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3-甲基吲哚抑制脂质过氧化。

3-Methylindole inhibits lipid peroxidation.

作者信息

Adams J D, Heins M C, Yost G S

机构信息

Pharmacology/Toxicology Program, College of Pharmacy, Washington State University, Pullman 99164-6510.

出版信息

Biochem Biophys Res Commun. 1987 Nov 30;149(1):73-8. doi: 10.1016/0006-291x(87)91606-8.

Abstract

The mechanism of pneumotoxicity of 3-methylindole has been postulated to occur via protein alkylation or lipid peroxidation. This report describes the effects of the addition of 3-methylindole to goat lung microsomes to evaluate the possibility that this xenobiotic may increase NADPH-supported lipid peroxidation. Concentrations of malondialdehyde were measured as an index of lipid peroxidation. Instead of a stimulation of lipid peroxidation by 3-methylindole, a complete inhibition of lipid peroxidation was produced by concentrations of 3-methylindole as low as 10 microM. The addition of 3-methylindole to actively peroxidizing microsomes (NADPH-supported) caused an immediate cessation of malondialdehyde production. These results demonstrate that 3-methylindole pneumotoxicity does not proceed by a mechanism of lipid peroxidation, but in fact, this molecule may act as an effective antioxidant to prevent lipid peroxidation in pulmonary tissue.

摘要

3-甲基吲哚的肺毒性机制据推测是通过蛋白质烷基化或脂质过氧化作用发生的。本报告描述了向山羊肺微粒体中添加3-甲基吲哚的效果,以评估这种外源性物质可能增加NADPH支持的脂质过氧化作用的可能性。丙二醛的浓度作为脂质过氧化作用的指标进行测量。与3-甲基吲哚刺激脂质过氧化作用不同,低至10微摩尔浓度的3-甲基吲哚就能完全抑制脂质过氧化作用。向积极进行过氧化反应的微粒体(NADPH支持)中添加3-甲基吲哚会立即停止丙二醛的生成。这些结果表明,3-甲基吲哚的肺毒性并非通过脂质过氧化作用机制发生,实际上,该分子可能作为一种有效的抗氧化剂来防止肺组织中的脂质过氧化作用。

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