Beneficial Roles of Vitamin D and Exercise in Oxidative Stress and Apoptosis

Abstract

Background:  Vitamin D acts in the body like a hormone with a multitude of functions. The main source of vitamin D is solar UV radiation, which converts 7-dehydrocholesterol to provitamin D. Regarding its role as an antioxidant, it was  demonstrated that vitamin D is an antioxidant vitamin that can prevent iron-dependent lipid peroxidation in the cell membrane. Moreover, rat neuron culture studies showed that 1, 25(OH)₂ D3 increases glutathione levels in these cells. The reduced form of glutathione, a fundamental antioxidant protects cells against ROS and apoptosis caused by oxidation. This suggests an important neuro-protective effect for the active form of vitamin D3, by counteracting oxidative damage to the CNS. Physical exercise and lifestyle modification have an effective role to improve neurodegenerative diseases. Moderate exercise training has an anti-inflammatory and beneficial effects on immunological functions and it mediate an important role in protecting against diseases that are associated with low grade inflammation  as shown in Alzeimer disease (AD) animal models. Exercise is an important factor for inhibiting apoptosis an increase of expression of pro- apoptotic Bax and cytochrome c was revealed , while expression of anti- apoptotic Bcl-2 was decreased in the old rats that underwent social isolation, which promoted apoptosis. In contrast, swimming exercise suppressed Bax and cytochrome c expression and increased Bcl-2 expression, which inhibited apoptosis. It has been postulated that regular physical exercise can promote a beneficial effect on the health of individuals and is considered an important autophagic inducer . It was observed that treadmill exercise (8 weeks) in mice modulated the levels of autophagy associated proteins, including Beclin1, LC3-II in the brain  and reduce the expression of p62 and improved autophagy.