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Obesity- or diabetes-induced oxidative stress is discussed as a major risk factor for DNA damage. Vitamin E and many polyphenols exhibit antioxidative activities with consequences on epigenetic regulation of inflammation and DNA repair. The present study investigated the counteraction of oxidative stress by vitamin E in the colorectal cancer cell line Caco-2 under normal (1 g/l) and high (4.5 g/l) glucose cell culture condition. Malondialdehyde (MDA) as a surrogate marker of lipid peroxidation and reactive oxygen species (ROS) was analyzed. Gene expression and promoter methylation of the DNA repair gene  MutL homolog 1  ( MLH1 ) and the  DNA methyltransferase 1  ( DNMT1 ) as well as global methylation by  LINE-1  were investigated. Results revealed a dose-dependent counteracting effect of vitamin E on H 2 O 2 -induced oxidative stress. Thereby, 10  μ M vitamin E proved to be more efficient than did 50  μ M in reducing MDA. Further, an induction of  MLH1  and  DNMT1  gene expression was noticed, accompanied by an increase in global methylation. Whether  LINE-1  hypomethylation is a cause or effect of oxidative stress is still unclear. In conclusion, supplementation of exogenous antioxidants like vitamin E  in vitro  exhibits beneficial effects concerning oxidative stress as well as epigenetic regulation involved in DNA repair.

oxidative medicine and cellular longevity

Counteraction of Oxidative Stress by Vitamin E Affects Epigenetic Regulation by Increasing Global Methylation and Gene Expression of <i>MLH1</i> and <i>DNMT1</i> Dose Dependently in Caco-2 Cells

Counteraction of Oxidative Stress by Vitamin E Affects Epigenetic Regulation by Increasing Global Methylation and Gene Expression of MLH1 and DNMT1 Dose Dependently in Caco-2 Cells