Mitochondrial DNA and aging

被引：94

作者：

Alexeyev, MF ^{[1
]}

LeDoux, SP ^{[1
]}

'Wilson, GL ^{[1
]}

机构：

[1] Univ S Alabama, Dept Cell Biol & Neurosci, Mobile, AL 36688 USA

来源：

CLINICAL SCIENCE | 2004年 / 107卷 / 04期

关键词：

aging; DNA damage; mitochondrial DNA; oxidative stress; reactive oxygen species; repair;

D O I：

10.1042/CS20040148

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

Among the numerous theories that explain the process of aging, the mitochondrial theory of aging has received the most attention. This theory states that electrons leaking from the ETC (electron transfer chain) reduce molecular oxygen to form O-2(.-) (superoxide anion radicals). O-2(.-), through both enzymic and non-enzymic reactions, can cause the generation of other ROS (reactive oxygen species). The ensuing state of oxidative stress results in damage to ETC components and mtDNA (mitochondrial DNA), thus increasing further the production of ROS. Ultimately, this 'vicious cycle' leads to a physiological decline in function, or aging. This review focuses on recent developments in aging research related to the role played by mtDNA. Both Supportive and contradictory evidence is discussed.

引用

页码：355 / 364

页数：10

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