PEROXISOME PROLIFERATORS PROTECT AGAINST PARACETAMOL HEPATOTOXICITY IN MICE

被引：27

作者：

NICHOLLSGRZEMSKI, FA ^{[1
]}

CALDER, IC ^{[1
]}

PRIESTLY, BG ^{[1
]}

机构：

[1] S AUSTRALIAN HLTH COMMISS,ADELAIDE,SA 5000,AUSTRALIA

来源：

BIOCHEMICAL PHARMACOLOGY | 1992年 / 43卷 / 07期

关键词：

D O I：

10.1016/0006-2952(92)90193-M

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

The hepatotoxicity of paracetamol is thought to be mediated by an electrophilic intermediate N-acetyl-p-benzoquinone imine (NAPQI). Conjugation of NAPQI with reduced glutathione (GSH) is a primary detoxicarion mechanism, but it is possible that other cellular antioxidants may play a role, by scavenging oxyradicals produced by a NAPQI-related redox cycling reaction. Peroxisome proliferation is a condition in which excess oxyradical formation occurs when the H2O2-producing enzymes involved in fatty acid β-oxidation are markedly induced while the H202-degrading enzymes are either increased marginally (catalase) or reduced in activity (GSH peroxidase) [1]. The purpose of this study was to determine whether a change in oxidant status associated with hepatic peroxisome proliferation in mice could alter susceptibility to paracetamol-induced hepatotoxicity. © 1992.

引用

页码：1395 / 1396

页数：2

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