Prevention of flight activity prolongs the life span of the housefly, Musca domestica, and attenuates the age-associated oxidative damamge to specific mitochondrial proteins

Liang Jun Yan, Rajindar S. Sohal

Research output: Contribution to journalArticle

86 Scopus citations

Abstract

The purpose of this study was to explore the mechanisms by which oxidative stress affects the aging process. The hypothesis that the rate of accumulation of oxidative damage to specific mitochondrial proteins is linked to the life expectancy of animals was tested in the housefly. The rate of oxygen consumption and life expectancy of the flies were experimentally altered by confining the flies in small jars, where they were unable to fly. Prevention of flight activity decreased the rate of oxygen utilization of flies and almost tripled their life span as compared to those permitted to fly. Rate of mitochondrial H2O2 generation at various ages was lower in the low activity flies than in the high activity flies. Oxidative damage to mitochondrial proteins, adenine nucelotide translocase, and aconitase, detected as carbonyl modifications, was attenuated; and the loss in their functional activity occurring with age was retarded in the long-lived low activity flies as compared to the short-lived high activity flies. The two proteins were previously identified to be the only mitochondrial proteins exhibiting age-related increases in carbonylation. Results support the hypothesis that accrual of oxidative damage to specific protein targets and the consequent loss of their function may constitute a mechanism by which oxidative stress controls the aging process. Copyright (C) 2000 Elsevier Science Inc.

Original languageEnglish
Pages (from-to)1143-1150
Number of pages8
JournalFree Radical Biology and Medicine
Volume29
Issue number11
DOIs
StatePublished - 1 Dec 2000

Keywords

  • Aconitase
  • Adenine nucleotide translocase (ANT)
  • Aging
  • Free radicals
  • Metabolic rate
  • Mitochondria
  • Oxidative damage
  • Protein carbonyls

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