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体内用异氰酸甲酯处理大鼠时脂质过氧化在复合物I处线粒体功能损伤中的作用

Role of lipid peroxidation in impairment of mitochondrial function at complex I by methyl isocyanate treatment of rats in vivo.

作者信息

Jeevaratnam K, Vidya S, Vaidyanathan C S

机构信息

Division of Pharmacology & Toxicology, Defence Research and Development Establishment, Gwalior, India.

出版信息

Biochem Mol Biol Int. 1993 Jul;30(3):411-7.

PMID:8401298
Abstract

The subcutaneous administration of methyl isocyanate (MIC) in 1.0 LD50 dose in rats caused a significant effect on hepatic mitochondrial function only at complex I region of the respiratory chain. MIC administration at 1.0 LD50 dose also resulted in significant increases in malondialdehyde and ferrous ion concentration in liver mitochondria. It is suggested that the augmented lipid peroxidation in hepatic mitochondria, catalyzed by iron, possibly mobilized from intracellular stores leads to the inhibition of enzymes of mitochondrial respiration at complex I region, in vivo, in rats receiving a lethal dose of MIC subcutaneously.

摘要

给大鼠皮下注射1.0半数致死剂量(LD50)的异氰酸甲酯(MIC),仅对呼吸链复合体I区域的肝线粒体功能产生显著影响。以1.0 LD50剂量注射MIC还导致肝线粒体中丙二醛和亚铁离子浓度显著增加。有人提出,在体内,接受致死剂量皮下注射MIC的大鼠中,可能从细胞内储存库动员出来的铁催化肝线粒体中脂质过氧化作用增强,从而导致线粒体呼吸酶在复合体I区域受到抑制。

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引用本文的文献

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