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线粒体在谷氨酸毒性机制中的作用。

Role of mitochondria in the mechanisms of glutamate toxicity.

作者信息

Isaev N K, Andreeva N A, Stel'mashuk E V, Zorov D B

机构信息

Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, 119992 Moscow, Russia.

出版信息

Biochemistry (Mosc). 2005 Jun;70(6):611-8. doi: 10.1007/s10541-005-0160-x.

Abstract

Current data on glutamate-induced functional and morphological changes in mitochondria correlating with or being a result of their membrane potential changes are reviewed. The important role of Ca2+, Na+, and H+ in the potentiation of such changes is considered. It is assumed that glutamate-induced loss of mitochondrial potential is mediated by Ca2+ overload resulting in the induction of nonspecific permeability of the inner mitochondrial membrane.

摘要

本文综述了谷氨酸诱导的线粒体功能和形态变化的当前数据,这些变化与线粒体膜电位变化相关或由其引起。文中考虑了Ca2+、Na+和H+在增强此类变化中的重要作用。据推测,谷氨酸诱导的线粒体电位丧失是由Ca2+超载介导的,导致线粒体内膜非特异性通透性的诱导。

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