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胡椒基丁醚或别嘌呤醇对氰化物诱导的小鼠脑脂质过氧化的影响。

Effect of piperonyl butoxide or allopurinol on cyanide-induced lipid peroxidation in mouse brain.

作者信息

Yamamoto H

机构信息

Institute of Community Medicine, University of Tsukuba, Ibaraki, Japan.

出版信息

Toxicol Lett. 1998 Feb;94(3):167-73. doi: 10.1016/s0378-4274(97)00113-6.

Abstract

The effect of piperonyl butoxide or allopurinol on cyanide-induced lipid peroxidation was investigated using homogenates from whole brain of mice. The brain homogenate exposed to a low concentration of potassium cyanide (10, 50, or 100 microM) was significantly increased in their concentration of malondialdehyde (MDA) + 4-hydroxyalkenals (4-MDA) as compared to control samples, in a concentration-dependent manner. The increased lipid peroxidation induced by cyanide was inhibited by piperonyl butoxide (1 mM), an inhibitor of mixed function oxidase, but not by allopurinol (0.1 mM), an inhibitor of xanthine oxidase. Furthermore, when a brain homogenate heated at 86 degrees C for 1 min was incubated with or without cyanide at 37 degrees C for 20 min, MDA + 4-MDA levels in the homogenate were not changed between cyanide treatment and untreated. An intraperitoneal injection of piperonyl butoxide (1 g/kg) significantly inhibited cyanide-induced seizures in mice. These results suggest that cyanide-induced seizures may be partly involved in the lipid peroxidation produced by the heat unstable and piperonyl butoxide dependent factors in brain.

摘要

使用小鼠全脑匀浆研究了胡椒基丁醚或别嘌呤醇对氰化物诱导的脂质过氧化的影响。与对照样品相比,暴露于低浓度氰化钾(10、50或100微摩尔)的脑匀浆中丙二醛(MDA)+4-羟基烯醛(4-MDA)的浓度显著增加,呈浓度依赖性。氰化物诱导的脂质过氧化增加被混合功能氧化酶抑制剂胡椒基丁醚(1毫摩尔)抑制,但未被黄嘌呤氧化酶抑制剂别嘌呤醇(0.1毫摩尔)抑制。此外,当在86℃加热1分钟的脑匀浆在37℃与氰化物一起或不与氰化物一起孵育20分钟时,氰化物处理组和未处理组之间匀浆中的MDA+4-MDA水平没有变化。腹腔注射胡椒基丁醚(1克/千克)可显著抑制小鼠氰化物诱导的惊厥。这些结果表明,氰化物诱导的惊厥可能部分与脑中热不稳定且依赖胡椒基丁醚的因素产生的脂质过氧化有关。

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