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酒精与肝脏氧化损伤

Alcohol and oxidative liver injury.

作者信息

Dey Aparajita, Cederbaum Arthur I

机构信息

Department of Pharmacology and Biological Chemistry, Mount Sinai School of Medicine, New York, NY, USA.

出版信息

Hepatology. 2006 Feb;43(2 Suppl 1):S63-74. doi: 10.1002/hep.20957.

Abstract

Acute and chronic ethanol treatment has been shown to increase the production of reactive oxygen species, lower cellular antioxidant levels, and enhance 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. Many of the seminal reports in this topic have been published in Hepatology , and it is fitting to review this research area for the 25th Anniversary Issue of the Journal.

摘要

急性和慢性乙醇处理已被证明会增加活性氧的产生,降低细胞抗氧化水平,并增强许多组织(尤其是肝脏)中的氧化应激。乙醇诱导的氧化应激在乙醇导致肝损伤的机制中起主要作用。许多途径在乙醇诱导氧化应激的过程中起关键作用。本综述总结了一些主要途径,并讨论了它们对酒精性肝损伤作用的证据。该主题的许多开创性报告已发表在《肝脏病学》上,因此在该杂志第25周年纪念刊上对这一研究领域进行综述是恰当的。

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