Oxidative stress, caloric restriction, and aging

Science. 1996 Jul 5;273(5271):59-63. doi: 10.1126/science.273.5271.59.

Abstract

Under normal physiological conditions, the use of oxygen by cells of aerobic organisms generates potentially deleterious reactive oxygen metabolites. A chronic state of oxidative stress exists in cells because of an imbalance between prooxidants and antioxidants. The amount of oxidative damage increases as an organism ages and is postulated to be a major causal factor of senescence. Support for this hypothesis includes the following observations: (i) Overexpression of antioxidative enzymes retards the age-related accrual of oxidative damage and extends the maximum life-span of transgenic Drosophila melanogaster. (ii) Variations in longevity among different species inversely correlate with the rates of mitochondrial generation of the superoxide anion radical (O2) and hydrogen peroxide. (iii) Restriction of caloric intake lowers steady-state levels of oxidative stress and damage, retards age-associated changes, and extends the maximum life-span in mammals.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Aging*
  • Animals
  • Drosophila melanogaster / physiology
  • Energy Intake*
  • Hydrogen Peroxide / metabolism
  • Longevity
  • Mammals / physiology
  • Mitochondria / metabolism
  • Oxidative Stress*
  • Oxygen Consumption
  • Superoxides / metabolism

Substances

  • Superoxides
  • Hydrogen Peroxide