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7812246 
Journal Article 
Review 
Oxidative stress, mitochondrial DNA mutation, and apoptosis in aging 
Lee, HC; Wei, YH 
2007 
Yes 
Experimental Biology and Medicine
ISSN: 1535-3702
EISSN: 1535-3699 
232 
5 
592-606 
English 
17463155 
WOS:000246160600001 
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. 
Aging/genetics/physiology; Animals; Apoptosis/physiology; DNA, Mitochondrial/genetics; Models, Biological; Mutation; Oxidative Stress/physiology