Oxidative stress, mitochondrial DNA mutation, and apoptosis in aging

Hsin Chen Lee, Yau Huei Wei*

*Corresponding author for this work

Research output: Contribution to journalShort surveypeer-review

226 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)592-606
Number of pages15
JournalExperimental Biology and Medicine
Volume232
Issue number5
StatePublished - 05 2007
Externally publishedYes

Keywords

  • Aging
  • Apoptosis
  • Mitochondria
  • Oxidative damage
  • Oxidative stress
  • mtDNA

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