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Articles in PresS, published online ahead of print March 12, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00387.2001
Submitted on August 27, 2001
Accepted on February 1, 2002
1 Endocrinology, Mayo Clinic, Rochester, MN, USA
* To whom correspondence should be addressed. E-mail: nair.sree{at}mayo.edu.
Rodent skeletal muscle mitochondrial DNA has been shown to be a potential site of oxidative damage during aging. Caloric restriction is reported to reduce oxidative stress and prolong life expectancy in rodents. Gene expression profiling and measurement of mitochondrial ATP production capacity were performed in skeletal muscle of male rats after feeding either a control diet or caloric restricted diet (60% of control diet) for 36 weeks in order to determine the potential mechanism of the beneficial effects of caloric restriction. Caloric restriction enhanced the transcripts of genes involved in reactive oxygen free radical scavenging function, tissue development and energy metabolism while decreasing expression of those genes involved in signal transduction, stress response, structural and contractile proteins. Real-time PCR measurments confirmed the changes in transcript levels of cytochrome c oxidase III, superoxide dismutase (SOD) 1 and 2 noted by the microarray approach. Mitochondrial ATP production and citrate synthase were unaltered by the dietary changes. We conclude that CR alters transcript levels of several genes in skeletal muscle and that mitochondrial function in skeletal muscle remains unaltered by the dietary intervention. Alterations in transcripts of many genes involved in reactive oxygen scavenging function may contribute to the increase in longevity reported with CR.
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