acetyl-l-carnitine fed to old rats

From: Doug Skrecky (oberon@vcn.bc.ca)
Date: Fri May 07 1999 - 00:12:02 MDT


Authors
  Hagen TM. Ingersoll RT. Wehr CM. Lykkesfeldt J. Vinarsky V. Bartholomew
  JC. Song MH. Ames BN.
Institution
  Department of Molecular and Cell Biology, University of California, Berkeley,
  CA 94720, USA.
Title
  Acetyl-L-carnitine fed to
  old rats partially restores mitochondrial function and
  ambulatory activity.
Source
  Proceedings of the National Academy of Sciences of the United States of
  America. 95(16):9562-6, 1998 Aug 4.
Abstract
  Mitochondrial function and ambulatory activity were monitored after feeding
  old rats acetyl-L-carnitine (ALCAR). Young
  (3-5 mo) and old (22-28 mo) rats were given a 1.5% (wt/vol)
  solution of ALCAR in their drinking water for 1 mo, were sacrificed, and
  their liver parenchymal cells were isolated. ALCAR supplementation
  significantly reverses the age-associated decline of mitochondrial membrane
  potential, as assessed by rhodamine 123 staining. Cardiolipin, which declines
  significantly with age, is also restored. ALCAR increases cellular oxygen
  consumption, which declines with age, to the level of young rats. However,
  the oxidant production per oxygen consumed, as measured by
  2',7'-dichlorofluorescin fluorescence levels, is approximately 30% higher
  than in untreated old rats. Cellular glutathione and
  ascorbate levels were nearly 30% and 50% lower, respectively, in cells from
  ALCAR-supplemented old rats than in untreated
  old rats, further indicating that ALCAR supplementation
  might increase oxidative stress. Ambulatory activity in young and
  old rats was quantified as a general measure of metabolic
  activity. Ambulatory activity, defined as mean total distance traveled, in
  old rats is almost 3-fold lower than in
  young animals. ALCAR supplementation increases ambulatory activity
  significantly in both young and old rats, with the increase
  being larger in old rats. Thus, ALCAR supplementation to
  old rats markedly reverses the age-associated decline in
  many indices of mitochondrial function and general metabolic activity, but
  may increase oxidative stress.

  Additional note by poster:

     Low dose lipoic acid also helps reverse mitochondrial function, but
  does not increase oxidative stress, so this may be a preferable
  supplement for fragile elderly humans to try. Lipoic acid does have the
  side effect of increasing biotin requirements, so extra biotin should be
  given as well to prevent a deficiency.
     Pyruvate is another supplement that may be helpful in the elderly.



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