[Oxidative stress in the cardiovascular system of rats with chronic deficiency of cerebral dopamine].

The physiological significance of cardiac mitochondrial reactive oxygen species (ROS) regulation is unknown. In the current study, mitochondrial ROS (O2- and OH) generation, stable 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 erytrocytes 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.