Protective Effects of Different Antioxidants against the Molecular Toxicity, Genetic and Epigenetic Alterations induced by 3,5- dimethylaminophenol-A Review of the Recent Work

Extensive human exposure to the monocyclic aromatic amines (MAAs), particularly to 3,5- dimethylaniline (3,5-DMA) has been clearly demonstrated and was significantly associated with bladder cancer. One of the mechanisms underlying their toxicity is suggested to be oxidative stress. 3,5-dimethylaminophenol (3,5-DMAP) is the major metabolite of 3,5-DMA. In mammalian cells, 3,5-DMAP became embedded in the cellular matrix in a form capable of continued redox cycling and induced dose-dependent increase of apoptosis mediated via caspase-3 activation. 3,5-DMAP also caused alterations in the antioxidant enzyme activities, decreases in reduced glutathione levels and increases in lipid peroxidation and protein oxidation. Cellular stress caused by 3,5-DMAP caused both genetic and epigenetic changes, which can eventually lead to cancer. Ascorbic acid and different selenocompounds were found to be protective its toxicity. The protection was observed for both nucleus and cytoplasm, suggesting that the amelioration arises from their antioxidant effects on different subcellular fractions.