氯仿的肝毒性作用:生化改变的短期动力学和剂量效应关系。

M Skrzypińska-Gawrysiak, J K Piotrowski, J Koralewska
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引用次数: 0

摘要

Balb/c小鼠以约致死剂量的1/8至1为单次剂量给予氯仿。在给药后的不同时间段,处死小鼠。测定血清谷氨酸-丙酮酸转氨酶(SGPT)、山梨醇脱氢酶(SDH)及肝脏谷胱甘肽(GSH)、丙二醛(MDA)水平。超过近似致死剂量1/8的所有剂量均发现SGPT和SDH水平升高。在所有剂量下,谷胱甘肽的消耗水平都保持在40%以内。肝脏丙二醛水平升高2 ~ 4倍。肝GSH的消耗和血清SGPT和SDH在一定程度上的增加呈双相发生。这些生化变化的剂量效应函数只能在作用的第二个延迟阶段构建。推测氯仿的肝毒性主要依赖于生物转化过程中自由基的形成。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The hepatotoxic action of chloroform: short-time dynamics of biochemical alterations and dose-effect relationships.

Chloroform was administered ip to Balb/c mice as a single dose ranging from 1/8 to 1 of the approximate lethal dose. At different time periods after administration, mice were sacrificed. Serum glutamate-pyruvate transaminase (SGPT) and sorbitol dehydrogenase (SDH) as well as glutathione (GSH) and malondialdehyde (MDA) levels in the liver were determined. Increased SGPT and SDH levels were found for all doses exceeding 1/8 of the approximate lethal dose. The depletion of GSH level was kept within 40% for all doses. A 2-4 fold increase of hepatic MDA level was found. The depletion of hepatic GSH and, to some extent the increase of serum SGPT and SDH, occurred in biphasic fashion. Dose-effect functions for these biochemical alterations could only be constructed for the second, delayed phase of action. It is postulated that the hepatotoxicity of chloroform is mainly dependent on radical formation in the course of biotransformation.

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