Department of Nutritional Sciences, University of Vienna, 1090 Vienna, Austria.
Department of Toxicology, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany.
Oxid Med Cell Longev. 2018 Mar 22;2018:3734250. doi: 10.1155/2018/3734250. eCollection 2018.
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 () and the () as well as global methylation by were investigated. Results revealed a dose-dependent counteracting effect of vitamin E on HO-induced oxidative stress. Thereby, 10 M vitamin E proved to be more efficient than did 50 M in reducing MDA. Further, an induction of and gene expression was noticed, accompanied by an increase in global methylation. Whether hypomethylation is a cause or effect of oxidative stress is still unclear. In conclusion, supplementation of exogenous antioxidants like vitamin E exhibits beneficial effects concerning oxidative stress as well as epigenetic regulation involved in DNA repair.
肥胖或糖尿病引起的氧化应激被认为是 DNA 损伤的一个主要危险因素。维生素 E 和许多多酚具有抗氧化活性，可影响炎症和 DNA 修复的表观遗传调控。本研究在正常（1g/L）和高（4.5g/L）葡萄糖细胞培养条件下，调查了维生素 E 对结直肠癌细胞系 Caco-2 中氧化应激的拮抗作用。分析了丙二醛（MDA）作为脂质过氧化和活性氧（ROS）的替代标志物。研究了 DNA 修复基因（）和（）的基因表达和启动子甲基化，以及通过进行的整体甲基化。结果显示，维生素 E 对 HO 诱导的氧化应激具有剂量依赖性的拮抗作用。因此，10μM 维生素 E 比 50μM 更能有效降低 MDA。此外，还注意到和基因表达的诱导，同时伴有整体甲基化的增加。是否是氧化应激的原因或结果尚不清楚。总之，补充外源性抗氧化剂，如维生素 E，可对氧化应激以及涉及 DNA 修复的表观遗传调控产生有益影响。
