Maximum Life Span - Research Data Concerning Maximum Life Span

Research Data Concerning Maximum Life Span

  • A comparison of the heart mitochondria in rats (7-year maximum life span) and pigeons (35-year maximum life span) showed that pigeon mitochondria leak fewer free-radicals than rat mitochondria, despite the fact that both animals have similar metabolic rate and cardiac output
  • For mammals there is a direct relationship between mitochondrial membrane fatty acid saturation and maximum life span
  • Studies of the liver lipids of mammals and a bird (pigeon) show an inverse relationship between maximum life span and number of double bonds
  • Selected species of birds and mammals show an inverse relationship between telomere rate of change (shortening) and maximum life span
  • Maximum life span correlates negatively with antioxidant enzyme levels and free-radicals production and positively with rate of DNA repair
  • Female mammals express more Mn−SOD and glutathione peroxidase antioxidant enzymes than males. This has been hypothesized as the reason they live longer However, mice entirely lacking in glutathione peroxidase 1 do not show a reduction in lifespan.
  • The maximum life span of transgenic mice has been extended about 20% by overexpression of human catalase targeted to mitochondria
  • A comparison of 7 non-primate mammals (mouse, hamster, rat, guinea-pig, rabbit, pig and cow) showed that the rate of mitochondrial superoxide and hydrogen peroxide production in heart and kidney were inversely correlated with maximum life span
  • A study of 8 non-primate mammals showed an inverse correlation between maximum life span and oxidative damage to mtDNA (Mitochondrial DNA) in heart & brain
  • A study of several species of mammals and a bird (pigeon) indicated a linear relationship between oxidative damage to protein and maximum life span
  • There is a direct correlation between DNA repair and maximum life span for mammalian species
  • Drosophila (fruit-flies) bred for 15 generations by only using eggs that were laid toward the end of reproductive life achieved maximum life spans 30% greater than that of controls
  • Overexpression of the enzyme which synthesizes glutathione in long-lived transgenic Drosophila (fruit-flies) extended maximum lifespan by nearly 50%
  • A mutation in the age−1 gene of the nematode worm Caenorhabditis elegans increased mean life span 65% and maximum life span 110%. However, the degree of lifespan extension in relative terms by both the age-1 and daf-2 mutations is strongly dependent on ambient temperature, with ~10% extension at 16 °C and 65% extension at 27 °C.
  • Fat-specific Insulin Receptor KnockOut (FIRKO) mice have reduced fat mass, normal calorie intake and an increased maximum life span of 18%.
  • The capacity of mammalian species to detoxify the carcinogenic chemical benzo(a)pyrene to a water-soluble form also correlates well with maximum life span.
  • Short-term induction of oxidative stress due to calorie restriction increases life span in Caenorhabditis elegans by promoting stress defense, specifically by inducing an enzyme called catalase. As shown by Michael Ristow and co-workers nutritive antioxidants completely abolish this extension of life span by inhibiting a process called mitohormesis.

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