X-Message-Number: 26337
Date: Wed, 15 Jun 2005 17:34:27 -0700 (PDT)
From: Doug Skrecky <>
Subject: nuclear free radical theory of aging disproved

  [There is accumulating data indicating that free radicals have little
or no effect on aging in "normal" long lived or wild type animals. In
contrast short lived mutants often do suffer from diseases with a
significant degree of free radical related pathology. A typical example
of this would age and free radical related renal failure in Fisher 344
rats.
  The nucleus and mitochondria have been believed to the most important
cellular sites of free radical damage. The present experiment largely
eliminates the nucleus from further consideration, which I am sure will
come as a shock to some (but not all) gerontologists.
   Mitochondria based theories of aging have run afoul from
contradictory results as well. Hopefully this matter will be resolved
soon. Until the impact (or lack thereof) of free radicals on aging is
elucidated, other competing theories are likely to remain on the back
burner.]

 Science. 2005 May 5; [Epub ahead of print]
Extension of Murine Lifespan by Overexpression of Catalase Targeted
to Mitochondria.
    To determine the role of reactive oxygen species in mammalian
longevity, we generated transgenic mice that overexpress human
catalase localized to the peroxisome (PCAT), nucleus (NCAT), or
mitochondrion (MCAT). Median and maximum lifespans were maximally
increased (average 5 months, and 5.5 months, respectively) in MCAT
animals. Cardiac pathology and cataract development were delayed,
oxidative damage was reduced, H2O2 production and H2O2-induced
aconitase inactivation were attenuated, and the development of
mitochondrial deletions was reduced. These results support the
free radical theory of aging and reinforce the importance of
mitochondria as a source of these radicals.

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