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MINIREVIEW

Oxidative Stress, Mitochondrial DNA Mutation, and Apoptosis in Aging

Hsin-Chen Lee^* and Yau-Huei Wei^,1

^* Department of Pharmacology and Department of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei 112, Taiwan

To whom requests for reprints should be addressed at ¹ Department of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei, Taiwan 112, Republic of China. E-mail: joeman{at}ym.edu.tw

A wide spectrum of alterations in mitochondria and mitochondrial DNA (mtDNA) with aging has been observed in animals and humans. These include (i) decline in mitochondrial respiratory function; (ii) increase in mitochondrial production of reactive oxygen species (ROS) and the extent of oxidative damage to DNA, proteins, and lipids; (iii) accumulation of point mutations and large-scale deletions of mtDNA; and (iv) enhanced apoptosis. Recent studies have provided abundant evidence to substantiate the importance of mitochondrial production of ROS in aging. On the other hand, somatic mtDNA mutations can cause premature aging without increasing ROS production. In this review, we focus on the roles that ROS play in the aging-associated decline of mitochondrial respiratory function, accumulation of mtDNA mutations, apoptosis, and alteration of gene expression profiles. Taking these findings together, we suggest that mitochondrial dysfunction, enhanced oxidative stress, subsequent accumulation of mtDNA mutations, altered expression of a few clusters of genes, and apoptosis are important contributors to human aging.

Key Words: aging • mtDNA • mitochondria • oxidative stress • oxidative damage • apoptosis

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