free radical production and aging

From: Doug Skrecky (oberon@vcn.bc.ca)
Date: Sun Feb 14 1999 - 05:35:55 MST


Authors
  Barja G. Cadenas S. Rojas C. Lopez-Torres M. Perez-Campo R.
Institution
  Department of Animal Biology-II (Animal Physiology), Faculty of Biology,
  Complutense University, Madrid, Spain.
Title
  A decrease of free radical
  production near critical targets as a cause of maximum longevity in animals.
Source
  Comparative Biochemistry & Physiology. Biochemistry & Molecular Biology.
  108(4):501-12, 1994 Aug.
Abstract
  A comprehensive study was performed on the brains of various vertebrate
  species showing different life energy potentials in order to find out if
  free radicals are important determinants of
  species-specific maximum life span. Brain superoxide dismutase, catalase,
  Se-dependent and independent GSH-peroxidases, GSH-reductase, and ascorbic
  acid showed significant inverse correlations with maximum longevity, whereas
  GSH, uric acid, GSSG/GSH, in vitro peroxidation (thiobarbituric acid test),
  and malondialdehyde (measured by HPLC), did not correlate with maximum life
  span. Superoxide dismutase, catalase, GSH-peroxidase, GSH and ascorbate
  results agree with those previously reported in various independent works
  using different animal species. GSSG/GSH, and true malondialdehyde (HPLC)
  results are reported for the first time in relation to maximum longevity. The
  results suggest that longevous species simultaneously show low antioxidant
  concentrations and low levels of in vivo free
  radical production (a low free
  radical turnover) in their tissues. The
  "free radical production hypothesis of
  aging" is proposed: a decrease in oxygen
  radical production per unit of O2 consumption near critical
  DNA targets (mitochondria or nucleus) increases the maximum life span of
  extraordinarily long-lived species like birds, primates, and man.
  Free radical production near these DNA
  sites would be a main factor responsible for aging in all the species, in
  those following Pearl's (Rubner's) metabolic rule as well as in those not
  following it.



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