[Pathobiochemistry of alcoholism].

J P von Wartburg
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引用次数: 0

Abstract

Liver alcohol dehydrogenase (ADH) represents the main enzyme of normal alcohol metabolism. Total activity of this enzyme varies largely due to the occurrence of isoenzymes and of genetic polymorphisms. One genetic variant, called "atypical", is characterized by a higher specific activity. In carriers of this variant enzyme an initially faster rate of ethanol metabolism leads to higher blood acetaldehyde levels. Acetaldehyde, as a toxic intermediary metabolite, causes tachycardia, nausea and flushing of the face. A high frequency for "atypical" ADH is observed in mongolid races and consequently a hypersensitivity to alcohol is often observed in Orientals. Hence, certain genetically determined enzyme patterns may represent an aversive factor with regard to alcohol consumption. In Caucasians the phenotypes with "atypical" ADH are less frequent. However, in individuals with the "atypical" variant regular intake of alcohol may lead to an increased organotoxicity due to acetaldehyde.

[酒精中毒的病理生化]。
肝脏酒精脱氢酶(ADH)是正常酒精代谢的主要酶。这种酶的总活性在很大程度上取决于同工酶和遗传多态性的发生。一种被称为“非典型”的基因变异,其特点是具有更高的特异性活性。在这种变异酶的携带者中,最初更快的乙醇代谢率导致更高的血液乙醛水平。乙醛作为一种有毒的中间代谢物,会引起心动过速、恶心和面部潮红。“非典型”ADH在蒙古人种中发病率很高,因此在东方人中经常观察到对酒精过敏。因此,某些基因决定的酶模式可能代表一个关于酒精消费的厌恶因素。在白种人中,“非典型”ADH的表型较少出现。然而,在具有“非典型”变体的个体中,经常摄入酒精可能导致乙醛引起的器官毒性增加。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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