Mitochondria in organismal aging and degeneration

Gino A Cortopassi, Alice Wong

Research output: Contribution to journalArticle

156 Scopus citations

Abstract

Several lines of experimentation support the view that the genetic, biochemical and bioenergetic functions of somatic mitochondria deteriorate during normal aging. Deletion mutations of the mitochondrial genome accumulate exponentially with age in nerve and muscle tissue of humans and multiple other species. In muscle, a tissue that undergoes age-related fiber loss and atrophy in humans, there is an exponential rise in the number of cytochrome-oxidase-deficient fibers, which is first detectable in the fourth decile of age. Most biochemical studies of animal mitochondrial activity indicate a decline in electron transport activity with age, as well as decreased bioenergetic capacity with age, as measured by mitochondrial membrane potential. Mitochondrial mutations may be both the result of mitochondrial oxidative stress, and cells bearing pure populations of pathogenic mitochondrial mutations are sensitized to oxidant stress. Oxidant stress to mitochondria is known to induce the mitochondrial permeability transition, which has recently been implicated in the release of cytochrome c and the initiation of apoptosis. Thus several lines of evidence support a contribution of mitochondrial dysfunction to the phenotypic changes associated with aging. Copyright (C) 1999 Elsevier Science B.V.

Original languageEnglish (US)
Pages (from-to)183-193
Number of pages11
JournalBiochimica et Biophysica Acta - Bioenergetics
Volume1410
Issue number2
DOIs
StatePublished - Feb 9 1999

ASJC Scopus subject areas

  • Biophysics

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