TY  - JOUR
AU  - Đurđević, Dragan
AU  - Đukić, Mirjana
AU  - Ninković, Milica
AU  - Stevanović, Ivana
AU  - Jovanović, Marina
AU  - Vasić, Una
PY  - 2013
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/2062
AB  - Diquat (DQ) neurotoxicity mechanisms are unknown, although, it's systemic toxicity is mediated by free radical reactions. The role of glutathione cycle was assessed by glutathione reductase (GR) applied in the pre-treatment of DQ poisoning. Wistar rats were used and tested compounds were administered intrastriatally (i.s.) in one single dose. Total glutathione (tGSH), glutathione disulfide (GSSG) and glutathione peroxidase (GPx) were measured in the vulnerable brain regions (VBRs) (striatum, hippocampus and cortex), at 30 minutes, 24 hours and 7 days post treatment. Results from the intact and the sham operated groups were not statistically different. Rapid spatial spreading of oxidative stress was confirmed in the examined VBRs.. Mortality (30-40%, within 24hrs) and signs of lethargy were observed in the DQ group. Activity of GPx activity was elevated and GSSG/GSH was higher in the examined VBRs during the experiment, compared to the controls. The i.s. pre-treatment with GR achieved neuroprotective role against DQ induced neurotoxicity, based on animal survival, absence of lethargy and decreased GPx activity and GSSG/GSH in the examined VBRs during the experiment, compared to the DQ group. Our results confirmed that oxidation of GSH was the reason for the reduced antioxidative defense against DQ neurotoxicity.
AB  - Mehanizmi neurotoksičnosti dikvata (DK) su nepoznati, mada se zna da je sistemska toksičnost posredovana reakcijama slobodnih radikala. Uloga glutationskog ciklusa je isptivana primenom glutation reduktaze (GR) u predtretmanu trovanja DK. Wistar pacovi su korišćeni i testirana jedinjenja intrastrjiatalno (i.s.) primenjena u jednokratnoj dozi. Ukupni glutation (tGSH), glutation-disulfid (GSSG) i aktivnost glutation peroksidaze (GPx) su mereni u selektivno osetljivim regionima mozga (strijatum, hipokampus i korteks), 30. minuta, 24. sata i 7. dana posle tretmana. Rezultati netretiranih (intaktna grupa) i lažno operisanih pacova se ne razlikuju statistički. Vremensko i prostorno širenje oksidativnog stresa je potvrđeno kod ispitivanih moždanih struktura. Mortalitet (30-40%, u roku od 24 casa) i znaci letargije su uočeni u samo u DK grupi. Statistički povećana aktivnost GPx, kao i odnosa GSSG/GSH u ispitivanim moždanim strukturama tokom eksperimenta, potvrđuje oksidativno narušenu ravnotežu i oštećenja moždanog tkiva. Predtretman i.s. sa GR je ispoljio neurozaštitni efekat od neurotoksičnosti DK, bazirano na preživljavanju životinja, odsustvu letargije i smanjenoj aktivnost GPx i odnosa GSSG / GSH ispitivanih moždanih struktura tokom eksperimenta, u odnosu na DK grupu. Naši rezultati ukazuju da je oksidacija GSH kljucna za smanjenje antioksidativne odbrane od DK neurotoksicnosti.
PB  - Univerzitet u Beogradu - Fakultet veterinarske medicine, Beograd
T2  - Acta veterinaria
T1  - Glutathione cycle in diquat neurotoxicity: Assessed by intrastriatal pre-treatment with glutathione reductase
T1  - Uloga glutationskog ciklusa u neurotoksičnosti dikvata - ispitivano primenom intrastrijatalnog predtretmana sa glutation reduktazom
VL  - 63
IS  - 2-3
SP  - 159
EP  - 175
DO  - 10.2298/AVB1303159D
ER  - 

@article{
author = "Đurđević, Dragan and Đukić, Mirjana and Ninković, Milica and Stevanović, Ivana and Jovanović, Marina and Vasić, Una",
year = "2013",
abstract = "Diquat (DQ) neurotoxicity mechanisms are unknown, although, it's systemic toxicity is mediated by free radical reactions. The role of glutathione cycle was assessed by glutathione reductase (GR) applied in the pre-treatment of DQ poisoning. Wistar rats were used and tested compounds were administered intrastriatally (i.s.) in one single dose. Total glutathione (tGSH), glutathione disulfide (GSSG) and glutathione peroxidase (GPx) were measured in the vulnerable brain regions (VBRs) (striatum, hippocampus and cortex), at 30 minutes, 24 hours and 7 days post treatment. Results from the intact and the sham operated groups were not statistically different. Rapid spatial spreading of oxidative stress was confirmed in the examined VBRs.. Mortality (30-40%, within 24hrs) and signs of lethargy were observed in the DQ group. Activity of GPx activity was elevated and GSSG/GSH was higher in the examined VBRs during the experiment, compared to the controls. The i.s. pre-treatment with GR achieved neuroprotective role against DQ induced neurotoxicity, based on animal survival, absence of lethargy and decreased GPx activity and GSSG/GSH in the examined VBRs during the experiment, compared to the DQ group. Our results confirmed that oxidation of GSH was the reason for the reduced antioxidative defense against DQ neurotoxicity., Mehanizmi neurotoksičnosti dikvata (DK) su nepoznati, mada se zna da je sistemska toksičnost posredovana reakcijama slobodnih radikala. Uloga glutationskog ciklusa je isptivana primenom glutation reduktaze (GR) u predtretmanu trovanja DK. Wistar pacovi su korišćeni i testirana jedinjenja intrastrjiatalno (i.s.) primenjena u jednokratnoj dozi. Ukupni glutation (tGSH), glutation-disulfid (GSSG) i aktivnost glutation peroksidaze (GPx) su mereni u selektivno osetljivim regionima mozga (strijatum, hipokampus i korteks), 30. minuta, 24. sata i 7. dana posle tretmana. Rezultati netretiranih (intaktna grupa) i lažno operisanih pacova se ne razlikuju statistički. Vremensko i prostorno širenje oksidativnog stresa je potvrđeno kod ispitivanih moždanih struktura. Mortalitet (30-40%, u roku od 24 casa) i znaci letargije su uočeni u samo u DK grupi. Statistički povećana aktivnost GPx, kao i odnosa GSSG/GSH u ispitivanim moždanim strukturama tokom eksperimenta, potvrđuje oksidativno narušenu ravnotežu i oštećenja moždanog tkiva. Predtretman i.s. sa GR je ispoljio neurozaštitni efekat od neurotoksičnosti DK, bazirano na preživljavanju životinja, odsustvu letargije i smanjenoj aktivnost GPx i odnosa GSSG / GSH ispitivanih moždanih struktura tokom eksperimenta, u odnosu na DK grupu. Naši rezultati ukazuju da je oksidacija GSH kljucna za smanjenje antioksidativne odbrane od DK neurotoksicnosti.",
publisher = "Univerzitet u Beogradu - Fakultet veterinarske medicine, Beograd",
journal = "Acta veterinaria",
title = "Glutathione cycle in diquat neurotoxicity: Assessed by intrastriatal pre-treatment with glutathione reductase, Uloga glutationskog ciklusa u neurotoksičnosti dikvata - ispitivano primenom intrastrijatalnog predtretmana sa glutation reduktazom",
volume = "63",
number = "2-3",
pages = "159-175",
doi = "10.2298/AVB1303159D"
}

Đurđević, D., Đukić, M., Ninković, M., Stevanović, I., Jovanović, M.,& Vasić, U.. (2013). Glutathione cycle in diquat neurotoxicity: Assessed by intrastriatal pre-treatment with glutathione reductase. in Acta veterinaria
Univerzitet u Beogradu - Fakultet veterinarske medicine, Beograd., 63(2-3), 159-175.
https://doi.org/10.2298/AVB1303159D

Đurđević D, Đukić M, Ninković M, Stevanović I, Jovanović M, Vasić U. Glutathione cycle in diquat neurotoxicity: Assessed by intrastriatal pre-treatment with glutathione reductase. in Acta veterinaria. 2013;63(2-3):159-175.
doi:10.2298/AVB1303159D .

Đurđević, Dragan, Đukić, Mirjana, Ninković, Milica, Stevanović, Ivana, Jovanović, Marina, Vasić, Una, "Glutathione cycle in diquat neurotoxicity: Assessed by intrastriatal pre-treatment with glutathione reductase" in Acta veterinaria, 63, no. 2-3 (2013):159-175,
https://doi.org/10.2298/AVB1303159D . .

TY  - JOUR
AU  - Đukić, Mirjana
AU  - Jovanović, Marina
AU  - Ninković, Milica
AU  - Stevanović, Ivana
AU  - Ćurčić, Marijana
AU  - Topić, Aleksandra
AU  - Vujanović, Dragana
AU  - Đurđević, Dragan
PY  - 2012
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/1663
AB  - Introduction: Contact herbicide diquat (DQ), redox cycling compound, mediates its systemic toxicity throughout the enlarged production of free radicals. Target organs are liver and kidney in humans. To-date, the mechanism of DQ-induced neurotoxicity has not been rationalized. Objective: The objectives of the study were to examine the ability of DQ to induce oxidative stress (OS) and/or nitrosative stress (NS) upon intrastriatal (i.s.) administration and to investigate the role of nitric oxide (NOx) using NG-nitro-L-arginine methyl ester (L-NAME), a non-selective inhibitor of nitric oxide synthase (NOS) in the pretreatment of DQ i.s. administration. Material and Methods: The experiment was conducted on Wistar rats, randomly divided in experimental groups, receiving different treatments i.s. applied. Parameters of OS/NS such as: superoxide anion radical (O-2(center dot-)), superoxide dismutase (SOD), malondialdehyde (MDA) and nitrates (NO3-) were measured in the cortex (bilaterally), at 30th min, 24 hours and 7 days after the treatments. Results: Lethargy and high mortality rate were observed only in the DQ group (within 24 hours and 2-3 hours, respectively) after awakening from anesthesia. Markedly increased production of NOx and O-2(center dot-) along with elevated lipid peroxidation altogether contributed to DQ neurotoxicity. The most importantly, the L-NAME i.s. pretreatment protected treated animals from dying and diminished OS/NS response against DQ-induced neurotoxicity. Conclusion: The i.s. pretreatment with L-NAME resulted in neuroprotection against DQ neurotoxity, based on animal survival and reduced LPO in the cortex.
PB  - Inst Agricultural Medicine, Lublin
T2  - Annals of Agricultural and Environmental Medicine
T1  - Intrastriatal pre-treatment with L-NAME protects rats from diquat neurotoxcity
VL  - 19
IS  - 4
SP  - 666
EP  - 672
UR  - https://hdl.handle.net/21.15107/rcub_farfar_1663
ER  - 

@article{
author = "Đukić, Mirjana and Jovanović, Marina and Ninković, Milica and Stevanović, Ivana and Ćurčić, Marijana and Topić, Aleksandra and Vujanović, Dragana and Đurđević, Dragan",
year = "2012",
abstract = "Introduction: Contact herbicide diquat (DQ), redox cycling compound, mediates its systemic toxicity throughout the enlarged production of free radicals. Target organs are liver and kidney in humans. To-date, the mechanism of DQ-induced neurotoxicity has not been rationalized. Objective: The objectives of the study were to examine the ability of DQ to induce oxidative stress (OS) and/or nitrosative stress (NS) upon intrastriatal (i.s.) administration and to investigate the role of nitric oxide (NOx) using NG-nitro-L-arginine methyl ester (L-NAME), a non-selective inhibitor of nitric oxide synthase (NOS) in the pretreatment of DQ i.s. administration. Material and Methods: The experiment was conducted on Wistar rats, randomly divided in experimental groups, receiving different treatments i.s. applied. Parameters of OS/NS such as: superoxide anion radical (O-2(center dot-)), superoxide dismutase (SOD), malondialdehyde (MDA) and nitrates (NO3-) were measured in the cortex (bilaterally), at 30th min, 24 hours and 7 days after the treatments. Results: Lethargy and high mortality rate were observed only in the DQ group (within 24 hours and 2-3 hours, respectively) after awakening from anesthesia. Markedly increased production of NOx and O-2(center dot-) along with elevated lipid peroxidation altogether contributed to DQ neurotoxicity. The most importantly, the L-NAME i.s. pretreatment protected treated animals from dying and diminished OS/NS response against DQ-induced neurotoxicity. Conclusion: The i.s. pretreatment with L-NAME resulted in neuroprotection against DQ neurotoxity, based on animal survival and reduced LPO in the cortex.",
publisher = "Inst Agricultural Medicine, Lublin",
journal = "Annals of Agricultural and Environmental Medicine",
title = "Intrastriatal pre-treatment with L-NAME protects rats from diquat neurotoxcity",
volume = "19",
number = "4",
pages = "666-672",
url = "https://hdl.handle.net/21.15107/rcub_farfar_1663"
}

Đukić, M., Jovanović, M., Ninković, M., Stevanović, I., Ćurčić, M., Topić, A., Vujanović, D.,& Đurđević, D.. (2012). Intrastriatal pre-treatment with L-NAME protects rats from diquat neurotoxcity. in Annals of Agricultural and Environmental Medicine
Inst Agricultural Medicine, Lublin., 19(4), 666-672.
https://hdl.handle.net/21.15107/rcub_farfar_1663

Đukić M, Jovanović M, Ninković M, Stevanović I, Ćurčić M, Topić A, Vujanović D, Đurđević D. Intrastriatal pre-treatment with L-NAME protects rats from diquat neurotoxcity. in Annals of Agricultural and Environmental Medicine. 2012;19(4):666-672.
https://hdl.handle.net/21.15107/rcub_farfar_1663 .

Đukić, Mirjana, Jovanović, Marina, Ninković, Milica, Stevanović, Ivana, Ćurčić, Marijana, Topić, Aleksandra, Vujanović, Dragana, Đurđević, Dragan, "Intrastriatal pre-treatment with L-NAME protects rats from diquat neurotoxcity" in Annals of Agricultural and Environmental Medicine, 19, no. 4 (2012):666-672,
https://hdl.handle.net/21.15107/rcub_farfar_1663 .

TY  - JOUR
AU  - Đukić, Mirjana
AU  - Jovanović, Marina
AU  - Ninković, Milica
AU  - Stevanović, Ivana
AU  - Đurđević, Dragan
AU  - Vasić, Una
PY  - 2012
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/1792
AB  - In this study we examined if the response of the cortex against diquat (DQ), intrastriatally (i.s.) applied to Wistar rats, was mediated by oxidative/nitrosative stress (OS/NS). In particular, we were focused on the glutathione (GSH) antioxidative role, thus we applied i.s. glutathione reductase (GR) in the pre-treatment of DQ administration. Superoxide anion radical (O2 •-), nitrate (NO3 -), malondialdehyde (MDA) and superoxide dismutase (SOD), were measured in ipsi- and contra- lateral sides of the cortex, at 30 minutes, 24 hours and 7 days post treatment. The redox balance was not significantly changed in the cortex of sham operated and intact groups. Also, no differences were observed between the ipsi- and contra- lateral side of the cortex. Lethargy and mortality (30-40%) of the animals in the DQ group within 24 hrs, coincided with rapidly developed lipid peroxidation supported by OS/NS upon i.s. DQ administration. Strong redox potential of DQ probably resulted in a huge deprivation of molecular oxygen. The pretreatment with GR acted neuro-protectively, based on animal survival and absence of lethargy, although, lipid peroxidation was not developed in the GR+DQ group, OS was documented by a high concentration of O2 •- (within 24 hrs), descending and eventually inhibiting SOD activity (at 7 days).
AB  - U ovoj studiji smo ispitali da li je oksidativni/nitrosativni stres (OS/NS), uključen u odgovor korteksa Wistar pacova nakon intrastrijatalne (i.s.) izloženosti dikvatu (DK). Posebno smo ispitivali značaj antioksidativne uloge glutationa (GSH), zbog čega smo primenili glutation reduktazu (GR) u predtretmanu davanja DK. Superoksid anjon radikal (O2•¯), nitrati (NO3¯), malondialdehid (MDA) i superoksid dismutaza (SOD), su mereni u obostranom korteksu (ipsi- i kontrastrana), nakon 30 minuta, 24 sati i 7 dana od tretmana. Redoks balans se nije značajno promenio u korteksu lažno operisanih i netretiranih pacova. Takođe, ne postoji statistički značajna razlika između ipsi- i kontra- strane korteksa. Letargija i mortalitet (30-40%) kod životinja u DK grupi su uočene tokom 24 časa od i.s. trovanja DK, što se poklopilo sa naglim razvojem OS/NS i lipidne peroksidacije. Visok redoks potencijal DK verovatno rezultira opsežnim utroškom molekularnog kiseonika. Zaključeno je da je ostvaren neuroprotektivni učinak predtretmana sa GR, na osnovu preživljavanja životinja i odsustva letargije. Lipidna peroksidacija nije bila razvijena u grupi predtretiranoj sa GR ali je ipak izmerena visoka koncentracija O2•¯ (tokom 24 sata) koja zatim opada i na kraju 7. dana u potpunosti inhibira aktivnost SOD.
PB  - Univerzitet u Beogradu - Fakultet veterinarske medicine, Beograd
T2  - Acta veterinaria
T1  - Influence of glutathione reductase on diquat neurotoxcity assessed by oxidative/nitrosative stress in the cortex of intrastriatally treated rats
T1  - Uticaj glutation reduktaze na neurotoksičnost dikvata - ispitivan je oksidativni/nitrozativni stres u korteksu intrastrijatalno tretiranih pacova
VL  - 62
IS  - 5-6
SP  - 553
EP  - 568
DO  - 10.2298/AVB1206553D
ER  - 

@article{
author = "Đukić, Mirjana and Jovanović, Marina and Ninković, Milica and Stevanović, Ivana and Đurđević, Dragan and Vasić, Una",
year = "2012",
abstract = "In this study we examined if the response of the cortex against diquat (DQ), intrastriatally (i.s.) applied to Wistar rats, was mediated by oxidative/nitrosative stress (OS/NS). In particular, we were focused on the glutathione (GSH) antioxidative role, thus we applied i.s. glutathione reductase (GR) in the pre-treatment of DQ administration. Superoxide anion radical (O2 •-), nitrate (NO3 -), malondialdehyde (MDA) and superoxide dismutase (SOD), were measured in ipsi- and contra- lateral sides of the cortex, at 30 minutes, 24 hours and 7 days post treatment. The redox balance was not significantly changed in the cortex of sham operated and intact groups. Also, no differences were observed between the ipsi- and contra- lateral side of the cortex. Lethargy and mortality (30-40%) of the animals in the DQ group within 24 hrs, coincided with rapidly developed lipid peroxidation supported by OS/NS upon i.s. DQ administration. Strong redox potential of DQ probably resulted in a huge deprivation of molecular oxygen. The pretreatment with GR acted neuro-protectively, based on animal survival and absence of lethargy, although, lipid peroxidation was not developed in the GR+DQ group, OS was documented by a high concentration of O2 •- (within 24 hrs), descending and eventually inhibiting SOD activity (at 7 days)., U ovoj studiji smo ispitali da li je oksidativni/nitrosativni stres (OS/NS), uključen u odgovor korteksa Wistar pacova nakon intrastrijatalne (i.s.) izloženosti dikvatu (DK). Posebno smo ispitivali značaj antioksidativne uloge glutationa (GSH), zbog čega smo primenili glutation reduktazu (GR) u predtretmanu davanja DK. Superoksid anjon radikal (O2•¯), nitrati (NO3¯), malondialdehid (MDA) i superoksid dismutaza (SOD), su mereni u obostranom korteksu (ipsi- i kontrastrana), nakon 30 minuta, 24 sati i 7 dana od tretmana. Redoks balans se nije značajno promenio u korteksu lažno operisanih i netretiranih pacova. Takođe, ne postoji statistički značajna razlika između ipsi- i kontra- strane korteksa. Letargija i mortalitet (30-40%) kod životinja u DK grupi su uočene tokom 24 časa od i.s. trovanja DK, što se poklopilo sa naglim razvojem OS/NS i lipidne peroksidacije. Visok redoks potencijal DK verovatno rezultira opsežnim utroškom molekularnog kiseonika. Zaključeno je da je ostvaren neuroprotektivni učinak predtretmana sa GR, na osnovu preživljavanja životinja i odsustva letargije. Lipidna peroksidacija nije bila razvijena u grupi predtretiranoj sa GR ali je ipak izmerena visoka koncentracija O2•¯ (tokom 24 sata) koja zatim opada i na kraju 7. dana u potpunosti inhibira aktivnost SOD.",
publisher = "Univerzitet u Beogradu - Fakultet veterinarske medicine, Beograd",
journal = "Acta veterinaria",
title = "Influence of glutathione reductase on diquat neurotoxcity assessed by oxidative/nitrosative stress in the cortex of intrastriatally treated rats, Uticaj glutation reduktaze na neurotoksičnost dikvata - ispitivan je oksidativni/nitrozativni stres u korteksu intrastrijatalno tretiranih pacova",
volume = "62",
number = "5-6",
pages = "553-568",
doi = "10.2298/AVB1206553D"
}

Đukić, M., Jovanović, M., Ninković, M., Stevanović, I., Đurđević, D.,& Vasić, U.. (2012). Influence of glutathione reductase on diquat neurotoxcity assessed by oxidative/nitrosative stress in the cortex of intrastriatally treated rats. in Acta veterinaria
Univerzitet u Beogradu - Fakultet veterinarske medicine, Beograd., 62(5-6), 553-568.
https://doi.org/10.2298/AVB1206553D

Đukić M, Jovanović M, Ninković M, Stevanović I, Đurđević D, Vasić U. Influence of glutathione reductase on diquat neurotoxcity assessed by oxidative/nitrosative stress in the cortex of intrastriatally treated rats. in Acta veterinaria. 2012;62(5-6):553-568.
doi:10.2298/AVB1206553D .

Đukić, Mirjana, Jovanović, Marina, Ninković, Milica, Stevanović, Ivana, Đurđević, Dragan, Vasić, Una, "Influence of glutathione reductase on diquat neurotoxcity assessed by oxidative/nitrosative stress in the cortex of intrastriatally treated rats" in Acta veterinaria, 62, no. 5-6 (2012):553-568,
https://doi.org/10.2298/AVB1206553D . .

TY  - JOUR
AU  - Đukić, Mirjana
AU  - Jovanović, Marina
AU  - Ninković, Milica
AU  - Stevanović, Ivana
AU  - Ilić, Katarina
AU  - Ćurčić, Marijana
AU  - Vekić, Jelena
PY  - 2012
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/1653
AB  - Paraquat (PQ), a widely used herbicide is a well-known free radical producing agent. The mechanistic pathways of PQ neurotoxicity were examined by assessing oxidative/nitrosative stress markers. Focus was on the role of glutathione (GSH) cycle and to examine whether the pre-treatment with enzyme glutathione reductase (GR) could protect the vulnerable brain regions (VBRs) against harmful oxidative effect of PQ. The study was conducted on Wistar rats, randomly divided in five groups: intact-control group, (n = 8) and four experimental groups (n = 24). All tested compounds were administered intrastriatally (i.s.) in one single dose. The following parameters of oxidative status were measured in the striatum, hippocampus and cortex, at 30 min, 24 h and 7 days post treatment: superoxide anion radical (O-2(center dot-)), nitrate (NO3-). malondialdehyde (MDA), superoxide dismutase (SOD), total GSH (tGSH) and its oxidized, disulfide form (GSSG) and glutathione peroxidase (GPx). Results obtained from the intact and the sham operated groups were not statistically different, confirming that invasive i.s. route of administration would not influence the reliability of results. Also, similar pattern of changes were observed between ipsi- and contra- lateral side of examined VBRs, indicating rapid spatial spreading of oxidative stress. Mortality of the animals (10%), within 24 h, along with symptoms of Parkinsonism, after awakening from anesthesia for 2-3 h, were observed in the PQ group, only. Increased levels of O2(center dot-), NO3- and MDA, increased ratio of GSSG/GSH and considerably high activity of GPx were measured at 30 min after the treatment. Cytotoxic effect of PQ was documented by drastic drop of all measured parameters and extremely high peak of the ratio GSSG/GSH at 24th hrs after the PQ i.s. injection. In the GR + PQ group, markedly low activity of GPx and low content of NO3- (in striatum and cortex) were measured during whole experiment, while increase value was observed only for O-2(center dot-), at 7th days. We concluded that oxidative/nitrosative stress and excitotoxicity are the most important events since the early stage of PQ induced neurotoxicity. Based on the ratio GSSG/GSH, the oxidation of GSH to GSSG is probably dominant way of GHS depletion and main reason for reduced antioxidative defense against PQ harmful oxidative effect. The GR pre-treatment resulted in the absence of Parkinson's disease-like symptoms and mortality of the rats. Additionally, oxidative/nitrosative stress did not developed, as well as almost diminished metabolism of the VBRs at 24th hours (as has been documented in the PQgroup) did not occurred in the GR + PQ suggesting a neuroprotective role for the GR in PQ induced neurotoxicity.
PB  - Elsevier Ireland Ltd, Clare
T2  - Chemico-Biological Interactions
T1  - Protective role of glutathione reductase in paraquat induced neurotoxicity
VL  - 199
IS  - 2
SP  - 74
EP  - 86
DO  - 10.1016/j.cbi.2012.05.008
ER  - 

@article{
author = "Đukić, Mirjana and Jovanović, Marina and Ninković, Milica and Stevanović, Ivana and Ilić, Katarina and Ćurčić, Marijana and Vekić, Jelena",
year = "2012",
abstract = "Paraquat (PQ), a widely used herbicide is a well-known free radical producing agent. The mechanistic pathways of PQ neurotoxicity were examined by assessing oxidative/nitrosative stress markers. Focus was on the role of glutathione (GSH) cycle and to examine whether the pre-treatment with enzyme glutathione reductase (GR) could protect the vulnerable brain regions (VBRs) against harmful oxidative effect of PQ. The study was conducted on Wistar rats, randomly divided in five groups: intact-control group, (n = 8) and four experimental groups (n = 24). All tested compounds were administered intrastriatally (i.s.) in one single dose. The following parameters of oxidative status were measured in the striatum, hippocampus and cortex, at 30 min, 24 h and 7 days post treatment: superoxide anion radical (O-2(center dot-)), nitrate (NO3-). malondialdehyde (MDA), superoxide dismutase (SOD), total GSH (tGSH) and its oxidized, disulfide form (GSSG) and glutathione peroxidase (GPx). Results obtained from the intact and the sham operated groups were not statistically different, confirming that invasive i.s. route of administration would not influence the reliability of results. Also, similar pattern of changes were observed between ipsi- and contra- lateral side of examined VBRs, indicating rapid spatial spreading of oxidative stress. Mortality of the animals (10%), within 24 h, along with symptoms of Parkinsonism, after awakening from anesthesia for 2-3 h, were observed in the PQ group, only. Increased levels of O2(center dot-), NO3- and MDA, increased ratio of GSSG/GSH and considerably high activity of GPx were measured at 30 min after the treatment. Cytotoxic effect of PQ was documented by drastic drop of all measured parameters and extremely high peak of the ratio GSSG/GSH at 24th hrs after the PQ i.s. injection. In the GR + PQ group, markedly low activity of GPx and low content of NO3- (in striatum and cortex) were measured during whole experiment, while increase value was observed only for O-2(center dot-), at 7th days. We concluded that oxidative/nitrosative stress and excitotoxicity are the most important events since the early stage of PQ induced neurotoxicity. Based on the ratio GSSG/GSH, the oxidation of GSH to GSSG is probably dominant way of GHS depletion and main reason for reduced antioxidative defense against PQ harmful oxidative effect. The GR pre-treatment resulted in the absence of Parkinson's disease-like symptoms and mortality of the rats. Additionally, oxidative/nitrosative stress did not developed, as well as almost diminished metabolism of the VBRs at 24th hours (as has been documented in the PQgroup) did not occurred in the GR + PQ suggesting a neuroprotective role for the GR in PQ induced neurotoxicity.",
publisher = "Elsevier Ireland Ltd, Clare",
journal = "Chemico-Biological Interactions",
title = "Protective role of glutathione reductase in paraquat induced neurotoxicity",
volume = "199",
number = "2",
pages = "74-86",
doi = "10.1016/j.cbi.2012.05.008"
}

Đukić, M., Jovanović, M., Ninković, M., Stevanović, I., Ilić, K., Ćurčić, M.,& Vekić, J.. (2012). Protective role of glutathione reductase in paraquat induced neurotoxicity. in Chemico-Biological Interactions
Elsevier Ireland Ltd, Clare., 199(2), 74-86.
https://doi.org/10.1016/j.cbi.2012.05.008

Đukić M, Jovanović M, Ninković M, Stevanović I, Ilić K, Ćurčić M, Vekić J. Protective role of glutathione reductase in paraquat induced neurotoxicity. in Chemico-Biological Interactions. 2012;199(2):74-86.
doi:10.1016/j.cbi.2012.05.008 .

Đukić, Mirjana, Jovanović, Marina, Ninković, Milica, Stevanović, Ivana, Ilić, Katarina, Ćurčić, Marijana, Vekić, Jelena, "Protective role of glutathione reductase in paraquat induced neurotoxicity" in Chemico-Biological Interactions, 199, no. 2 (2012):74-86,
https://doi.org/10.1016/j.cbi.2012.05.008 . .

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  - 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, Mirjana
AU  - Ninković, Milica
AU  - Jovanović, Marina
PY  - 2008
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/1040
AB  - Elevated free radical production and/or insufficient antioxidative defense results in cellular oxidant stress responses. Sustained and/or intense oxidative insults can overcome cell defenses resulting in accumulated damage to macromolecules, leading to loss of cell function, membrane damage, and ultimately to cell death. Oxidative stress (OS) can result from conditions including excessive physical stress, exposure to environmental pollution and xenobiotics, and smoking. Oxidative stress, as a pathophysiological mechanism, has been linked to numerous pathologies, poisonings, and the ageing process. Reactive oxygen species and reactive nitrogen species, endogenously or exogenously produced, can readily attack all classes of macromolecules (proteins, DNA, unsaturated fatty acid). The disrupted oxidative-reductive milieu proceeds via lipid peroxidation, altered antioxidative enzyme activities and depletion of non-enzymatic endogenous antioxidants, several of which can de detected in the pre-symptomatic phase of many diseases. Therefore, they could represent markers of altered metabolic and physiological homeostasis. Accordingly, from the point of view of routine clinical-diagnostic practice, it would be valuable to routinely analyze OS status parameters to earlier recognize potential disease states and provide the basis for preventative advance treatment with appropriate medicines.
AB  - Povećano stvaranje slobodnih radikala i/ili nedovoljna antioksidativna zaštita dovodi do oksidativnog stre sa (OS) u ćeliji. Produženi i/ili snažan oksidativni insult prevazilazi ćelijski antioksidativni odbrambreni kapacitet, dolazi do oštećenja makromolekula, gubi se ćelijska funkcija, oštećuju se membrane, što sve zajedno dovodi do smrti ćelije. Stanja organizma kao što su povećana fizička aktivnost, izloženost zagađenju čovekove okoline, ksenobioticima, pušenje itd. rezultiraju OS. Oksidativni stres, kao patofiziološki mehanizam, je potvrđen u brojnim patologijama, trovanjima i starenju. Reaktivne kiseonične vrste i reaktivne azotove vrste, endogenog ili egzogenog porekla, mogu lako da napadnu sve klase biomolekula (proteni, DNK, nezasićene masne kiseline). Narušen oksido-reduktivni milje, koji posreduje povećanju lipidne peroksidacije, promeni aktivnosti direktnih ili indirektnih antioksidativnih enzima, kao i smanjenom sadržaju neenzimskih antioksidanasa, može biti prepoznat u presimptomatskoj fazi brojnih bolesti. U tom smislu može biti pokazatelj izmenjenih metaboličkih i funkcionalnih zbivanja. U svakodnevnoj kliničko-dijagnostičkoj praksi analize parametara OS u biološkom materijalu bi trebalo da imaju svoje mesto, radi rane dijagnoze bolesti, prevencije i unapređivanja terapije. .
PB  - Društvo medicinskih biohemičara Srbije, Beograd i Versita
T2  - Journal of Medical Biochemistry
T1  - Oxidative stress: Clinical diagnostic significance
VL  - 27
IS  - 4
SP  - 409
EP  - 425
UR  - https://hdl.handle.net/21.15107/rcub_farfar_1040
ER  - 

@article{
author = "Đukić, Mirjana and Ninković, Milica and Jovanović, Marina",
year = "2008",
abstract = "Elevated free radical production and/or insufficient antioxidative defense results in cellular oxidant stress responses. Sustained and/or intense oxidative insults can overcome cell defenses resulting in accumulated damage to macromolecules, leading to loss of cell function, membrane damage, and ultimately to cell death. Oxidative stress (OS) can result from conditions including excessive physical stress, exposure to environmental pollution and xenobiotics, and smoking. Oxidative stress, as a pathophysiological mechanism, has been linked to numerous pathologies, poisonings, and the ageing process. Reactive oxygen species and reactive nitrogen species, endogenously or exogenously produced, can readily attack all classes of macromolecules (proteins, DNA, unsaturated fatty acid). The disrupted oxidative-reductive milieu proceeds via lipid peroxidation, altered antioxidative enzyme activities and depletion of non-enzymatic endogenous antioxidants, several of which can de detected in the pre-symptomatic phase of many diseases. Therefore, they could represent markers of altered metabolic and physiological homeostasis. Accordingly, from the point of view of routine clinical-diagnostic practice, it would be valuable to routinely analyze OS status parameters to earlier recognize potential disease states and provide the basis for preventative advance treatment with appropriate medicines., Povećano stvaranje slobodnih radikala i/ili nedovoljna antioksidativna zaštita dovodi do oksidativnog stre sa (OS) u ćeliji. Produženi i/ili snažan oksidativni insult prevazilazi ćelijski antioksidativni odbrambreni kapacitet, dolazi do oštećenja makromolekula, gubi se ćelijska funkcija, oštećuju se membrane, što sve zajedno dovodi do smrti ćelije. Stanja organizma kao što su povećana fizička aktivnost, izloženost zagađenju čovekove okoline, ksenobioticima, pušenje itd. rezultiraju OS. Oksidativni stres, kao patofiziološki mehanizam, je potvrđen u brojnim patologijama, trovanjima i starenju. Reaktivne kiseonične vrste i reaktivne azotove vrste, endogenog ili egzogenog porekla, mogu lako da napadnu sve klase biomolekula (proteni, DNK, nezasićene masne kiseline). Narušen oksido-reduktivni milje, koji posreduje povećanju lipidne peroksidacije, promeni aktivnosti direktnih ili indirektnih antioksidativnih enzima, kao i smanjenom sadržaju neenzimskih antioksidanasa, može biti prepoznat u presimptomatskoj fazi brojnih bolesti. U tom smislu može biti pokazatelj izmenjenih metaboličkih i funkcionalnih zbivanja. U svakodnevnoj kliničko-dijagnostičkoj praksi analize parametara OS u biološkom materijalu bi trebalo da imaju svoje mesto, radi rane dijagnoze bolesti, prevencije i unapređivanja terapije. .",
publisher = "Društvo medicinskih biohemičara Srbije, Beograd i Versita",
journal = "Journal of Medical Biochemistry",
title = "Oxidative stress: Clinical diagnostic significance",
volume = "27",
number = "4",
pages = "409-425",
url = "https://hdl.handle.net/21.15107/rcub_farfar_1040"
}

Đukić, M., Ninković, M.,& Jovanović, M.. (2008). Oxidative stress: Clinical diagnostic significance. in Journal of Medical Biochemistry
Društvo medicinskih biohemičara Srbije, Beograd i Versita., 27(4), 409-425.
https://hdl.handle.net/21.15107/rcub_farfar_1040

Đukić M, Ninković M, Jovanović M. Oxidative stress: Clinical diagnostic significance. in Journal of Medical Biochemistry. 2008;27(4):409-425.
https://hdl.handle.net/21.15107/rcub_farfar_1040 .

Đukić, Mirjana, Ninković, Milica, Jovanović, Marina, "Oxidative stress: Clinical diagnostic significance" in Journal of Medical Biochemistry, 27, no. 4 (2008):409-425,
https://hdl.handle.net/21.15107/rcub_farfar_1040 .

TY  - JOUR
AU  - Ćurčić-Jovanović, Marijana
AU  - Đukić, Mirjana
AU  - Vasiljević, Ivana
AU  - Ninković, Milica
AU  - Jovanović, Marina
PY  - 2007
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/1021
AB  - This work was a part of an initial study regarding the involvement of reactive nitrogen species (RNS) in paraquat (PQ) neurotoxicity. The nitrate concentration in the vulnerable regions of the brain (cortex, striatum and hippocampus) of Wistar rats was used as a measure of nitric oxide (NO) production or catabolism of the formed RNS. The tissue homogenates were deproteinized with acetonitrile and then centrifuged. Nitrate was measured in filtrated supernatants by simple and rapid isocratic ion-exchange high performance liquid chromatography with UV detection (IE-HPLC-UV) at 214 nm. The mobile phase (pH 8.5) consisted of borate buffer/gluconate concentrate, methanol, acetonitrile and deionized water (2:12:12:74, v/v/v/v), and the flow rate was 1.3 mL/min. Physiological nitrate levels (18.8 ± 6.1 nmol/mg of proteins), as well as a diverse range of nitrate concentrations could be determined with good precision (CV = 2.2 %) and accuracy (recovery of spiked samples was 99 ± 4%) in the brain tissue homogenates. Linearity was achieved in the range of nitrate from 0-80 μM. The retention time of nitrate anion was 5.3 ± 0.3 min. .
AB  - Prezentovani rad je deo započete studije o uključenosti reaktivnih vrsta azota (RNS) u neurotoksičnost parakvata (PQ). Sadržaj nitrata u selektivno osetljivim moždanim regijama (cortex, striatum i hippocampus) Wistar pacova može se koristiti kao merilo produkcije azotmonoksida ili katabolizma drugih RNS. Homogenizati moždanog tkiva su najpre deproteinizovani, zatim centrifugirani. Nitrati su određivani u filtriranom supernatantu brzom i jednostavnom izokratskom metodom visoko efikasne tečne hromatografije sa diode-array detekcijom (IE-HPLC-UV) na 214 nm. Korišćena je mobilna faza sastava: boratni pufer/glukonat koncentrat : metanol : acetonitril : dejonizovana voda (2:12:12:74, v/v/v/v), pH 8,5, pri protoku 1,3 mL/min. Širok opseg koncentracija nitrata kao i njihovi fiziološki nivoi (18,8 ± 6,1 nmol/mg proteina) mogu se meriti sa dobrom preciznošću (CV = 2,2%) i tačnošću (recovery opterećenih uzoraka 99 ± 4%) u homogenizatima moždanih tkiva. Linearnost je dobijena u opsegu 0-80 μmol/L nitrata dok je retenciono vreme bilo 5,3 ± 0,3 min. .
PB  - Srpsko hemijsko društvo, Beograd
T2  - Journal of the Serbian Chemical Society
T1  - Determination of nitrate by the IE-HPLC-UV method in the brain tissues of Wistar rats poisoned with paraquat
T1  - Određivanje nitrata IE-HPLC-UV metodom u moždanim tkivima Wistar pacova trovanih parakvatom
VL  - 72
IS  - 4
SP  - 347
EP  - 356
DO  - 10.2298/JSC0704347C
ER  - 

@article{
author = "Ćurčić-Jovanović, Marijana and Đukić, Mirjana and Vasiljević, Ivana and Ninković, Milica and Jovanović, Marina",
year = "2007",
abstract = "This work was a part of an initial study regarding the involvement of reactive nitrogen species (RNS) in paraquat (PQ) neurotoxicity. The nitrate concentration in the vulnerable regions of the brain (cortex, striatum and hippocampus) of Wistar rats was used as a measure of nitric oxide (NO) production or catabolism of the formed RNS. The tissue homogenates were deproteinized with acetonitrile and then centrifuged. Nitrate was measured in filtrated supernatants by simple and rapid isocratic ion-exchange high performance liquid chromatography with UV detection (IE-HPLC-UV) at 214 nm. The mobile phase (pH 8.5) consisted of borate buffer/gluconate concentrate, methanol, acetonitrile and deionized water (2:12:12:74, v/v/v/v), and the flow rate was 1.3 mL/min. Physiological nitrate levels (18.8 ± 6.1 nmol/mg of proteins), as well as a diverse range of nitrate concentrations could be determined with good precision (CV = 2.2 %) and accuracy (recovery of spiked samples was 99 ± 4%) in the brain tissue homogenates. Linearity was achieved in the range of nitrate from 0-80 μM. The retention time of nitrate anion was 5.3 ± 0.3 min. ., Prezentovani rad je deo započete studije o uključenosti reaktivnih vrsta azota (RNS) u neurotoksičnost parakvata (PQ). Sadržaj nitrata u selektivno osetljivim moždanim regijama (cortex, striatum i hippocampus) Wistar pacova može se koristiti kao merilo produkcije azotmonoksida ili katabolizma drugih RNS. Homogenizati moždanog tkiva su najpre deproteinizovani, zatim centrifugirani. Nitrati su određivani u filtriranom supernatantu brzom i jednostavnom izokratskom metodom visoko efikasne tečne hromatografije sa diode-array detekcijom (IE-HPLC-UV) na 214 nm. Korišćena je mobilna faza sastava: boratni pufer/glukonat koncentrat : metanol : acetonitril : dejonizovana voda (2:12:12:74, v/v/v/v), pH 8,5, pri protoku 1,3 mL/min. Širok opseg koncentracija nitrata kao i njihovi fiziološki nivoi (18,8 ± 6,1 nmol/mg proteina) mogu se meriti sa dobrom preciznošću (CV = 2,2%) i tačnošću (recovery opterećenih uzoraka 99 ± 4%) u homogenizatima moždanih tkiva. Linearnost je dobijena u opsegu 0-80 μmol/L nitrata dok je retenciono vreme bilo 5,3 ± 0,3 min. .",
publisher = "Srpsko hemijsko društvo, Beograd",
journal = "Journal of the Serbian Chemical Society",
title = "Determination of nitrate by the IE-HPLC-UV method in the brain tissues of Wistar rats poisoned with paraquat, Određivanje nitrata IE-HPLC-UV metodom u moždanim tkivima Wistar pacova trovanih parakvatom",
volume = "72",
number = "4",
pages = "347-356",
doi = "10.2298/JSC0704347C"
}

Ćurčić-Jovanović, M., Đukić, M., Vasiljević, I., Ninković, M.,& Jovanović, M.. (2007). Determination of nitrate by the IE-HPLC-UV method in the brain tissues of Wistar rats poisoned with paraquat. in Journal of the Serbian Chemical Society
Srpsko hemijsko društvo, Beograd., 72(4), 347-356.
https://doi.org/10.2298/JSC0704347C

Ćurčić-Jovanović M, Đukić M, Vasiljević I, Ninković M, Jovanović M. Determination of nitrate by the IE-HPLC-UV method in the brain tissues of Wistar rats poisoned with paraquat. in Journal of the Serbian Chemical Society. 2007;72(4):347-356.
doi:10.2298/JSC0704347C .

Ćurčić-Jovanović, Marijana, Đukić, Mirjana, Vasiljević, Ivana, Ninković, Milica, Jovanović, Marina, "Determination of nitrate by the IE-HPLC-UV method in the brain tissues of Wistar rats poisoned with paraquat" in Journal of the Serbian Chemical Society, 72, no. 4 (2007):347-356,
https://doi.org/10.2298/JSC0704347C . .

TY  - JOUR
AU  - Đukić, Mirjana
AU  - Ćurčić-Jovanović, Marijana
AU  - Ninković, Milica
AU  - Vasijević, Ivana
AU  - Jovanović, Marina
PY  - 2007
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/908
AB  - The role of nitric oxide (NO) in paraquat (PQ)-induced neurotoxicity is still not fully understood. In this study we used N-G-nitro-L-arginine methyl ester (L-NAME), a non-selective nitric oxide synthase (NOS) inhibitor, in order to examine the effects of NO, reactive oxygen species (ROS) generation and lipid peroxidation (LPO) development during PQ-mediated neurotoxicity. Oxidative stress development in the striatum of Wistar rats intrastriatally (i.s.) poisoned with PQ (and in some cases pre-treated with L-NAME) was investigated by measuring superoxide anion (O-2(center dot-)), malondialdehyde (MDA) and nitrate (NO3-), 30 min, 24 hours and 7 days after treatment. L-NAME pretreatment provided the possibility to distinguish the role of ROS from reactive nitrogen species (RNS) in oxidative stress development induced by PQ. Our results confirm the involvement of NO in PQ-mediated neurotoxicity and reduced LPO by L-NAME pretreatment implying that the latter has a protective role.
PB  - Inst Agricultural Medicine, Lublin
T2  - Annals of Agricultural and Environmental Medicine
T1  - The role of nitric oxide in paraquat-induced oxidative stress in rat striatum
VL  - 14
IS  - 2
SP  - 247
EP  - 252
UR  - https://hdl.handle.net/21.15107/rcub_farfar_908
ER  - 

@article{
author = "Đukić, Mirjana and Ćurčić-Jovanović, Marijana and Ninković, Milica and Vasijević, Ivana and Jovanović, Marina",
year = "2007",
abstract = "The role of nitric oxide (NO) in paraquat (PQ)-induced neurotoxicity is still not fully understood. In this study we used N-G-nitro-L-arginine methyl ester (L-NAME), a non-selective nitric oxide synthase (NOS) inhibitor, in order to examine the effects of NO, reactive oxygen species (ROS) generation and lipid peroxidation (LPO) development during PQ-mediated neurotoxicity. Oxidative stress development in the striatum of Wistar rats intrastriatally (i.s.) poisoned with PQ (and in some cases pre-treated with L-NAME) was investigated by measuring superoxide anion (O-2(center dot-)), malondialdehyde (MDA) and nitrate (NO3-), 30 min, 24 hours and 7 days after treatment. L-NAME pretreatment provided the possibility to distinguish the role of ROS from reactive nitrogen species (RNS) in oxidative stress development induced by PQ. Our results confirm the involvement of NO in PQ-mediated neurotoxicity and reduced LPO by L-NAME pretreatment implying that the latter has a protective role.",
publisher = "Inst Agricultural Medicine, Lublin",
journal = "Annals of Agricultural and Environmental Medicine",
title = "The role of nitric oxide in paraquat-induced oxidative stress in rat striatum",
volume = "14",
number = "2",
pages = "247-252",
url = "https://hdl.handle.net/21.15107/rcub_farfar_908"
}

Đukić, M., Ćurčić-Jovanović, M., Ninković, M., Vasijević, I.,& Jovanović, M.. (2007). The role of nitric oxide in paraquat-induced oxidative stress in rat striatum. in Annals of Agricultural and Environmental Medicine
Inst Agricultural Medicine, Lublin., 14(2), 247-252.
https://hdl.handle.net/21.15107/rcub_farfar_908

Đukić M, Ćurčić-Jovanović M, Ninković M, Vasijević I, Jovanović M. The role of nitric oxide in paraquat-induced oxidative stress in rat striatum. in Annals of Agricultural and Environmental Medicine. 2007;14(2):247-252.
https://hdl.handle.net/21.15107/rcub_farfar_908 .

Đukić, Mirjana, Ćurčić-Jovanović, Marijana, Ninković, Milica, Vasijević, Ivana, Jovanović, Marina, "The role of nitric oxide in paraquat-induced oxidative stress in rat striatum" in Annals of Agricultural and Environmental Medicine, 14, no. 2 (2007):247-252,
https://hdl.handle.net/21.15107/rcub_farfar_908 .

TY  - CONF
AU  - Ćurčić, Marijana
AU  - Đukić, Mirjana
AU  - Ninković, Milica
AU  - Vasijević, Ivana
AU  - Jovanović, Marina
PY  - 2007
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/981
PB  - Elsevier Ireland Ltd, Clare
C3  - Toxicology Letters
T1  - Differences in nitric oxide release in CNS caused by paraquat and diquat
VL  - 172
IS  - Supplement
SP  - S41
EP  - S41
DO  - 10.1016/j.toxlet.2007.05.136
ER  - 

@conference{
author = "Ćurčić, Marijana and Đukić, Mirjana and Ninković, Milica and Vasijević, Ivana and Jovanović, Marina",
year = "2007",
publisher = "Elsevier Ireland Ltd, Clare",
journal = "Toxicology Letters",
title = "Differences in nitric oxide release in CNS caused by paraquat and diquat",
volume = "172",
number = "Supplement",
pages = "S41-S41",
doi = "10.1016/j.toxlet.2007.05.136"
}

Ćurčić, M., Đukić, M., Ninković, M., Vasijević, I.,& Jovanović, M.. (2007). Differences in nitric oxide release in CNS caused by paraquat and diquat. in Toxicology Letters
Elsevier Ireland Ltd, Clare., 172(Supplement), S41-S41.
https://doi.org/10.1016/j.toxlet.2007.05.136

Ćurčić M, Đukić M, Ninković M, Vasijević I, Jovanović M. Differences in nitric oxide release in CNS caused by paraquat and diquat. in Toxicology Letters. 2007;172(Supplement):S41-S41.
doi:10.1016/j.toxlet.2007.05.136 .

Ćurčić, Marijana, Đukić, Mirjana, Ninković, Milica, Vasijević, Ivana, Jovanović, Marina, "Differences in nitric oxide release in CNS caused by paraquat and diquat" in Toxicology Letters, 172, no. Supplement (2007):S41-S41,
https://doi.org/10.1016/j.toxlet.2007.05.136 . .

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 . .

TY  - CONF
AU  - Đukić, Mirjana
AU  - Jovanović, Marina
AU  - Nedeljković, Mirjana
PY  - 2002
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/358
PB  - Savez farmaceutskih udruženja Srbije, Beograd
C3  - Arhiv za farmaciju
T1  - Influence of disulfiram treatment on 5-HIAA excretions in alcoholics
T1  - Uticaj terapije disulfiramom na 5-HIAA ekskreciju kod alkoholičara
VL  - 52
IS  - 4
SP  - 766
EP  - 767
UR  - https://hdl.handle.net/21.15107/rcub_farfar_358
ER  - 

@conference{
author = "Đukić, Mirjana and Jovanović, Marina and Nedeljković, Mirjana",
year = "2002",
publisher = "Savez farmaceutskih udruženja Srbije, Beograd",
journal = "Arhiv za farmaciju",
title = "Influence of disulfiram treatment on 5-HIAA excretions in alcoholics, Uticaj terapije disulfiramom na 5-HIAA ekskreciju kod alkoholičara",
volume = "52",
number = "4",
pages = "766-767",
url = "https://hdl.handle.net/21.15107/rcub_farfar_358"
}

Đukić, M., Jovanović, M.,& Nedeljković, M.. (2002). Influence of disulfiram treatment on 5-HIAA excretions in alcoholics. in Arhiv za farmaciju
Savez farmaceutskih udruženja Srbije, Beograd., 52(4), 766-767.
https://hdl.handle.net/21.15107/rcub_farfar_358

Đukić M, Jovanović M, Nedeljković M. Influence of disulfiram treatment on 5-HIAA excretions in alcoholics. in Arhiv za farmaciju. 2002;52(4):766-767.
https://hdl.handle.net/21.15107/rcub_farfar_358 .

Đukić, Mirjana, Jovanović, Marina, Nedeljković, Mirjana, "Influence of disulfiram treatment on 5-HIAA excretions in alcoholics" in Arhiv za farmaciju, 52, no. 4 (2002):766-767,
https://hdl.handle.net/21.15107/rcub_farfar_358 .