For debate: Defective mitochondria, free radicals, cell death, aging-reality or myth-ochondria?

Pierre Rustin, Jurgen Christoph Von Kleist-Retzow, Zoltan Vajo, Agnes Rotig, Amold Munnich

Research output: Contribution to journalArticle

32 Citations (Scopus)


As both experimental evidence and theoretical considerations may suggest that free radicals and mitochondria might be associated as key factors in aging, these organelles have been implicated in various versions of the free radical theory of aging. However, except for a few cases, no evidence for a death process specifically activated in respiratory defective cells could be found in patients with a mitochondrial disorder, including those harboring high levels of mutant mtDNA associated with profound respiratory chain deficiencies. This and more recent evidence suggest that damages produced by free-radicals endogenously generated in the mitochondria result in a distinctive biochemical profile, only occur under exceptional conditions and that a dysfunction of the respiratory chain does not cause opening of the permeability transition pore and is not sufficient per se to trigger massive entrance of cells into death processes, neither apoptosis nor necrosis. Therefore, defective mitochondria and their particular genome, should not be considered as a major and primary source of free radicals either leading cells into a death cascade or resulting in an accelerated aging process. Copyright (C) 2000 Elsevier Science Ireland Ltd.

Original languageEnglish
Pages (from-to)201-206
Number of pages6
JournalMechanisms of Ageing and Development
Issue number3
Publication statusPublished - Apr 14 2000


  • Aging
  • Free radicals
  • Mitochondrium
  • Oxidation

ASJC Scopus subject areas

  • Ageing
  • Developmental Biology

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