期刊
CLINICAL SCIENCE
卷 107, 期 4, 页码 355-364出版社
PORTLAND PRESS LTD
DOI: 10.1042/CS20040148
关键词
aging; DNA damage; mitochondrial DNA; oxidative stress; reactive oxygen species; repair
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.
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