Vitamin A and Retinoids as Mitochondrial Toxicants

Figure 3

A general view of the effects of in vivo vitamin A supplementation in an animal experimental model. It has been hypothesized that vitamin A may induce mitochondrial dysfunction by different ways as follows: (1) by decreasing BDNF levels, (2) by inducing ER stress and calcium ion metabolism deregulation, and/or (3) by increasing α-synuclein levels. The increased levels may induce redox unbalance in the organelle that, in turn, may generate more in a vicious cycle. Increased H₂O₂ production (by Mn-SOD and MAO enzymes) may disseminate redox impairment from one region to another.