Mitochondrial DNA repair and aging

被引:245
|
作者
Mandavilli, BS [1 ]
Santos, JH [1 ]
Van Houten, B [1 ]
机构
[1] NIEHS, Mol Genet Lab, NIH, Res Triangle Pk, NC 27709 USA
关键词
mitochondria; DNA damage; DNA repair; animal models; C; elegans; Drosophila; yeast;
D O I
10.1016/S0027-5107(02)00220-8
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
The mitochondrial electron transport chain plays an important role in energy production in aerobic organisms and is also a significant source of reactive oxygen species that damage DNA, RNA and proteins in the cell. Oxidative damage to the mitochondrial DNA is implicated in various degenerative diseases, cancer and aging. The importance of mitochondrial ROS in age-related degenerative diseases is further strengthened by studies using animal models, Caenorhabditis elegans, Drosophila and yeast. Research in the last several years shows that mitochondrial DNA is more susceptible to various carcinogens and ROS when compared to nuclear DNA. DNA damage in mammalian mitochondria is repaired by base excision repair (BER). Studies have shown that mitochondria contain all the enzymes required for BER. Mitochondrial DNA damage, if not repaired, leads to disruption of electron transport chain and production of more ROS. This vicious cycle of ROS production and mtDNA damage ultimately leads to energy depletion in the cell and apoptosis. Published by Elsevier Science B.V.
引用
收藏
页码:127 / 151
页数:25
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