SOD isoforms play no role in lifespan in ad lib or dietary restricted conditions, but mutational inactivation of SOD-1 reduces life extension by cold

Kelvin Yen, Harshil B. Patel, Alex L. Lublin, Charles V. Mobbs

Research output: Contribution to journalArticlepeer-review

41 Scopus citations

Abstract

The free radical theory of aging is one of the most prominent theories of aging and senescence, but has yet to be definitively proven. If free radicals are the cause of senescence, then the cellular anti-oxidant system should play a large role in lifespan determination. Because superoxide dismutase (SOD) plays a central role in detoxifying superoxide radicals, we have examined the effects of mutational inactivation of each isoform of sod on normal lifespan and lifespan extension by dietary restriction (DR) or cold-/hypothermic-induced longevity (CHIL). We find no significant decrease in lifespan for control worms or worms undergoing DR when sod isoforms are knocked-out even though sod mutational inactivation produces hypersensitivity to paraquat. In contrast, sod-1 inactivation significantly reduces lifespan extension by CHIL, suggesting that CHIL requires a specific genetic program beyond simple reduction in metabolic rate. Furthermore, CHIL paradoxically increases lifespan while reducing resistance to oxidative stress, further disassociating oxidative stress resistance and lifespan.

Original languageEnglish
Pages (from-to)173-178
Number of pages6
JournalMechanisms of Ageing and Development
Volume130
Issue number3
DOIs
StatePublished - Mar 2009

Keywords

  • Aging
  • Free radicals
  • Lifespan
  • Oxidative stress
  • Senescence

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