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This version published online on May 26, 2005
Endocrinology, doi:10.1210/en.2005-0378
A more recent version of this article appeared on September 1, 2005
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Submitted on March 31, 2005
Accepted on May 10, 2005

The Role of Oxidative Stress in relation to Caloric Restriction and Longevity

Ricardo Gredilla and Gustavo Barja*

Department of Animal Physiology-II, Faculty of Biology, Complutense University, Madrid 28040, Spain

* To whom correspondence should be addressed. E-mail: barja{at}bio.ucm.es.

Reduction of the caloric intake without malnutrition is one of the most consistent experimental interventions increasing mean and maximum life span in different species. For over seventy years caloric restriction has been studied, and during the last years the number of investigations on such nutritional intervention and aging has dramatically increased. Since caloric restriction decreases the aging rate, it constitutes an excellent approach to better understand the mechanisms underlying the aging process. Different investigations have reported reductions in steady-state oxidative damage to proteins, lipids and DNA in animals subjected to restricted caloric intake. Most interestingly, several investigations have reported that these decreases in oxidative damage are related to a lowering of mitochondrial free radical generation rate in different tissues of the restricted animals. Thus, similarly to what has been described for long-lived animals in comparative studies, a decrease in mitochondrial free radical generation has been suggested to be one of the main determinants of the extended life span observed in restricted animals. Here we review recent studies on caloric restriction and longevity, focusing on mitochondrial oxidative stress and the proposed mechanisms leading to an extended longevity in caloric restricted animals.


Key words: Caloric restriction • longevity • mitochondria




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