Abstract
Oxidative stress in rat heart mitochondria under a rotenone model of Parkinson’ disease: a corrective effect of capicor treatment
Highlights
IntroductionBiochemical and genetic mechanisms of oxidative stress (OS) developing in rat heart mitochondria were studied in a rotenone model of Parkinson’s disease (PD), and the effect of Capicor (combination of meldonium dihydrate and gamma-butyrobetain dihydrate) on these mechanisms was evaluated
Biochemical and genetic mechanisms of oxidative stress (OS) developing in rat heart mitochondria were studied in a rotenone model of Parkinson’s disease (PD), and the effect of Capicor on these mechanisms was evaluated
Prolonged systemic rotenone administration induced OS developing in rat heart mitochondria: in witness of that was an increase in intensities of lipid peroxidation, protein oxidative modification, and H2O2 production as well as a decrease in GSH content, GSH/GSSG ratio, and glutathione peroxidase (GPx) activity
Summary
Biochemical and genetic mechanisms of oxidative stress (OS) developing in rat heart mitochondria were studied in a rotenone model of Parkinson’s disease (PD), and the effect of Capicor (combination of meldonium dihydrate and gamma-butyrobetain dihydrate) on these mechanisms was evaluated. Rotenone intoxication increased the intensity of lipid peroxidation, protein oxidative modification, and H2O2 production. These events were accompanied by decreased in GSH content, GSH/GSSG ratio, and GPx activity. Regarding the correction of oxidative stress induced by rotenone administration, there was recently shown that treatment of rats with Capicor (combination of Meldonium dihydrate and gamma-butyrobe tain dihydrate, Olainpharm, Latvia) led to reduction of OS in the brain and liver mitochondria [3, 9].
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