Mitochondria, oxidative stress and aging

Free Radic Res. 2000 Mar;32(3):189-98. doi: 10.1080/10715760000300201.

Abstract

In the eighties, Miquel and Fleming suggested that mitochondria play a key role in cellular aging. Mitochondria, and specially mitochondrial DNA (mtDNA), are major targets of free radical attack. At present, it is well established that mitochondrial deficits accumulate upon aging due to oxidative damage. Thus, oxidative lesions to mtDNA accumulate with age in human and rodent tissues. Furthermore, levels of oxidative damage to mtDNA are several times higher than those of nuclear DNA. Mitochondrial size increases whereas mitochondrial membrane potential decreases with age in brain and liver. Recently, we have shown that treatment with certain antioxidants, such as sulphur-containing antioxidants, vitamins C and E or the Ginkgo biloba extract EGb 761, protects against the age-associated oxidative damage to mtDNA and oxidation of mitochondrial glutathione. Moreover, the extract EGb 761 also prevents changes in mitochondrial morphology and function associated with aging of the brain and liver. Thus, mitochondrial aging may be prevented by antioxidants. Furthermore, late onset administration of certain antioxidants is also able to prevent the impairment in physiological performance, particularly motor co-ordination, that occurs upon aging.

Publication types

  • Review

MeSH terms

  • Age Factors
  • Aging*
  • Antioxidants / pharmacology
  • DNA Damage
  • Free Radicals / metabolism
  • Mitochondria / metabolism*
  • Oxidative Stress*
  • Reactive Oxygen Species / metabolism

Substances

  • Antioxidants
  • Free Radicals
  • Reactive Oxygen Species