X-Message-Number: 11926
Date: Tue, 8 Jun 1999 13:37:38 -0700 (PDT)
From: Doug Skrecky <>
Subject: ALC and PBN reverse mitochondrial decay

  Hagen TM.  Wehr CM.  Ames BN.
  Department of Molecular and Cell Biology, University of California at
  Berkeley 94720, USA. 
  Mitochondrial decay in aging. Reversal
  through supplementation of acetyl-L-carnitine and
  Annals of the New York Academy of Sciences.  854:214-23, 1998 Nov 20.
  We show that mitochondrial function in the majority of
  hepatocytes isolated from old rats (24 mo) is significantly impaired.
  Mitochondrial membrane potential, cardiolipin levels,
  respiratory control ratio, and overall cellular O2 consumption decline, and
  the level of oxidants increases. To examine whether dietary supplementation
  of micronutrients that may have become essential with age could reverse the
  decline in mitochondrial function, we supplemented the diet
  of old rats with 1% (w/v) acetyl-L-carnitine (ALCAR) in drinking water. ALCAR
  supplementation (1 month) resulted in significant increases in cellular
  respiration, mitochondrial membrane potential, and
  cardiolipin values. However, supplementation also increased the rate of
  oxidant production, indicating that the efficiency of
  mitochondrial electron transport had not improved. To
  counteract the potential increase in oxidative stress, animals were
  administered N-tert-butyl-alpha-phenyl-nitrone (30 mg/kg) (PBN) with or
  without ALCAR. Results showed that PBN significantly lowered oxidant
  production as measured by 2,7'-dichlorofluorescin diacetate (DCFH), even when
  ALCAR was coadministered to the animals. Thus, dietary supplementation with
  ALCAR, particularly in combination with PBN, improves
  mitochondrial function without a significant increase in
  oxidative stress.

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