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International Journal of Physiology and Pathophysiology
SJR: 0.116

ISSN 印刷: 2155-014X
ISSN オンライン: 2155-0158

Archives: Volume 1, 2010 to Volume 9, 2018

International Journal of Physiology and Pathophysiology

DOI: 10.1615/IntJPhysPathophys.v1.i1.30
pages 17-24

Oxidative Stress in a Cardiovascular System of Rats with Persistent Deficiency of Cerebral Dopamine

Sergiy O. Talanov
Bogomoletz Institute of Physiology of the National Academy of Sciences of Ukraine, Kyiv, Ukraine
Anatoliy V. Kotsuruba
Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine
Yulia P. Korkach
Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine

要約

Physiological significance of cardiac mitochondrial reactive oxygen species (ROS) regulation is still unknown. In the current study, mitochondrial ROS (O2 and OH) generation, stabile H2O2 and lipids peroxidation marker (malonic dialdehyde, MDA) pools, as well as pools of potent antioxidants − urea and uric acid − were determined in rat heart, miocardial mitochondria and in blood plasma and erythrocytes at low 44% and high 96% levels of cerebral dopamine-synthesis neurons destruction (by 6-hydroxidopamine treatment). In the untreated rats ROS generation, H2O2 and MDA levels were low but in rats with chronic 3−4 month deficiency of cerebral dopamine synthesis by nigro-striatal dopaminergic system ROS generation and lipids peroxidation were progressively increased. Dopamine deficiency can improve mitochondrial efficiency of oxidative phosphorylation due to oxidative stress.