Mitochondrial DNA mutation, oxidative stress, and alteration of gene expression in human aging

Hsin Chen Lee, Yau Huei Wei

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

1 Scopus citations

Abstract

A decline in respiratory function and increase in oxidative stressin mitochondria have been proposed as important contributors to human aging. A wide spectrum of alterations in mitochondria and mitochondrial DNA (mtDNA) has been observed in aged individuals and senescent cells. These include: • Decline in mitochondrial respiratory function • Accumulation of mtDNA mutations • Alteration in the expression of the mitochondrial genes • Increase in the rate of production of reactive oxygen species (ROS) • Increase in the extent of oxidative damage to DNA, proteins, and lipids. Responses to oxidative stress and their subsequent consequences in affected tissues play an important role in the deleterious effects of ROS on cellular function and on the apoptotic process, which culminate in aging and degenerative diseases. In this review, we focus on the roles that ROS play in aging-associated oxidative damage to mtDNA and proteins and on the oxidative stress responses of human cells at the molecular and cellular levels. The alterations of gene expression profiles elicited by oxidative stress in aging animals are discussed. Taking recent findings from this and other laboratories together, we suggest that the decline in respiratory function and increase in mitochondrial production of ROS and subsequent accumulation of mtDNA mutations and alteration in the expression of a few clusters of genes play an important role in the aging process.

Original languageEnglish
Title of host publicationMitochondria in Health and Disease
PublisherCRC Press
Pages319-362
Number of pages44
ISBN (Electronic)9781420028843
ISBN (Print)0824754425, 9780824754426
StatePublished - 01 01 2005
Externally publishedYes

Bibliographical note

Publisher Copyright:
© 2005 by Taylor & Francis Group.

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