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[碘苯中毒诱导的肝脏谷胱甘肽耗竭及其与脂质过氧化和坏死的关系]

[Depletion of liver glutathione induced by iodobenzene poisoning and its relation to lipid peroxidation and necrosis].

作者信息

Casini A F, Pompella A, Comporti M

出版信息

Boll Soc Ital Biol Sper. 1983 Nov 30;59(11):1725-31.

PMID:6667314
Abstract

The mechanisms underlying iodobenzene hepatotoxicity were investigated in Albino mice in which the hepatic glutathione (GSH) content had been decreased by nearly 50% by starvation for 16 h before poisoning. After iodobenzene administration (9 mmol/Kg, p.o.) the hepatic GSH content decreased progressively and liver necrosis, as measured by the plasma transaminase (GPT, GOT) levels, occurred in many animals at 12 and 16 h. A clear cut necrosis was evident only when the hepatic GSH depletion reached a threshold value (3.5-2.5 nmol/mg protein). The same threshold value was evident for the occurrence of lipid peroxidation (measured as both carbonyl functions and conjugated dienes in liver phospholipids). The highly significant correlation found between lipid peroxidation and liver necrosis supports the possibility of a cause-effect relationship between the two phenomena.

摘要

在白化小鼠中研究了碘苯肝毒性的潜在机制,这些小鼠在中毒前经16小时饥饿处理,其肝脏谷胱甘肽(GSH)含量降低了近50%。给予碘苯(9 mmol/Kg,口服)后,肝脏GSH含量逐渐降低,许多动物在12小时和16小时时出现肝坏死,通过血浆转氨酶(GPT、GOT)水平来衡量。只有当肝脏GSH耗竭达到阈值(3.5 - 2.5 nmol/mg蛋白质)时,才会出现明显的坏死。脂质过氧化(以肝脏磷脂中的羰基功能和共轭二烯来衡量)的发生也有相同的阈值。脂质过氧化与肝坏死之间发现的高度显著相关性支持了这两种现象之间存在因果关系的可能性。

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