TY  - JOUR
AU  - Ninković, Milica
AU  - Maliević, Ivorad M.
AU  - Jelenković, Ankica V.
AU  - Đukić, Mirjana
AU  - Jovanović, Marina
AU  - Stevanović, Ivana
PY  - 2009
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/1169
AB  - Oxidative stress development in different brain structures and the influence of nitric oxide (NO) overproduction during sepsis was investigated using male Wistar rats. Rats were subjected to cecal ligation and puncture (CLP) or were sham-operated. To evaluate the source of NO production, 30 min before the operation septic and control animals were treated with single intraperitoneal doses of NO synthase (NOS) inhibitors: L-NAME and aminoguanidine (AG) (10, 30 or 90 mg/kg) and 7-nitroindazole (7-NI) (30 mg/kg). The concentration of GSH in the cortex, brain stem, cerebellum, striatum and hippocampus significantly decreased post CLP at both early and late stage sepsis. Lipid peroxidation also occurred in the cortex and cerebellum in late stage sepsis. Pre-treatment with a non-selective NOS inhibitor (L-NAME) and with selective inducible and neuronal NOS inhibitors (AG and 7-NI) revealed benefit effects on the GSH concentrations. Unexpectedly, NOS inhibition resulted in diverse effects on TBARS concentrations, suggesting the importance of specific quantities of NO in specific brain structures during sepsis.
PB  - General Physiol And Biophysics, Bratislava
T2  - General Physiology and Biophysics
T1  - Nitric oxide synthase inhibitors partially inhibit oxidative stress development in the rat brain during sepsis provoked by cecal ligation and puncture
VL  - 28
SP  - 243
EP  - 250
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1476
ER  - 

@article{
author = "Ninković, Milica and Maliević, Ivorad M. and Jelenković, Ankica V. and Đukić, Mirjana and Jovanović, Marina and Stevanović, Ivana",
year = "2009",
abstract = "Oxidative stress development in different brain structures and the influence of nitric oxide (NO) overproduction during sepsis was investigated using male Wistar rats. Rats were subjected to cecal ligation and puncture (CLP) or were sham-operated. To evaluate the source of NO production, 30 min before the operation septic and control animals were treated with single intraperitoneal doses of NO synthase (NOS) inhibitors: L-NAME and aminoguanidine (AG) (10, 30 or 90 mg/kg) and 7-nitroindazole (7-NI) (30 mg/kg). The concentration of GSH in the cortex, brain stem, cerebellum, striatum and hippocampus significantly decreased post CLP at both early and late stage sepsis. Lipid peroxidation also occurred in the cortex and cerebellum in late stage sepsis. Pre-treatment with a non-selective NOS inhibitor (L-NAME) and with selective inducible and neuronal NOS inhibitors (AG and 7-NI) revealed benefit effects on the GSH concentrations. Unexpectedly, NOS inhibition resulted in diverse effects on TBARS concentrations, suggesting the importance of specific quantities of NO in specific brain structures during sepsis.",
publisher = "General Physiol And Biophysics, Bratislava",
journal = "General Physiology and Biophysics",
title = "Nitric oxide synthase inhibitors partially inhibit oxidative stress development in the rat brain during sepsis provoked by cecal ligation and puncture",
volume = "28",
pages = "243-250",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1476"
}

Ninković, M., Maliević, I. M., Jelenković, A. V., Đukić, M., Jovanović, M.,& Stevanović, I.. (2009). Nitric oxide synthase inhibitors partially inhibit oxidative stress development in the rat brain during sepsis provoked by cecal ligation and puncture. in General Physiology and Biophysics
General Physiol And Biophysics, Bratislava., 28, 243-250.
https://hdl.handle.net/21.15107/rcub_ibiss_1476

Ninković M, Maliević IM, Jelenković AV, Đukić M, Jovanović M, Stevanović I. Nitric oxide synthase inhibitors partially inhibit oxidative stress development in the rat brain during sepsis provoked by cecal ligation and puncture. in General Physiology and Biophysics. 2009;28:243-250.
https://hdl.handle.net/21.15107/rcub_ibiss_1476 .

Ninković, Milica, Maliević, Ivorad M., Jelenković, Ankica V., Đukić, Mirjana, Jovanović, Marina, Stevanović, Ivana, "Nitric oxide synthase inhibitors partially inhibit oxidative stress development in the rat brain during sepsis provoked by cecal ligation and puncture" in General Physiology and Biophysics, 28 (2009):243-250,
https://hdl.handle.net/21.15107/rcub_ibiss_1476 .

TY  - JOUR
AU  - Stevanović, Nana D.
AU  - Jovanović, Marina
AU  - Jelenković, Ankica V.
AU  - Ninković, Milica
AU  - Đukić, Mirjana
AU  - Stojanović, Ivana
AU  - Čolić, Miodrag
PY  - 2009
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/1182
AB  - The goal of the present study was to examine the effectiveness of a non-specific nitric oxide synthase (NOS) inhibitor N-nitro-L-arginine methyl ester (L-NAME) to modulate the toxicity of aluminium chloride (AlCl3). Rats were killed at 3 h and at 30 days after treatments and the striatum was removed. Nitrite, superoxide, superoxide dismutase activity, malondialdehyde and reduced glutathione were determined. AlCl3 exposure promoted oxidative stress in the striatum. The biochemical changes observed in neuronal tissues show that aluminium acts as pro-oxidant, while the NOS inhibitor exerts antioxidant action in AlCl3-treated rats. We conclude that L-NAME can efficiently protect neuronal tissue from AlCl3-induced toxicity.
PB  - General Physiol And Biophysics, Bratislava
T2  - General Physiology and Biophysics
T1  - The effect of inhibition of nitric oxide synthase on aluminium-induced toxicity in the rat brain
VL  - 28
SP  - 235
EP  - 242
UR  - https://hdl.handle.net/21.15107/rcub_farfar_1182
ER  - 

@article{
author = "Stevanović, Nana D. and Jovanović, Marina and Jelenković, Ankica V. and Ninković, Milica and Đukić, Mirjana and Stojanović, Ivana and Čolić, Miodrag",
year = "2009",
abstract = "The goal of the present study was to examine the effectiveness of a non-specific nitric oxide synthase (NOS) inhibitor N-nitro-L-arginine methyl ester (L-NAME) to modulate the toxicity of aluminium chloride (AlCl3). Rats were killed at 3 h and at 30 days after treatments and the striatum was removed. Nitrite, superoxide, superoxide dismutase activity, malondialdehyde and reduced glutathione were determined. AlCl3 exposure promoted oxidative stress in the striatum. The biochemical changes observed in neuronal tissues show that aluminium acts as pro-oxidant, while the NOS inhibitor exerts antioxidant action in AlCl3-treated rats. We conclude that L-NAME can efficiently protect neuronal tissue from AlCl3-induced toxicity.",
publisher = "General Physiol And Biophysics, Bratislava",
journal = "General Physiology and Biophysics",
title = "The effect of inhibition of nitric oxide synthase on aluminium-induced toxicity in the rat brain",
volume = "28",
pages = "235-242",
url = "https://hdl.handle.net/21.15107/rcub_farfar_1182"
}

Stevanović, N. D., Jovanović, M., Jelenković, A. V., Ninković, M., Đukić, M., Stojanović, I.,& Čolić, M.. (2009). The effect of inhibition of nitric oxide synthase on aluminium-induced toxicity in the rat brain. in General Physiology and Biophysics
General Physiol And Biophysics, Bratislava., 28, 235-242.
https://hdl.handle.net/21.15107/rcub_farfar_1182

Stevanović ND, Jovanović M, Jelenković AV, Ninković M, Đukić M, Stojanović I, Čolić M. The effect of inhibition of nitric oxide synthase on aluminium-induced toxicity in the rat brain. in General Physiology and Biophysics. 2009;28:235-242.
https://hdl.handle.net/21.15107/rcub_farfar_1182 .

Stevanović, Nana D., Jovanović, Marina, Jelenković, Ankica V., Ninković, Milica, Đukić, Mirjana, Stojanović, Ivana, Čolić, Miodrag, "The effect of inhibition of nitric oxide synthase on aluminium-induced toxicity in the rat brain" in General Physiology and Biophysics, 28 (2009):235-242,
https://hdl.handle.net/21.15107/rcub_farfar_1182 .

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  - 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 . .