TY  - JOUR
AU  - Kotur-Stevuljević, Jelena
AU  - Bogavac-Stanojević, Nataša
AU  - Jelić-Ivanović, Zorana
AU  - Stefanović, Aleksandra
AU  - Gojković, Tamara
AU  - Joksić, Jelena
AU  - Sopić, Miron
AU  - Gulan, Brankica
AU  - Janać, Jelena
AU  - Milošević, Sanja
PY  - 2015
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/2407
AB  - Objective: The connection of oxidative stress with dyslipidemia creates a newly-emerging atherosclerosis risk factor involved in acute ischemic stroke development. This study analyzed the influence of oxidative stress on structural changes of high-density lipoprotein (HDL) particles connected with modification in protective paraoxonase 1 (PON1) activity. Methods: This study used 185 patients with acute ischemic stroke and 185 apparently healthy controls. Oxidative stress status, PON1 status, lipids and high-sensitivity C-reactive protein (hsCRP) were determined. In isolated HDL lipoprotein fraction we determined selected markers of oxidative stress (malondialdehyde, MDA) and the content of total sulfhydryl (SH) groups. The capability of oxidative and PON1 status parameters to discriminate patients according to survival status was evaluated. Results: Stroke patients had lower HDL-cholesterol than controls and a remarkable fall in PON1 activity (control group-227 U/L, survivors-42 U/L, lethal outcome group-61 U/L, p  lt  0.001), along with more prominent inflammation. Pronounced oxidative stress and impaired antioxidative protection was present among patients. HDL fraction analysis revealed a significant decrease of SH groups content (control group vs. patients, p  lt  0.05) and increased in MDA content in patients (lethal outcome vs. control group, p  lt  0.05). According to logistic regression analysis, the best predictor of disease outcome was oxidative stress marker - prooxidative-antioxidative balance (PAB). Conclusions: Pronounced oxidative stress in this group of acute ischemic stroke patients probably led to HDL structural changes, which could further cause an alteration or decrease of PON1 activity. Evidence of increased prooxidant level associated with decreased protective, antioxidative factors suggests their mutual involvement in this complex pathology.
PB  - Elsevier Ireland Ltd, Clare
T2  - Atherosclerosis
T1  - Oxidative stress and paraoxonase 1 status in acute ischemic stroke patients
VL  - 241
IS  - 1
SP  - 192
EP  - 198
DO  - 10.1016/j.atherosclerosis.2015.05.016
ER  - 

@article{
author = "Kotur-Stevuljević, Jelena and Bogavac-Stanojević, Nataša and Jelić-Ivanović, Zorana and Stefanović, Aleksandra and Gojković, Tamara and Joksić, Jelena and Sopić, Miron and Gulan, Brankica and Janać, Jelena and Milošević, Sanja",
year = "2015",
abstract = "Objective: The connection of oxidative stress with dyslipidemia creates a newly-emerging atherosclerosis risk factor involved in acute ischemic stroke development. This study analyzed the influence of oxidative stress on structural changes of high-density lipoprotein (HDL) particles connected with modification in protective paraoxonase 1 (PON1) activity. Methods: This study used 185 patients with acute ischemic stroke and 185 apparently healthy controls. Oxidative stress status, PON1 status, lipids and high-sensitivity C-reactive protein (hsCRP) were determined. In isolated HDL lipoprotein fraction we determined selected markers of oxidative stress (malondialdehyde, MDA) and the content of total sulfhydryl (SH) groups. The capability of oxidative and PON1 status parameters to discriminate patients according to survival status was evaluated. Results: Stroke patients had lower HDL-cholesterol than controls and a remarkable fall in PON1 activity (control group-227 U/L, survivors-42 U/L, lethal outcome group-61 U/L, p  lt  0.001), along with more prominent inflammation. Pronounced oxidative stress and impaired antioxidative protection was present among patients. HDL fraction analysis revealed a significant decrease of SH groups content (control group vs. patients, p  lt  0.05) and increased in MDA content in patients (lethal outcome vs. control group, p  lt  0.05). According to logistic regression analysis, the best predictor of disease outcome was oxidative stress marker - prooxidative-antioxidative balance (PAB). Conclusions: Pronounced oxidative stress in this group of acute ischemic stroke patients probably led to HDL structural changes, which could further cause an alteration or decrease of PON1 activity. Evidence of increased prooxidant level associated with decreased protective, antioxidative factors suggests their mutual involvement in this complex pathology.",
publisher = "Elsevier Ireland Ltd, Clare",
journal = "Atherosclerosis",
title = "Oxidative stress and paraoxonase 1 status in acute ischemic stroke patients",
volume = "241",
number = "1",
pages = "192-198",
doi = "10.1016/j.atherosclerosis.2015.05.016"
}

Kotur-Stevuljević, J., Bogavac-Stanojević, N., Jelić-Ivanović, Z., Stefanović, A., Gojković, T., Joksić, J., Sopić, M., Gulan, B., Janać, J.,& Milošević, S.. (2015). Oxidative stress and paraoxonase 1 status in acute ischemic stroke patients. in Atherosclerosis
Elsevier Ireland Ltd, Clare., 241(1), 192-198.
https://doi.org/10.1016/j.atherosclerosis.2015.05.016

Kotur-Stevuljević J, Bogavac-Stanojević N, Jelić-Ivanović Z, Stefanović A, Gojković T, Joksić J, Sopić M, Gulan B, Janać J, Milošević S. Oxidative stress and paraoxonase 1 status in acute ischemic stroke patients. in Atherosclerosis. 2015;241(1):192-198.
doi:10.1016/j.atherosclerosis.2015.05.016 .

Kotur-Stevuljević, Jelena, Bogavac-Stanojević, Nataša, Jelić-Ivanović, Zorana, Stefanović, Aleksandra, Gojković, Tamara, Joksić, Jelena, Sopić, Miron, Gulan, Brankica, Janać, Jelena, Milošević, Sanja, "Oxidative stress and paraoxonase 1 status in acute ischemic stroke patients" in Atherosclerosis, 241, no. 1 (2015):192-198,
https://doi.org/10.1016/j.atherosclerosis.2015.05.016 . .

TY  - JOUR
AU  - Matović, Vesna
AU  - Milošević, Sanja
AU  - Đukić, Danijela
PY  - 2003
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/437
AB  - Mechanisms of metal toxicity have not been fully understood. It was proven in the last decades that certain metals induce increased generation of free radicals, which react lipids, proteins and nucleic acids in the organism inducing tissue-damaging effects and cell death. Metals such as iron copper, chromium, etc. undergo redox cycling and directly catalyze production of free radicals, while mercury, nickel, lead and some others act indirectly by inhibition of antioxidative mechanisims. This paper presents basic understanding of free radicals, their influence on the organism and antioxidative system. Particular attention is given to oxidative mechanisms in which iron, copper, chromium, mercury and lead play role in generation of free radicals and oxidative stress, contrary to zinc which has a significant role in antioxidative cell protection.
AB  - Mehanizmi toksičnosti metala su još uvek nedovoljno proučeni. Poslednjih decenija dokazano je da određeni metali indukuju i povećanu produkciju slobodnih radikala koji reaguju sa lipidima, proteinima i nukleinskim kiselinama organizma, što rezultira različitim oštećenjima, pa i smrću ćelija. Metali sa promenljivom valencom, kao što su gvožđe, bakar, hrom i dr. direktno katalizuju produkciju slobodnih radikala u reakcijama redoks-ciklusa, dok kadmijum, živa, nikl, olovo i neki drugi metali deluju indirektno tako što inhibiraju antioksidativne mehanizme organizma. U radu su izneta osnovna saznanja o slobodnim radikalima, njihovom dejstvu na organizam i antioksidativnom sistemu organizma. Posebno su obrađeni oksidativni mehanizmi kojima metali gvožđe, bakar, hrom, kadmijum, živa i olovo ostvaruju ulogu u nastanku slobodnih radikala i oksidativnog stresa za razliku od cinka koji ima značajnu ulogu u antioksidativnoj zaštiti ćelija.
PB  - Savez farmaceutskih udruženja Srbije, Beograd
T2  - Arhiv za farmaciju
T1  - Oxidative mechanisms in metal toxicity
T1  - Oksidativni mehanizmi toksičnosti metala
VL  - 53
IS  - 6
SP  - 473
EP  - 492
UR  - https://hdl.handle.net/21.15107/rcub_farfar_437
ER  - 

@article{
author = "Matović, Vesna and Milošević, Sanja and Đukić, Danijela",
year = "2003",
abstract = "Mechanisms of metal toxicity have not been fully understood. It was proven in the last decades that certain metals induce increased generation of free radicals, which react lipids, proteins and nucleic acids in the organism inducing tissue-damaging effects and cell death. Metals such as iron copper, chromium, etc. undergo redox cycling and directly catalyze production of free radicals, while mercury, nickel, lead and some others act indirectly by inhibition of antioxidative mechanisims. This paper presents basic understanding of free radicals, their influence on the organism and antioxidative system. Particular attention is given to oxidative mechanisms in which iron, copper, chromium, mercury and lead play role in generation of free radicals and oxidative stress, contrary to zinc which has a significant role in antioxidative cell protection., Mehanizmi toksičnosti metala su još uvek nedovoljno proučeni. Poslednjih decenija dokazano je da određeni metali indukuju i povećanu produkciju slobodnih radikala koji reaguju sa lipidima, proteinima i nukleinskim kiselinama organizma, što rezultira različitim oštećenjima, pa i smrću ćelija. Metali sa promenljivom valencom, kao što su gvožđe, bakar, hrom i dr. direktno katalizuju produkciju slobodnih radikala u reakcijama redoks-ciklusa, dok kadmijum, živa, nikl, olovo i neki drugi metali deluju indirektno tako što inhibiraju antioksidativne mehanizme organizma. U radu su izneta osnovna saznanja o slobodnim radikalima, njihovom dejstvu na organizam i antioksidativnom sistemu organizma. Posebno su obrađeni oksidativni mehanizmi kojima metali gvožđe, bakar, hrom, kadmijum, živa i olovo ostvaruju ulogu u nastanku slobodnih radikala i oksidativnog stresa za razliku od cinka koji ima značajnu ulogu u antioksidativnoj zaštiti ćelija.",
publisher = "Savez farmaceutskih udruženja Srbije, Beograd",
journal = "Arhiv za farmaciju",
title = "Oxidative mechanisms in metal toxicity, Oksidativni mehanizmi toksičnosti metala",
volume = "53",
number = "6",
pages = "473-492",
url = "https://hdl.handle.net/21.15107/rcub_farfar_437"
}

Matović, V., Milošević, S.,& Đukić, D.. (2003). Oxidative mechanisms in metal toxicity. in Arhiv za farmaciju
Savez farmaceutskih udruženja Srbije, Beograd., 53(6), 473-492.
https://hdl.handle.net/21.15107/rcub_farfar_437

Matović V, Milošević S, Đukić D. Oxidative mechanisms in metal toxicity. in Arhiv za farmaciju. 2003;53(6):473-492.
https://hdl.handle.net/21.15107/rcub_farfar_437 .

Matović, Vesna, Milošević, Sanja, Đukić, Danijela, "Oxidative mechanisms in metal toxicity" in Arhiv za farmaciju, 53, no. 6 (2003):473-492,
https://hdl.handle.net/21.15107/rcub_farfar_437 .