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氧化应激作为丙戊酸相关肝毒性的一种机制。

Oxidative stress as a mechanism of valproic acid-associated hepatotoxicity.

作者信息

Chang Thomas K H, Abbott Frank S

机构信息

Faculty of Pharmaceutical Sciences, The University of British Columbia, Vancouver, British Columbia, Canada.

出版信息

Drug Metab Rev. 2006;38(4):627-39. doi: 10.1080/03602530600959433.

Abstract

Valproic acid (2-n-propylpentanoic acid; VPA) has several therapeutic indications, but it is used primarily as an anticonvulsant. VPA is a relatively safe drug, but its use is associated with idiosyncratic hepatotoxicity, which in some cases may lead to fatality. The underlying mechanism responsible for the hepatotoxicity is still not well understood, but various hypotheses have been proposed, including oxidative stress. This article discusses the experimental evidence on the effect of VPA on the various indices of oxidative stress and on the potential role of oxidative stress in VPA-associated hepatotoxicity.

摘要

丙戊酸(2-正丙基戊酸;VPA)有多种治疗适应症,但主要用作抗惊厥药。VPA是一种相对安全的药物,但其使用与特异质性肝毒性有关,在某些情况下可能导致死亡。肝毒性的潜在机制仍未完全明确,但已提出了各种假说,包括氧化应激。本文讨论了关于VPA对氧化应激各项指标的影响以及氧化应激在VPA相关肝毒性中的潜在作用的实验证据。

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