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Oxidative stress and alcoholic liver disease.

机译:氧化应激和酒精性肝病。

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摘要

Reactive oxygen species (ROS) are highly reactive molecules that are naturally generated in small amounts during the body's metabolic reactions and can react with and damage complex cellular molecules such as lipids, proteins, or DNA. This review describes pathways involved in ROS formation, why ROS are toxic to cells, and how the liver protects itself against ROS. Acute and chronic ethanol treatment increases the production of ROS, lowers cellular antioxidant levels, and enhances oxidative stress in many tissues, especially the liver. Ethanol-induced oxidative stress plays a major role in the mechanisms by which ethanol produces liver injury. Many pathways play a key role in how ethanol induces oxidative stress. This review summarizes some of the leading pathways and discusses the evidence for their contribution to alcohol-induced liver injury.
机译:活性氧(ROS)是高活性分子,在人体的新陈代谢反应中会自然生成少量,并且会与复杂的细胞分子(例如脂质,蛋白质或DNA)发生反应并对其造成损害。这篇综述描述了ROS形成的途径,为什么ROS对细胞有毒以及肝脏如何保护自己免受ROS侵害。急性和慢性乙醇治疗会增加ROS的产生,降低细胞的抗氧化剂水平,并增加许多组织(尤其是肝脏)的氧化应激。乙醇诱导的氧化应激在乙醇产生肝损伤的机制中起主要作用。许多途径在乙醇如何诱导氧化应激中起关键作用。这篇综述总结了一些主要途径,并讨论了其对酒精诱导的肝损伤的作用的证据。

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