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乙醇诱导性脂肪肝发病机制中肝脏脂质的过氧化作用

Peroxidation of liver lipids in the pathogenesis of the ethanol-induced fatty liver.

作者信息

Kalish G H, Di Luzio N R

出版信息

Science. 1966 Jun 3;152(3727):1390-2. doi: 10.1126/science.152.3727.1390-a.

Abstract

Administration of an acutely intoxicating dose of ethanol produced significant increases in the concentration of liver triglyceride and enhanced the peroxidation of liver lipids in rats. Adipose triglyceride and lipid peroxide concentrations were unaltered. Coenzyme Q(4), an effective antioxidant, significantly inhibited accumulation of liver triglyceride following ethanol intoxication and prevented the peroxidation of liver lipids. These results, which demonstrate the selective ability of ethanol to induce peroxidation of liver lipids, together with the effectiveness of antioxidants, support the previously proposed hypothesis that peroxidation of liver lipids following ethanol intoxication is a factor in the pathogenesis of ethanol-induced liver injury.

摘要

给大鼠急性注射能引起中毒剂量的乙醇,会使其肝脏甘油三酯浓度显著升高,并增强肝脏脂质的过氧化作用。而脂肪组织中的甘油三酯和脂质过氧化物浓度未发生改变。辅酶Q(4)作为一种有效的抗氧化剂,能显著抑制乙醇中毒后肝脏甘油三酯的积累,并防止肝脏脂质的过氧化。这些结果表明乙醇具有选择性诱导肝脏脂质过氧化的能力,同时也体现了抗氧化剂的有效性,支持了之前提出的假说,即乙醇中毒后肝脏脂质的过氧化是乙醇性肝损伤发病机制中的一个因素。

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