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首页> 外文期刊>Journal of Neurochemistry: Offical Journal of the International Society for Neurochemistry >Impaired one carbon metabolism and DNA methylation in alcohol toxicity
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Impaired one carbon metabolism and DNA methylation in alcohol toxicity

机译：酒精毒性损害一种碳代谢和DNA甲基化

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摘要

Excessive alcohol consumption is a prominent problem and one of the major causes of mortality and morbidity around the world. Long-term, heavy alcohol consumption is associated with a number of deleterious health consequences, such as cancer, heart and liver disease, a variety of neurological, cognitive, and behavioral deficits. Alcohol consumption is also associated with developmental defects. The causes of alcohol-induced toxicity are presently unclear. One of the mechanisms underlying alcohol toxicity has to do with its interaction with folic acid/homocysteine or one-carbon metabolism (OCM). OCM is a major donor of methyl groups for methylation, particularly DNA methylation critical for epigenetic regulation of gene expression, and its disturbance may compromise DNA methylation, thereby affecting gene expression. OCM disturbance mediated by nutrient deficits is a well-known risk factor for various disorders and developmental defects (e.g., neural tube defects). In this review, we summarize the role of OCM disturbance and associated epigenetic aberrations in chronic alcohol-induced toxicity.
机译：过量饮酒是一个突出的问题，是世界范围内死亡率和发病率的主要原因之一。长期大量饮酒与多种有害健康的后果有关，例如癌症，心脏病和肝病，各种神经，认知和行为缺陷。饮酒也与发育缺陷有关。目前尚不清楚酒精引起的毒性的原因。酒精中毒的潜在机制之一与其与叶酸/高半胱氨酸或单碳代谢（OCM）的相互作用有关。 OCM是用于甲基化的甲基的主要供体，特别是对基因表达的表观遗传调控至关重要的DNA甲基化，其干扰可能会损害DNA甲基化，从而影响基因表达。由营养缺乏引起的OCM紊乱是各种疾病和发育缺陷（例如神经管缺陷）的众所周知的危险因素。在这篇综述中，我们总结了OCM紊乱和相关表观遗传畸变在慢性酒精诱导的毒性中的作用。

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