The Interactive Effects of The Aerobic Exercise and Vitamin E Supplementation on Parkinson's Rat Model.

In Parkinson's disease (PD), mitochondrial defects and oxidative stress cause an increase in free radicals and the death of dopaminergic neurons in the substantia nigra. By preventing lipid peroxidation and protecting against peroxide radicals, vitamin E is the most important antioxidant of biological membranes that can neutralize free radicals. Also, the improvement of the functional status of mitochondria can be influenced by exercise, which can be partially the result of changes in the mitochondrial mitophagy and dynamics system. This study aimed to investigate the interactive effects of six weeks of vitamin E (VE) consumption and training on the mitochondrial function [Cytochrome C (Cyt-C), Adenosine triphosphate (Atp) synthase, optical atrophy1 mitochondrial dynamics like guanosine triphosphatase (GTPase), 8-Oxodequanosin and Pten induced kinase 1 (Pink1) is a protein coding gene] in the hippocampus tissue of PD rats.