From: Doug Skrecky (oberon@vcn.bc.ca)
Date: Tue Jun 08 1999 - 14:38:34 MDT
Authors
Hagen TM. Wehr CM. Ames BN.
Institution
Department of Molecular and Cell Biology, University of California at
Berkeley 94720, USA. tory.hagen@orst.edu
Title
Mitochondrial decay in aging. Reversal
through supplementation of acetyl-L-carnitine and
N-tert-butyl-alpha-phenyl-nitrone.
Source
Annals of the New York Academy of Sciences. 854:214-23, 1998 Nov 20.
Abstract
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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