Ireland Ltd, Clare
C3  - Toxicology Letters
T1  - Renal superoxide dismutase activity in mice exposed to acute and subacute cadmium intoxication: The role of magnesium pretreatment
VL  - 189
IS  - Supplement
SP  - S222
EP  - S222
DO  - 10.1016/j.toxlet.2009.06.518
ER  - 

@conference{
author = "Đukić-Ćosić, Danijela and Plamenac-Bulat, Zorica and Ninković, Milica and Maličević, Živorad and Matović, Vesna",
year = "2009",
publisher = "Elsevier Ireland Ltd, Clare",
journal = "Toxicology Letters",
title = "Renal superoxide dismutase activity in mice exposed to acute and subacute cadmium intoxication: The role of magnesium pretreatment",
volume = "189",
number = "Supplement",
pages = "S222-S222",
doi = "10.1016/j.toxlet.2009.06.518"
}

Đukić-Ćosić, D., Plamenac-Bulat, Z., Ninković, M., Maličević, Ž.,& Matović, V.. (2009). Renal superoxide dismutase activity in mice exposed to acute and subacute cadmium intoxication: The role of magnesium pretreatment. in Toxicology Letters
Elsevier Ireland Ltd, Clare., 189(Supplement), S222-S222.
https://doi.org/10.1016/j.toxlet.2009.06.518

Đukić-Ćosić D, Plamenac-Bulat Z, Ninković M, Maličević Ž, Matović V. Renal superoxide dismutase activity in mice exposed to acute and subacute cadmium intoxication: The role of magnesium pretreatment. in Toxicology Letters. 2009;189(Supplement):S222-S222.
doi:10.1016/j.toxlet.2009.06.518 .

Đukić-Ćosić, Danijela, Plamenac-Bulat, Zorica, Ninković, Milica, Maličević, Živorad, Matović, Vesna, "Renal superoxide dismutase activity in mice exposed to acute and subacute cadmium intoxication: The role of magnesium pretreatment" in Toxicology Letters, 189, no. Supplement (2009):S222-S222,
https://doi.org/10.1016/j.toxlet.2009.06.518 . .

TY  - JOUR
AU  - Ninković, Milica
AU  - Maličević, Živorad
AU  - Stojanović, Dragica
AU  - Vasiljević, Ivana
AU  - Jovanović, Marina
AU  - Đukić, Mirjana
PY  - 2008
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/1121
AB  - Although brain complications in sepsis are not rare, early pathophysiologic events had not been made clear yet. We have considered antioxidative components-glutathione peroxidase (GSHPx) activity and reduced glutathione (GSH) concentration in two brain integrative centers, Le the brain stem (BS) and thalamus. Sepsis was induced in adult male Wistar rats (200-250 g) by cecal ligation and perforation (CLP) with inoculation of Escherichia coli suspension (ATCC 25922) (n=40). The control group was sham operated (n=40). For each time point (0, 12, 24 and 72 hours) after treatment, ten animals within each group were decapitated. In BS, GSHPx activity increased at 12 and 24 hours after CLP, while in the thalamus, GSHPx activity increased at 72 hours, compared to controls. In BS, GSH concentration decreased at the 12(th) and 24(th) hour, and in the thalamus it decreased at the 72(nd) hour. Changed oxidative status in BS, recorded as soon as the 12(th) hour reflects a prompt reaction of the central nervous system. This could be of great consequence for disturbed vasomotor response during sepsis.
PB  - Univerzitet u Beogradu - Fakultet veterinarske medicine, Beograd
T2  - Acta veterinaria
T1  - Brain stem and thalamus antioxidative defensein experimental sepsis
VL  - 58
IS  - 2-3
SP  - 129
EP  - 137
DO  - 10.2298/AVB0803129N
ER  - 

@article{
author = "Ninković, Milica and Maličević, Živorad and Stojanović, Dragica and Vasiljević, Ivana and Jovanović, Marina and Đukić, Mirjana",
year = "2008",
abstract = "Although brain complications in sepsis are not rare, early pathophysiologic events had not been made clear yet. We have considered antioxidative components-glutathione peroxidase (GSHPx) activity and reduced glutathione (GSH) concentration in two brain integrative centers, Le the brain stem (BS) and thalamus. Sepsis was induced in adult male Wistar rats (200-250 g) by cecal ligation and perforation (CLP) with inoculation of Escherichia coli suspension (ATCC 25922) (n=40). The control group was sham operated (n=40). For each time point (0, 12, 24 and 72 hours) after treatment, ten animals within each group were decapitated. In BS, GSHPx activity increased at 12 and 24 hours after CLP, while in the thalamus, GSHPx activity increased at 72 hours, compared to controls. In BS, GSH concentration decreased at the 12(th) and 24(th) hour, and in the thalamus it decreased at the 72(nd) hour. Changed oxidative status in BS, recorded as soon as the 12(th) hour reflects a prompt reaction of the central nervous system. This could be of great consequence for disturbed vasomotor response during sepsis.",
publisher = "Univerzitet u Beogradu - Fakultet veterinarske medicine, Beograd",
journal = "Acta veterinaria",
title = "Brain stem and thalamus antioxidative defensein experimental sepsis",
volume = "58",
number = "2-3",
pages = "129-137",
doi = "10.2298/AVB0803129N"
}

Ninković, M., Maličević, Ž., Stojanović, D., Vasiljević, I., Jovanović, M.,& Đukić, M.. (2008). Brain stem and thalamus antioxidative defensein experimental sepsis. in Acta veterinaria
Univerzitet u Beogradu - Fakultet veterinarske medicine, Beograd., 58(2-3), 129-137.
https://doi.org/10.2298/AVB0803129N

Ninković M, Maličević Ž, Stojanović D, Vasiljević I, Jovanović M, Đukić M. Brain stem and thalamus antioxidative defensein experimental sepsis. in Acta veterinaria. 2008;58(2-3):129-137.
doi:10.2298/AVB0803129N .

Ninković, Milica, Maličević, Živorad, Stojanović, Dragica, Vasiljević, Ivana, Jovanović, Marina, Đukić, Mirjana, "Brain stem and thalamus antioxidative defensein experimental sepsis" in Acta veterinaria, 58, no. 2-3 (2008):129-137,
https://doi.org/10.2298/AVB0803129N . .

TY  - JOUR
AU  - Ninković, Milica
AU  - Selaković, Vesna
AU  - Đukić, Mirjana
AU  - Milosavljević, Petar
AU  - Vasiljević, Ivana
AU  - Jovanović, Marina
AU  - Maličević, Živorad
PY  - 2008
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/1060
AB  - Aim: The mechanism of MDMA (3,4-methylenedioxymethamphetamine)-induced toxicity is believed to be, in part, due to enhanced oxidative stress. As MDMA is eliminated via the kidney, the aim. of this study was to investigate whether MDMA created conditions of oxidative stress within rat kidney. Methods: Adult male Wistar rats were divided into three groups, control treatment (water), acute MDMA administration (single oral dose: 5, 10, 20 or 40 mg/kg body weight) and subacute MDMA administration (5, 10, or 20 mg/kg body weight per day during 14 days). Animals were sacrificed 8 h after the single oral MDMA administration in the acute MDMA administration group and after the last MDMA administration in the subacute MDMA administration group. Rectal temperature measurements, oxidative stress status parameters and histological examinations were performed. Results: In all MDMA-administered rats, rectal temperature markedly increased peaking approximately 1 h after MDMA ingestion. Superoxide dismutase activity and thiobarbituric acid reactive substances increased after MDMA administration. Histological examinations of the kidney revealed dose-dependent disruption of tissue structure in subacute MDMA-administered rats. The latter was not observed in acute MDMA-administered rats.
PB  - Wiley, Hoboken
T2  - Nephrology
T1  - Oxidative stress in rat kidneys due to 3,4-methylenedioxymetamphetamine (ecstasy) toxicity
VL  - 13
IS  - 1
SP  - 33
EP  - 37
DO  - 10.1111/j.1440-1797.2007.00886.x
ER  - 

@article{
author = "Ninković, Milica and Selaković, Vesna and Đukić, Mirjana and Milosavljević, Petar and Vasiljević, Ivana and Jovanović, Marina and Maličević, Živorad",
year = "2008",
abstract = "Aim: The mechanism of MDMA (3,4-methylenedioxymethamphetamine)-induced toxicity is believed to be, in part, due to enhanced oxidative stress. As MDMA is eliminated via the kidney, the aim. of this study was to investigate whether MDMA created conditions of oxidative stress within rat kidney. Methods: Adult male Wistar rats were divided into three groups, control treatment (water), acute MDMA administration (single oral dose: 5, 10, 20 or 40 mg/kg body weight) and subacute MDMA administration (5, 10, or 20 mg/kg body weight per day during 14 days). Animals were sacrificed 8 h after the single oral MDMA administration in the acute MDMA administration group and after the last MDMA administration in the subacute MDMA administration group. Rectal temperature measurements, oxidative stress status parameters and histological examinations were performed. Results: In all MDMA-administered rats, rectal temperature markedly increased peaking approximately 1 h after MDMA ingestion. Superoxide dismutase activity and thiobarbituric acid reactive substances increased after MDMA administration. Histological examinations of the kidney revealed dose-dependent disruption of tissue structure in subacute MDMA-administered rats. The latter was not observed in acute MDMA-administered rats.",
publisher = "Wiley, Hoboken",
journal = "Nephrology",
title = "Oxidative stress in rat kidneys due to 3,4-methylenedioxymetamphetamine (ecstasy) toxicity",
volume = "13",
number = "1",
pages = "33-37",
doi = "10.1111/j.1440-1797.2007.00886.x"
}

Ninković, M., Selaković, V., Đukić, M., Milosavljević, P., Vasiljević, I., Jovanović, M.,& Maličević, Ž.. (2008). Oxidative stress in rat kidneys due to 3,4-methylenedioxymetamphetamine (ecstasy) toxicity. in Nephrology
Wiley, Hoboken., 13(1), 33-37.
https://doi.org/10.1111/j.1440-1797.2007.00886.x

Ninković M, Selaković V, Đukić M, Milosavljević P, Vasiljević I, Jovanović M, Maličević Ž. Oxidative stress in rat kidneys due to 3,4-methylenedioxymetamphetamine (ecstasy) toxicity. in Nephrology. 2008;13(1):33-37.
doi:10.1111/j.1440-1797.2007.00886.x .

Ninković, Milica, Selaković, Vesna, Đukić, Mirjana, Milosavljević, Petar, Vasiljević, Ivana, Jovanović, Marina, Maličević, Živorad, "Oxidative stress in rat kidneys due to 3,4-methylenedioxymetamphetamine (ecstasy) toxicity" in Nephrology, 13, no. 1 (2008):33-37,
https://doi.org/10.1111/j.1440-1797.2007.00886.x . .

TY  - JOUR
AU  - Đukić-Ćosić, Danijela
AU  - Ćurčić-Jovanović, Marijana
AU  - Bulat, Zorica
AU  - Ninković, Milica
AU  - Maličević, Živorad
AU  - Matović, Vesna
PY  - 2008
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/1052
AB  - In this study the effect of acute and subacute cadmium (Cd) intoxication on iron (Fe) concentration and lipid peroxidation (LPO) was investigated in the livers of Swiss mice. Animals were divided into two groups: the Cd group mice intoxicated with Cd and controls. In acute time-response studies, Fe and malondialdehyde (NIDA) levels were determined at 4, 6, 12, 24 and 48 h after a single oral dose of Cd (20 mg Cd/kg b.w.). In the subacute experiment, mice were given 10 mg Cd/kg b.w. orally every day for 14 days; Fe and MDA contents were determined in liver after I and 2 weeks. Acute Cd intoxication induced a significantly increased hepatic Fe content after 4 and 6 It, and a statistically significant increase in NIDA 6, 12 and 24h after Cd administration, although a significantly decreased NIDA level was observed after 48 h. The results suggest development of early oxidative stress in livers of mice after acute intoxication with Cd. The decreased NIDA observed after 48 It occurred presumably due to the adaptive response of the organism. Subacute Cd intoxication induced a significant decrease of hepatic Fe and MDA levels at both investigated time intervals compared with control. These results indicate a positive correlation between hepatic Fe and NIDA content and suggest that prolonged Cd intoxication decreases hepatic LPO indirectly, by reducing the Fe content of mouse liver.
PB  - Elsevier Gmbh, Urban & Fischer Verlag, Jena
T2  - Journal of Trace Elements in Medicine and Biology
T1  - Relation between lipid peroxidation and iron concentration in mouse liver after acute and subacute cadmium intoxication
VL  - 22
IS  - 1
SP  - 66
EP  - 72
DO  - 10.1016/j.jtemb.2007.09.024
ER  - 

@article{
author = "Đukić-Ćosić, Danijela and Ćurčić-Jovanović, Marijana and Bulat, Zorica and Ninković, Milica and Maličević, Živorad and Matović, Vesna",
year = "2008",
abstract = "In this study the effect of acute and subacute cadmium (Cd) intoxication on iron (Fe) concentration and lipid peroxidation (LPO) was investigated in the livers of Swiss mice. Animals were divided into two groups: the Cd group mice intoxicated with Cd and controls. In acute time-response studies, Fe and malondialdehyde (NIDA) levels were determined at 4, 6, 12, 24 and 48 h after a single oral dose of Cd (20 mg Cd/kg b.w.). In the subacute experiment, mice were given 10 mg Cd/kg b.w. orally every day for 14 days; Fe and MDA contents were determined in liver after I and 2 weeks. Acute Cd intoxication induced a significantly increased hepatic Fe content after 4 and 6 It, and a statistically significant increase in NIDA 6, 12 and 24h after Cd administration, although a significantly decreased NIDA level was observed after 48 h. The results suggest development of early oxidative stress in livers of mice after acute intoxication with Cd. The decreased NIDA observed after 48 It occurred presumably due to the adaptive response of the organism. Subacute Cd intoxication induced a significant decrease of hepatic Fe and MDA levels at both investigated time intervals compared with control. These results indicate a positive correlation between hepatic Fe and NIDA content and suggest that prolonged Cd intoxication decreases hepatic LPO indirectly, by reducing the Fe content of mouse liver.",
publisher = "Elsevier Gmbh, Urban & Fischer Verlag, Jena",
journal = "Journal of Trace Elements in Medicine and Biology",
title = "Relation between lipid peroxidation and iron concentration in mouse liver after acute and subacute cadmium intoxication",
volume = "22",
number = "1",
pages = "66-72",
doi = "10.1016/j.jtemb.2007.09.024"
}

Đukić-Ćosić, D., Ćurčić-Jovanović, M., Bulat, Z., Ninković, M., Maličević, Ž.,& Matović, V.. (2008). Relation between lipid peroxidation and iron concentration in mouse liver after acute and subacute cadmium intoxication. in Journal of Trace Elements in Medicine and Biology
Elsevier Gmbh, Urban & Fischer Verlag, Jena., 22(1), 66-72.
https://doi.org/10.1016/j.jtemb.2007.09.024

Đukić-Ćosić D, Ćurčić-Jovanović M, Bulat Z, Ninković M, Maličević Ž, Matović V. Relation between lipid peroxidation and iron concentration in mouse liver after acute and subacute cadmium intoxication. in Journal of Trace Elements in Medicine and Biology. 2008;22(1):66-72.
doi:10.1016/j.jtemb.2007.09.024 .

Đukić-Ćosić, Danijela, Ćurčić-Jovanović, Marijana, Bulat, Zorica, Ninković, Milica, Maličević, Živorad, Matović, Vesna, "Relation between lipid peroxidation and iron concentration in mouse liver after acute and subacute cadmium intoxication" in Journal of Trace Elements in Medicine and Biology, 22, no. 1 (2008):66-72,
https://doi.org/10.1016/j.jtemb.2007.09.024 . .

TY  - JOUR
AU  - Bulat, Zorica
AU  - Đukić-Ćosić, Danijela
AU  - Maličević, Živorad
AU  - Bulat, Petar
AU  - Matović, Vesna
PY  - 2008
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/1104
AB  - The objective of this study was to examine the influence of oral supplementation with Zn or Mg on Cd content in the blood and organs of rabbits exposed to prolonged Cd intoxication. Rabbits were divided into the following groups: Cd group-received orally every day for 4 weeks 10 mg Cd/kg body weight (b.w.), Cd+Zn group and Cd+Mg group-exposed to Cd and supplemented with 20 mg Zn/kg b.w. or 40 mg Mg/kg b.w. 1 h after Cd treatment. Cd content in biological material was determined by atomic absorption spectrophotometry. Blood Cd concentration was determined in all investigated groups at time 0 and after 10, 14, 18, 22, 25, and 28 days, whereas Cd content in the brain, heart, lungs, liver, kidney, spleen, pancreas, skeletal muscle, and bone was determined after 28 days. Blood Cd concentration was significantly increased in all groups from the 14th day of Cd intoxication and lasted till the end of the experiment. Zn or Mg supplementation significantly reduced blood Cd content on the 18th and 25th days. Supplementation with Zn or Mg significantly decreased Cd concentration in the kidney, spleen, and bone and, in addition, Zn reduced Cd content in the brain. Supplementation with Zn or Mg in Cd-intoxicated rabbits caused similar reduction of blood Cd concentration; however, reduction of tissue Cd content was more pronounced in Zn- than in Mg-supplemented group.
PB  - Humana Press Inc, Totowa
T2  - Biological Trace Element Research
T1  - Zinc or magnesium supplementation modulates Cd intoxication in blood, kidney, spleen, and bone of rabbits
VL  - 124
IS  - 2
SP  - 110
EP  - 117
DO  - 10.1007/s12011-008-8128-5
ER  - 

@article{
author = "Bulat, Zorica and Đukić-Ćosić, Danijela and Maličević, Živorad and Bulat, Petar and Matović, Vesna",
year = "2008",
abstract = "The objective of this study was to examine the influence of oral supplementation with Zn or Mg on Cd content in the blood and organs of rabbits exposed to prolonged Cd intoxication. Rabbits were divided into the following groups: Cd group-received orally every day for 4 weeks 10 mg Cd/kg body weight (b.w.), Cd+Zn group and Cd+Mg group-exposed to Cd and supplemented with 20 mg Zn/kg b.w. or 40 mg Mg/kg b.w. 1 h after Cd treatment. Cd content in biological material was determined by atomic absorption spectrophotometry. Blood Cd concentration was determined in all investigated groups at time 0 and after 10, 14, 18, 22, 25, and 28 days, whereas Cd content in the brain, heart, lungs, liver, kidney, spleen, pancreas, skeletal muscle, and bone was determined after 28 days. Blood Cd concentration was significantly increased in all groups from the 14th day of Cd intoxication and lasted till the end of the experiment. Zn or Mg supplementation significantly reduced blood Cd content on the 18th and 25th days. Supplementation with Zn or Mg significantly decreased Cd concentration in the kidney, spleen, and bone and, in addition, Zn reduced Cd content in the brain. Supplementation with Zn or Mg in Cd-intoxicated rabbits caused similar reduction of blood Cd concentration; however, reduction of tissue Cd content was more pronounced in Zn- than in Mg-supplemented group.",
publisher = "Humana Press Inc, Totowa",
journal = "Biological Trace Element Research",
title = "Zinc or magnesium supplementation modulates Cd intoxication in blood, kidney, spleen, and bone of rabbits",
volume = "124",
number = "2",
pages = "110-117",
doi = "10.1007/s12011-008-8128-5"
}

Bulat, Z., Đukić-Ćosić, D., Maličević, Ž., Bulat, P.,& Matović, V.. (2008). Zinc or magnesium supplementation modulates Cd intoxication in blood, kidney, spleen, and bone of rabbits. in Biological Trace Element Research
Humana Press Inc, Totowa., 124(2), 110-117.
https://doi.org/10.1007/s12011-008-8128-5

Bulat Z, Đukić-Ćosić D, Maličević Ž, Bulat P, Matović V. Zinc or magnesium supplementation modulates Cd intoxication in blood, kidney, spleen, and bone of rabbits. in Biological Trace Element Research. 2008;124(2):110-117.
doi:10.1007/s12011-008-8128-5 .

Bulat, Zorica, Đukić-Ćosić, Danijela, Maličević, Živorad, Bulat, Petar, Matović, Vesna, "Zinc or magnesium supplementation modulates Cd intoxication in blood, kidney, spleen, and bone of rabbits" in Biological Trace Element Research, 124, no. 2 (2008):110-117,
https://doi.org/10.1007/s12011-008-8128-5 . .

TY  - CONF
AU  - Đukić-Ćosić, Danijela
AU  - Bulat, Zorica
AU  - Ninković, Milica
AU  - Maličević, Živorad
AU  - Matović, Vesna
PY  - 2007
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/985
PB  - Elsevier Ireland Ltd, Clare
C3  - Toxicology Letters
T1  - Effect of subacute cadmium intoxication on iron and lipid peroxidation in mouse liver
VL  - 172
IS  - Supplement
SP  - S209
EP  - S209
DO  - 10.1016/j.toxlet.2007.05.526
ER  - 

@conference{
author = "Đukić-Ćosić, Danijela and Bulat, Zorica and Ninković, Milica and Maličević, Živorad and Matović, Vesna",
year = "2007",
publisher = "Elsevier Ireland Ltd, Clare",
journal = "Toxicology Letters",
title = "Effect of subacute cadmium intoxication on iron and lipid peroxidation in mouse liver",
volume = "172",
number = "Supplement",
pages = "S209-S209",
doi = "10.1016/j.toxlet.2007.05.526"
}

Đukić-Ćosić, D., Bulat, Z., Ninković, M., Maličević, Ž.,& Matović, V.. (2007). Effect of subacute cadmium intoxication on iron and lipid peroxidation in mouse liver. in Toxicology Letters
Elsevier Ireland Ltd, Clare., 172(Supplement), S209-S209.
https://doi.org/10.1016/j.toxlet.2007.05.526

Đukić-Ćosić D, Bulat Z, Ninković M, Maličević Ž, Matović V. Effect of subacute cadmium intoxication on iron and lipid peroxidation in mouse liver. in Toxicology Letters. 2007;172(Supplement):S209-S209.
doi:10.1016/j.toxlet.2007.05.526 .

Đukić-Ćosić, Danijela, Bulat, Zorica, Ninković, Milica, Maličević, Živorad, Matović, Vesna, "Effect of subacute cadmium intoxication on iron and lipid peroxidation in mouse liver" in Toxicology Letters, 172, no. Supplement (2007):S209-S209,
https://doi.org/10.1016/j.toxlet.2007.05.526 . .

TY  - JOUR
AU  - Đukić-Ćosić, Danijela
AU  - Ninković, Milica
AU  - Maličević, Živorad
AU  - Matović, Vesna
AU  - Soldatović, Danilo
PY  - 2007
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/988
AB  - The study was designed to investigate the role of magnesium (Mg) pretreatment on reduced glutathione (GSH) levels in kidney, liver and testis of mice intoxicated with cadmium (Cd). Animals were divided into four groups: I - controls, 11 - Cd group: mice intoxicated with Cd, III - Mg+Cd group: mice given Mg 1 h before Cd, and IV - Mg group: mice given only Mg. In acute time - response studies, the single oral dose of Cd was 20 mg Cd/kg b.w. and 40 mg Mg/kg b.w. GSH levels were determined after 4, 6, 12, 24, and 48 h. In subacute experiments, mice were given 10 mg Cd/kg b.w. orally every day and 20 mg Mg/kg b.w., and GSH content was determined in investigated organs after 1 and 2 weeks. Acute cadmium intoxication significantly decreased the GSH content in liver 4, 6 and 12 h after Cd administration and increased GSH in kidney after 12, 24 and 48 h, but did not cause significant GSH alterations in testis. Mg pretreatment reduced the observed changes of GSH content in kidney and liver. Subacute Cd intoxication induced diminished renal GSH levels compared with the controls while the increased GSH levels were observed in liver and testes after 2 weeks Cd treatment. Mg pretreatment was efficient in restoring renal and testis GSH levels towards the control group, but had no effect on hepatic GSH.
PB  - John Libbey Eurotext Ltd, Montrouge
T2  - Magnesium Research
T1  - Effect of magnesium pretreatment on reduced glutathione levels in tissues of mice exposed to acute and subacute cadmium intoxication: a time course study
VL  - 20
IS  - 3
SP  - 177
EP  - 186
UR  - https://hdl.handle.net/21.15107/rcub_farfar_988
ER  - 

@article{
author = "Đukić-Ćosić, Danijela and Ninković, Milica and Maličević, Živorad and Matović, Vesna and Soldatović, Danilo",
year = "2007",
abstract = "The study was designed to investigate the role of magnesium (Mg) pretreatment on reduced glutathione (GSH) levels in kidney, liver and testis of mice intoxicated with cadmium (Cd). Animals were divided into four groups: I - controls, 11 - Cd group: mice intoxicated with Cd, III - Mg+Cd group: mice given Mg 1 h before Cd, and IV - Mg group: mice given only Mg. In acute time - response studies, the single oral dose of Cd was 20 mg Cd/kg b.w. and 40 mg Mg/kg b.w. GSH levels were determined after 4, 6, 12, 24, and 48 h. In subacute experiments, mice were given 10 mg Cd/kg b.w. orally every day and 20 mg Mg/kg b.w., and GSH content was determined in investigated organs after 1 and 2 weeks. Acute cadmium intoxication significantly decreased the GSH content in liver 4, 6 and 12 h after Cd administration and increased GSH in kidney after 12, 24 and 48 h, but did not cause significant GSH alterations in testis. Mg pretreatment reduced the observed changes of GSH content in kidney and liver. Subacute Cd intoxication induced diminished renal GSH levels compared with the controls while the increased GSH levels were observed in liver and testes after 2 weeks Cd treatment. Mg pretreatment was efficient in restoring renal and testis GSH levels towards the control group, but had no effect on hepatic GSH.",
publisher = "John Libbey Eurotext Ltd, Montrouge",
journal = "Magnesium Research",
title = "Effect of magnesium pretreatment on reduced glutathione levels in tissues of mice exposed to acute and subacute cadmium intoxication: a time course study",
volume = "20",
number = "3",
pages = "177-186",
url = "https://hdl.handle.net/21.15107/rcub_farfar_988"
}

Đukić-Ćosić, D., Ninković, M., Maličević, Ž., Matović, V.,& Soldatović, D.. (2007). Effect of magnesium pretreatment on reduced glutathione levels in tissues of mice exposed to acute and subacute cadmium intoxication: a time course study. in Magnesium Research
John Libbey Eurotext Ltd, Montrouge., 20(3), 177-186.
https://hdl.handle.net/21.15107/rcub_farfar_988

Đukić-Ćosić D, Ninković M, Maličević Ž, Matović V, Soldatović D. Effect of magnesium pretreatment on reduced glutathione levels in tissues of mice exposed to acute and subacute cadmium intoxication: a time course study. in Magnesium Research. 2007;20(3):177-186.
https://hdl.handle.net/21.15107/rcub_farfar_988 .

Đukić-Ćosić, Danijela, Ninković, Milica, Maličević, Živorad, Matović, Vesna, Soldatović, Danilo, "Effect of magnesium pretreatment on reduced glutathione levels in tissues of mice exposed to acute and subacute cadmium intoxication: a time course study" in Magnesium Research, 20, no. 3 (2007):177-186,
https://hdl.handle.net/21.15107/rcub_farfar_988 .

TY  - JOUR
AU  - Ninković, Milica
AU  - Maličević, Živorad
AU  - Jelenković, Ankica V.
AU  - Jovanović, D.M
AU  - Đukić, Mirjana
AU  - Vasiljević, Ivana
PY  - 2006
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/887
AB  - As a part of blood-brain barrier, brain capillaries participate in pathophysiological events during systemic inflammation. We investigated the effects of 7-nitroindazole (7-NI), selective neuronal nitric oxide synthase (NOS) inhibitor, to oxidative status (OS) of brain capillaries. Adult Wistar rats were randomized at groups: control group (CG) (sham operated), sepsis group (GS) (cecal ligation and perforation with inoculation of Escherichia coli (ATCC 25922), 7-NI group (G7-NI), (30 mg/ kg b/w i. p.) and 7-NI + sepsis group (G7-NIS), (7-NI was applied 30 minutes before operation). Lipid peroxidation index (LPI), nitrite concentration, superoxide dismutase (SOD) activity and superoxide anion (O2*-) content were determined 3, 6, 24 and 48 hour in each group. Cerebral capillaries were separated from non-vascular brain tissue using sucrose gradient. Compared to controls, LPI, nitrite and O2*- increased at SG. In the G7-NIS, LPI reached control values at the 24th and 48th hour, while nitrite were decreased at the 3rd and 24th hour, compared to controls. In the same group, O2*- decreased at the 3rd, 6th and 24th hour, although SOD showed variable activity. The systematic nNOS inhibition with 7-NI forces OS on early terms of sepsis, but lately it contributes to the normalization of OS in cerebral capillaries.
T2  - Acta Physiologica Hungarica
T1  - Oxidative stress in the rats brain capillaries in sepsis - The influence of 7-nitroindazole
VL  - 93
IS  - 4
SP  - 315
EP  - 323
DO  - 10.1556/APhysiol.93.2006.4.7
ER  - 

@article{
author = "Ninković, Milica and Maličević, Živorad and Jelenković, Ankica V. and Jovanović, D.M and Đukić, Mirjana and Vasiljević, Ivana",
year = "2006",
abstract = "As a part of blood-brain barrier, brain capillaries participate in pathophysiological events during systemic inflammation. We investigated the effects of 7-nitroindazole (7-NI), selective neuronal nitric oxide synthase (NOS) inhibitor, to oxidative status (OS) of brain capillaries. Adult Wistar rats were randomized at groups: control group (CG) (sham operated), sepsis group (GS) (cecal ligation and perforation with inoculation of Escherichia coli (ATCC 25922), 7-NI group (G7-NI), (30 mg/ kg b/w i. p.) and 7-NI + sepsis group (G7-NIS), (7-NI was applied 30 minutes before operation). Lipid peroxidation index (LPI), nitrite concentration, superoxide dismutase (SOD) activity and superoxide anion (O2*-) content were determined 3, 6, 24 and 48 hour in each group. Cerebral capillaries were separated from non-vascular brain tissue using sucrose gradient. Compared to controls, LPI, nitrite and O2*- increased at SG. In the G7-NIS, LPI reached control values at the 24th and 48th hour, while nitrite were decreased at the 3rd and 24th hour, compared to controls. In the same group, O2*- decreased at the 3rd, 6th and 24th hour, although SOD showed variable activity. The systematic nNOS inhibition with 7-NI forces OS on early terms of sepsis, but lately it contributes to the normalization of OS in cerebral capillaries.",
journal = "Acta Physiologica Hungarica",
title = "Oxidative stress in the rats brain capillaries in sepsis - The influence of 7-nitroindazole",
volume = "93",
number = "4",
pages = "315-323",
doi = "10.1556/APhysiol.93.2006.4.7"
}

Ninković, M., Maličević, Ž., Jelenković, A. V., Jovanović, D.M, Đukić, M.,& Vasiljević, I.. (2006). Oxidative stress in the rats brain capillaries in sepsis - The influence of 7-nitroindazole. in Acta Physiologica Hungarica, 93(4), 315-323.
https://doi.org/10.1556/APhysiol.93.2006.4.7

Ninković M, Maličević Ž, Jelenković AV, Jovanović D, Đukić M, Vasiljević I. Oxidative stress in the rats brain capillaries in sepsis - The influence of 7-nitroindazole. in Acta Physiologica Hungarica. 2006;93(4):315-323.
doi:10.1556/APhysiol.93.2006.4.7 .

Ninković, Milica, Maličević, Živorad, Jelenković, Ankica V., Jovanović, D.M, Đukić, Mirjana, Vasiljević, Ivana, "Oxidative stress in the rats brain capillaries in sepsis - The influence of 7-nitroindazole" in Acta Physiologica Hungarica, 93, no. 4 (2006):315-323,
https://doi.org/10.1556/APhysiol.93.2006.4.7 . .

TY  - CONF
AU  - Đukić-Ćosić, Danijela
AU  - Ninković, Milica
AU  - Maličević, Živorad
AU  - Matović, Vesna
PY  - 2006
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/694
PB  - Elsevier Ireland Ltd, Clare
C3  - Toxicology Letters
T1  - Effect of magnesium pretreatment on glutathione levels in kidney and liver of mice exposed to acute cadmium intoxication
VL  - 164, Supplement
SP  - S198
DO  - 10.1016/j.toxlet.2006.07.070
ER  - 

@conference{
author = "Đukić-Ćosić, Danijela and Ninković, Milica and Maličević, Živorad and Matović, Vesna",
year = "2006",
publisher = "Elsevier Ireland Ltd, Clare",
journal = "Toxicology Letters",
title = "Effect of magnesium pretreatment on glutathione levels in kidney and liver of mice exposed to acute cadmium intoxication",
volume = "164, Supplement",
pages = "S198",
doi = "10.1016/j.toxlet.2006.07.070"
}

Đukić-Ćosić, D., Ninković, M., Maličević, Ž.,& Matović, V.. (2006). Effect of magnesium pretreatment on glutathione levels in kidney and liver of mice exposed to acute cadmium intoxication. in Toxicology Letters
Elsevier Ireland Ltd, Clare., 164, Supplement, S198.
https://doi.org/10.1016/j.toxlet.2006.07.070

Đukić-Ćosić D, Ninković M, Maličević Ž, Matović V. Effect of magnesium pretreatment on glutathione levels in kidney and liver of mice exposed to acute cadmium intoxication. in Toxicology Letters. 2006;164, Supplement:S198.
doi:10.1016/j.toxlet.2006.07.070 .

Đukić-Ćosić, Danijela, Ninković, Milica, Maličević, Živorad, Matović, Vesna, "Effect of magnesium pretreatment on glutathione levels in kidney and liver of mice exposed to acute cadmium intoxication" in Toxicology Letters, 164, Supplement (2006):S198,
https://doi.org/10.1016/j.toxlet.2006.07.070 . .

TY  - JOUR
AU  - Đukić-Ćosić, Danijela
AU  - Ninković, Milica
AU  - Maličević, Živorad
AU  - Bulat, Zorica
AU  - Matović, Vesna
PY  - 2006
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/679
AB  - In this report, we present the results of our investigations on the effect of Mg pretreatment on Cd and bioelements (Cu and Zn) contents in kidney of mice exposed to acute and subacute Cd intoxication. Acute intoxication was performed on male Swiss mice given a single oral dose of 20 mg Cd/kg body weight and mice given the same dose of Cd but pretreated with 40 mg Mg/kg body weight. For subacute intoxication one group of mice was given 10 mg Cd/kg body weight every day, for 2 wk, and the other one received the same dose of Cd after oral Mg intake of 20 mg/kg body weight. Cd, Cu, and Zn content was determined in kidney by atomic absorption spectrophotometry. In acute Cd intoxication, Mg pretreatment resulted in significant decrease of Cd in kidney after 4 and 6 h, compared with animals given only Cd. Under the condition of subacute Cd intoxication, Mg supplementation reduced Cd kidney content after 2 wk for about 30%, compared with animals treated with Cd only. The effect of Mg on Cu and Zn kidney content was also beneficial.
PB  - Humana Press Inc, Totowa
T2  - Biological Trace Element Research
T1  - Effect of supplemental magnesium on the kidney levels of cadmium, zinc, and copper of mice exposed to toxic levels of cadmium
VL  - 114
IS  - 1-3
SP  - 281
EP  - 291
DO  - 10.1385/BTER:114:1:281
ER  - 

@article{
author = "Đukić-Ćosić, Danijela and Ninković, Milica and Maličević, Živorad and Bulat, Zorica and Matović, Vesna",
year = "2006",
abstract = "In this report, we present the results of our investigations on the effect of Mg pretreatment on Cd and bioelements (Cu and Zn) contents in kidney of mice exposed to acute and subacute Cd intoxication. Acute intoxication was performed on male Swiss mice given a single oral dose of 20 mg Cd/kg body weight and mice given the same dose of Cd but pretreated with 40 mg Mg/kg body weight. For subacute intoxication one group of mice was given 10 mg Cd/kg body weight every day, for 2 wk, and the other one received the same dose of Cd after oral Mg intake of 20 mg/kg body weight. Cd, Cu, and Zn content was determined in kidney by atomic absorption spectrophotometry. In acute Cd intoxication, Mg pretreatment resulted in significant decrease of Cd in kidney after 4 and 6 h, compared with animals given only Cd. Under the condition of subacute Cd intoxication, Mg supplementation reduced Cd kidney content after 2 wk for about 30%, compared with animals treated with Cd only. The effect of Mg on Cu and Zn kidney content was also beneficial.",
publisher = "Humana Press Inc, Totowa",
journal = "Biological Trace Element Research",
title = "Effect of supplemental magnesium on the kidney levels of cadmium, zinc, and copper of mice exposed to toxic levels of cadmium",
volume = "114",
number = "1-3",
pages = "281-291",
doi = "10.1385/BTER:114:1:281"
}

Đukić-Ćosić, D., Ninković, M., Maličević, Ž., Bulat, Z.,& Matović, V.. (2006). Effect of supplemental magnesium on the kidney levels of cadmium, zinc, and copper of mice exposed to toxic levels of cadmium. in Biological Trace Element Research
Humana Press Inc, Totowa., 114(1-3), 281-291.
https://doi.org/10.1385/BTER:114:1:281

Đukić-Ćosić D, Ninković M, Maličević Ž, Bulat Z, Matović V. Effect of supplemental magnesium on the kidney levels of cadmium, zinc, and copper of mice exposed to toxic levels of cadmium. in Biological Trace Element Research. 2006;114(1-3):281-291.
doi:10.1385/BTER:114:1:281 .

Đukić-Ćosić, Danijela, Ninković, Milica, Maličević, Živorad, Bulat, Zorica, Matović, Vesna, "Effect of supplemental magnesium on the kidney levels of cadmium, zinc, and copper of mice exposed to toxic levels of cadmium" in Biological Trace Element Research, 114, no. 1-3 (2006):281-291,
https://doi.org/10.1385/BTER:114:1:281 . .

TY  - JOUR
AU  - Vasiljević, Ivana D.
AU  - Jovanović, Marina
AU  - Čolić, Miodrag
AU  - Mihajlović, Rosa
AU  - Đukić, Mirjana
AU  - Ninković, Milica
AU  - Maličević, Živorad
PY  - 2004
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/562
AB  - The aetiology of neuronal death in neurodegenerative diseases, including Huntington-s disease, is still unknown. There could be a complex interplay among altered energy metabolism, excitotoxicity and oxidative stress. Our aim was to examine the effects of intrastriatal injection of a selective inhibitor of neuronal nitric oxide synthase, 7-nitroindazole, and a non-specific potent nitric oxide synthase inhibitor, Nw-nitro-L-arginine methyl ester, in order to study the possible involvement of glutathione, an important antioxidant, in quinolinic acid-induced striatal toxicity in the rat. Unilateral administration of quinolinic acid to rat striatum in a single dose of 150 nmol/L was used as a model of Huntington-s disease. The other group of animals were pretreated with 7- nitroindazole and Nw-nitro-L-arginine methyl ester, respectively. Control groups were treated with saline solution and olive oil, respectively. Content of total glutathione, was increased in the ipsi- and contralateral striatum, forebrain cortex, basal forebrain and hippocampus in the groups treated with nitric oxid synthase inhibitors and quinolinic acid compared to the quinolinic acid-treated animals. These results support the hypothesis that oxygen free radicals contribute to excitotoxic neuronal injury, and also that nitric oxide synthase inhibitors could be potential neuroprotective agents in Huntington-s disease.
AB  - Etiologija selektivnog umiranja neurona u neurodegenerativnim bolestima je nepoznata, iako postoje dokazi o defektu energetskog metabolizma, ekscitotoksičnosti i oksidativnom oštećenju. Verovatno je da ključnu ulogu ima kompleksna interakcija između ovih mehanizama. Cilj ovog rada bio je da se ispitaju efekti intrastrijatne primene selektivnog inhibitora neuronske azot oksid sintaze, 7-nitroindazola, kao i nespecifičnog inhibitora azot oksid sintaze, Nw-nitro-l-arginin metil estra, zbog moguće uključenosti glutationa, ključnog antioksidansa, u toksičnost strijatuma izazvanu hinolinskom kiselinom, kod pacova. Unilateralna aplikacija hinolinske kiseline, u strijatum pacova u pojedinačnoj dozi od 150 nmol/L korišćena je kao model Hantingtonove bolesti. Druge grupe životinja tretirane su 7-nitroindazolom, odnosno Nw-nitro-l-arginin metil estrom. Kontrolne grupe dobijale su fiziološki rastvor, odnosno maslinovo ulje. Sadržaj ukupnog glutationa je povećan u ipsi- i kontralateralnom strijatumu, kori prednjeg mozga, bazalnom prednjem mozgu i hipokampusu grupa životinja koje su pored hinolinske kiseline primile i odgovarajući inhibitor neuronske azot oksid sintaze, u poređenju sa grupom tretiranom samo neurotoksinom. Ovi podaci pokazuju da kiseonični slobodni radikali učestvuju u ekscitotoksičnom oštećenju neurona, kao i da inhibitori azot oksid sintaze mogu biti potencijalni neuroprotektivni agensi u Hantingtonovoj bolesti.
PB  - Društvo medicinskih biohemičara Srbije i Crne Gore, Beograd i Univerzitet u Beogradu - Farmaceutski fakultet, Beograd
T2  - Jugoslovenska medicinska biohemija
T1  - Effects of various nitric oxide synthase inhibitors on quinolinic acid-induced neuronal injury in rats
T1  - Efekti različitih inhibitora azot oksid sintaze na oštećenje neurona indukovano hinolinskom kiselinom kod pacova
VL  - 23
IS  - 1
SP  - 11
EP  - 18
DO  - 10.2298/JMH0401011V
ER  - 

@article{
author = "Vasiljević, Ivana D. and Jovanović, Marina and Čolić, Miodrag and Mihajlović, Rosa and Đukić, Mirjana and Ninković, Milica and Maličević, Živorad",
year = "2004",
abstract = "The aetiology of neuronal death in neurodegenerative diseases, including Huntington-s disease, is still unknown. There could be a complex interplay among altered energy metabolism, excitotoxicity and oxidative stress. Our aim was to examine the effects of intrastriatal injection of a selective inhibitor of neuronal nitric oxide synthase, 7-nitroindazole, and a non-specific potent nitric oxide synthase inhibitor, Nw-nitro-L-arginine methyl ester, in order to study the possible involvement of glutathione, an important antioxidant, in quinolinic acid-induced striatal toxicity in the rat. Unilateral administration of quinolinic acid to rat striatum in a single dose of 150 nmol/L was used as a model of Huntington-s disease. The other group of animals were pretreated with 7- nitroindazole and Nw-nitro-L-arginine methyl ester, respectively. Control groups were treated with saline solution and olive oil, respectively. Content of total glutathione, was increased in the ipsi- and contralateral striatum, forebrain cortex, basal forebrain and hippocampus in the groups treated with nitric oxid synthase inhibitors and quinolinic acid compared to the quinolinic acid-treated animals. These results support the hypothesis that oxygen free radicals contribute to excitotoxic neuronal injury, and also that nitric oxide synthase inhibitors could be potential neuroprotective agents in Huntington-s disease., Etiologija selektivnog umiranja neurona u neurodegenerativnim bolestima je nepoznata, iako postoje dokazi o defektu energetskog metabolizma, ekscitotoksičnosti i oksidativnom oštećenju. Verovatno je da ključnu ulogu ima kompleksna interakcija između ovih mehanizama. Cilj ovog rada bio je da se ispitaju efekti intrastrijatne primene selektivnog inhibitora neuronske azot oksid sintaze, 7-nitroindazola, kao i nespecifičnog inhibitora azot oksid sintaze, Nw-nitro-l-arginin metil estra, zbog moguće uključenosti glutationa, ključnog antioksidansa, u toksičnost strijatuma izazvanu hinolinskom kiselinom, kod pacova. Unilateralna aplikacija hinolinske kiseline, u strijatum pacova u pojedinačnoj dozi od 150 nmol/L korišćena je kao model Hantingtonove bolesti. Druge grupe životinja tretirane su 7-nitroindazolom, odnosno Nw-nitro-l-arginin metil estrom. Kontrolne grupe dobijale su fiziološki rastvor, odnosno maslinovo ulje. Sadržaj ukupnog glutationa je povećan u ipsi- i kontralateralnom strijatumu, kori prednjeg mozga, bazalnom prednjem mozgu i hipokampusu grupa životinja koje su pored hinolinske kiseline primile i odgovarajući inhibitor neuronske azot oksid sintaze, u poređenju sa grupom tretiranom samo neurotoksinom. Ovi podaci pokazuju da kiseonični slobodni radikali učestvuju u ekscitotoksičnom oštećenju neurona, kao i da inhibitori azot oksid sintaze mogu biti potencijalni neuroprotektivni agensi u Hantingtonovoj bolesti.",
publisher = "Društvo medicinskih biohemičara Srbije i Crne Gore, Beograd i Univerzitet u Beogradu - Farmaceutski fakultet, Beograd",
journal = "Jugoslovenska medicinska biohemija",
title = "Effects of various nitric oxide synthase inhibitors on quinolinic acid-induced neuronal injury in rats, Efekti različitih inhibitora azot oksid sintaze na oštećenje neurona indukovano hinolinskom kiselinom kod pacova",
volume = "23",
number = "1",
pages = "11-18",
doi = "10.2298/JMH0401011V"
}

Vasiljević, I. D., Jovanović, M., Čolić, M., Mihajlović, R., Đukić, M., Ninković, M.,& Maličević, Ž.. (2004). Effects of various nitric oxide synthase inhibitors on quinolinic acid-induced neuronal injury in rats. in Jugoslovenska medicinska biohemija
Društvo medicinskih biohemičara Srbije i Crne Gore, Beograd i Univerzitet u Beogradu - Farmaceutski fakultet, Beograd., 23(1), 11-18.
https://doi.org/10.2298/JMH0401011V

Vasiljević ID, Jovanović M, Čolić M, Mihajlović R, Đukić M, Ninković M, Maličević Ž. Effects of various nitric oxide synthase inhibitors on quinolinic acid-induced neuronal injury in rats. in Jugoslovenska medicinska biohemija. 2004;23(1):11-18.
doi:10.2298/JMH0401011V .

Vasiljević, Ivana D., Jovanović, Marina, Čolić, Miodrag, Mihajlović, Rosa, Đukić, Mirjana, Ninković, Milica, Maličević, Živorad, "Effects of various nitric oxide synthase inhibitors on quinolinic acid-induced neuronal injury in rats" in Jugoslovenska medicinska biohemija, 23, no. 1 (2004):11-18,
https://doi.org/10.2298/JMH0401011V . .

TY  - JOUR
AU  - Ninković, Milica
AU  - Jovanović, Marina
AU  - Maličević, Živorad
AU  - Jelenković, Ankica V.
AU  - Đukić, Mirjana
AU  - Vasiljević, Ivana
PY  - 2003
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/461
AB  - Quinolinic acid (QA) produces a pattern of selective cell loss in the striatum, that closely mimics that of Huntington's disease (HD). The aim of this study was to investigate the antioxidative status in the thalamus after intrastriatal application of QA and the influence of nerve growth factor (NGF) on such neurotoxicity. Wistar rats were treated intrastriatally (coordinates: 8.4A, 2.6L, 4.8V), using a stereotaxic instrument. The first group was treated with QA (150 nmol/l). The second group was treated with QA, followed by NGF (4.5 mg/kg b.w). The control group was treated with 0.9 % saline solution. Seven days after the treatment, we found decreased superoxide dismutase (SOD) activity in mitochondrial fractions of the striatum of both groups. In the thalamus, SOD activity showed no differences. The content of superoxide anion increased in the striatum of QA- treated animals. It was decreased in both structures in the group that was treated with QA and NGF. In the QA+ NGF-treated group, we found increased glutathione peroxidase (GSHPx) and GSH, compared to the group that was treated with QA only, but these values were lower than in the controls. Thus, NGF showed beneficial effects on the oxido-reduction status in the striatum, and also in the thalamus, a structure that is separated from but tightly connected with the striatum.
AB  - Hinolinska kiselina (HK) prouzrokuje takav selektivni gubitak ćelija u strijatumu, koji veoma dobro imitira onaj kod Huntingtonove bolesti. Cilj ovog istraživanja bio je da se ispita antioksidativni status u talamusu nakon aplikacije HK u strijatum i uticaj NGF na takvu neurotoksičnost. Wistar pacovi su tretirani intrastrijatno, pomoću stereotaksičnog instrumenta (koordinate: 8,4A, 2,6L, 4,8V). Prva grupa je bila tretirana HK (150 nmol/l). Druga grupa je bila tretirana HK, a nakon toga je dobila NGF (4.5 mg/ kg b.w). Kontrolna grupa je bila tretirana fiziološkim rastvorom. Sedam dana nakon tretmana, u mitohondrijskim frakcijama strijatuma, našli smo smanjenu aktivnost SOD u obema grupama. U talamusu, aktivnost SOD se nije promenila. Sadržaj superoksidnog anjona se povećao u strijatumu životinja koje su bile tretirane HK, a smanjio se u obema strukturama, u grupi koja je bila tretirana sa HK i NGF. U HK+ NGF-tretiranoj grupi, našli smo povećanu aktivnost GSHPx i GSH u odnosu na grupu koja je bila tretirana samo sa HK, ali su te vrednosti bile manje u odnosu na kontrolne. NGF je pokazao povoljne efekte na oksido-reduktivni status u strijatumu, ali takođe i u talamusu, strukturi koja je odvojena, ali veoma blisko povezana sa strijatumom.
PB  - Univerzitet u Beogradu - Fakultet veterinarske medicine, Beograd
T2  - Acta veterinaria
T1  - Antioxidative effect of nerve growth factor (NGF) in rat thalamus after quinolinic acid-induced neurotoxicity
T1  - Efekat NGF na antioksidativnu odbranu u talamusu pacova nakon neurotoksičnog delovanja hinolinske kiseline
VL  - 53
IS  - 2-3
SP  - 77
EP  - 86
DO  - 10.2298/AVB0303077N
ER  - 

@article{
author = "Ninković, Milica and Jovanović, Marina and Maličević, Živorad and Jelenković, Ankica V. and Đukić, Mirjana and Vasiljević, Ivana",
year = "2003",
abstract = "Quinolinic acid (QA) produces a pattern of selective cell loss in the striatum, that closely mimics that of Huntington's disease (HD). The aim of this study was to investigate the antioxidative status in the thalamus after intrastriatal application of QA and the influence of nerve growth factor (NGF) on such neurotoxicity. Wistar rats were treated intrastriatally (coordinates: 8.4A, 2.6L, 4.8V), using a stereotaxic instrument. The first group was treated with QA (150 nmol/l). The second group was treated with QA, followed by NGF (4.5 mg/kg b.w). The control group was treated with 0.9 % saline solution. Seven days after the treatment, we found decreased superoxide dismutase (SOD) activity in mitochondrial fractions of the striatum of both groups. In the thalamus, SOD activity showed no differences. The content of superoxide anion increased in the striatum of QA- treated animals. It was decreased in both structures in the group that was treated with QA and NGF. In the QA+ NGF-treated group, we found increased glutathione peroxidase (GSHPx) and GSH, compared to the group that was treated with QA only, but these values were lower than in the controls. Thus, NGF showed beneficial effects on the oxido-reduction status in the striatum, and also in the thalamus, a structure that is separated from but tightly connected with the striatum., Hinolinska kiselina (HK) prouzrokuje takav selektivni gubitak ćelija u strijatumu, koji veoma dobro imitira onaj kod Huntingtonove bolesti. Cilj ovog istraživanja bio je da se ispita antioksidativni status u talamusu nakon aplikacije HK u strijatum i uticaj NGF na takvu neurotoksičnost. Wistar pacovi su tretirani intrastrijatno, pomoću stereotaksičnog instrumenta (koordinate: 8,4A, 2,6L, 4,8V). Prva grupa je bila tretirana HK (150 nmol/l). Druga grupa je bila tretirana HK, a nakon toga je dobila NGF (4.5 mg/ kg b.w). Kontrolna grupa je bila tretirana fiziološkim rastvorom. Sedam dana nakon tretmana, u mitohondrijskim frakcijama strijatuma, našli smo smanjenu aktivnost SOD u obema grupama. U talamusu, aktivnost SOD se nije promenila. Sadržaj superoksidnog anjona se povećao u strijatumu životinja koje su bile tretirane HK, a smanjio se u obema strukturama, u grupi koja je bila tretirana sa HK i NGF. U HK+ NGF-tretiranoj grupi, našli smo povećanu aktivnost GSHPx i GSH u odnosu na grupu koja je bila tretirana samo sa HK, ali su te vrednosti bile manje u odnosu na kontrolne. NGF je pokazao povoljne efekte na oksido-reduktivni status u strijatumu, ali takođe i u talamusu, strukturi koja je odvojena, ali veoma blisko povezana sa strijatumom.",
publisher = "Univerzitet u Beogradu - Fakultet veterinarske medicine, Beograd",
journal = "Acta veterinaria",
title = "Antioxidative effect of nerve growth factor (NGF) in rat thalamus after quinolinic acid-induced neurotoxicity, Efekat NGF na antioksidativnu odbranu u talamusu pacova nakon neurotoksičnog delovanja hinolinske kiseline",
volume = "53",
number = "2-3",
pages = "77-86",
doi = "10.2298/AVB0303077N"
}

Ninković, M., Jovanović, M., Maličević, Ž., Jelenković, A. V., Đukić, M.,& Vasiljević, I.. (2003). Antioxidative effect of nerve growth factor (NGF) in rat thalamus after quinolinic acid-induced neurotoxicity. in Acta veterinaria
Univerzitet u Beogradu - Fakultet veterinarske medicine, Beograd., 53(2-3), 77-86.
https://doi.org/10.2298/AVB0303077N

Ninković M, Jovanović M, Maličević Ž, Jelenković AV, Đukić M, Vasiljević I. Antioxidative effect of nerve growth factor (NGF) in rat thalamus after quinolinic acid-induced neurotoxicity. in Acta veterinaria. 2003;53(2-3):77-86.
doi:10.2298/AVB0303077N .

Ninković, Milica, Jovanović, Marina, Maličević, Živorad, Jelenković, Ankica V., Đukić, Mirjana, Vasiljević, Ivana, "Antioxidative effect of nerve growth factor (NGF) in rat thalamus after quinolinic acid-induced neurotoxicity" in Acta veterinaria, 53, no. 2-3 (2003):77-86,
https://doi.org/10.2298/AVB0303077N . .