Detoxifying function of cytochrorne c against oxygen toxicity

被引:26
作者
Min, Lee [1 ]
Xu Jian-xing [1 ]
机构
[1] Chinese Acad Sci, Inst Biophys, Natl Lab Biomacromol, Beijing 100101, Peoples R China
基金
美国国家科学基金会;
关键词
oxygen toxicity; cytochrome c; reactive oxygen species (ROS); respiratory chain; mitochondria;
D O I
10.1016/j.mito.2006.11.011
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The detoxifying function of cytochrome c to scavenge O-2(-.) and H2O2 in mitochondria is confirmed experimentally. A model of respiratory chain operating with two electron-leak pathways mediated by cytochrome c is suggested to illustrate the controlling mechanism of ROS level in mitochondria. A concept of mitochondrial radical metabolism is suggested based on the two electron-leak pathways mediated by cytochrome c are metabolic routes of O-2(-.). Two portions of oxygen consumption can be found in mitochondria. The main portion of oxygen consumed in the electron transfer of respiratory chain is used in ATP synthesis, while a subordinate part of oxygen consumed by the leaked electrons contributes to ROS generation. It is found that the amount of electron leak of respiratory chain is not fixed, but varies with age and pathological states. The models of respiratory chain operating with two cytochrome c-mediated electron-leak pathways and a radical metabolism of mitochondria accompanied with energy metabolism are helpful to comprehend the pathological problems caused by oxygen toxicity. (c) 2006 Elsevier B.V. and Mitochondria Research Society. All rights reserved.
引用
收藏
页码:13 / 16
页数:4
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