Gredilla Ricardo, Barja Gustavo
Department of Animal Physiology-II, Faculty of Biology, Complutense University, Madrid, Spain.
Endocrinology. 2005 Sep;146(9):3713-7. doi: 10.1210/en.2005-0378. Epub 2005 May 26.
Reduction of caloric intake without malnutrition is one of the most consistent experimental interventions that increases mean and maximum life spans in different species. For over 70 yr, caloric restriction has been studied, and during the last years the number of investigations on such nutritional intervention and aging has dramatically increased. Because caloric restriction decreases the aging rate, it constitutes an excellent approach to better understand the mechanisms underlying the aging process. Various 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 various tissues of the restricted animals. Thus, similar 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. In this study we review recent reports of caloric restriction and longevity, focusing on mitochondrial oxidative stress and the proposed mechanisms leading to an extended longevity in calorie-restricted animals.
在不造成营养不良的情况下减少热量摄入，是在不同物种中延长平均寿命和最大寿命最可靠的实验性干预措施之一。七十多年来，人们一直在研究热量限制，在过去几年里，关于这种营养干预与衰老的研究数量急剧增加。由于热量限制能降低衰老速度，所以它是深入了解衰老过程潜在机制的绝佳方法。多项研究报告称，热量摄入受限的动物体内，蛋白质、脂质和DNA的稳态氧化损伤有所减少。最有意思的是，多项研究报告指出，这些氧化损伤的减少与热量受限动物各组织中线粒体自由基生成速率的降低有关。因此，正如在比较研究中对长寿动物所描述的那样，线粒体自由基生成的减少被认为是热量受限动物寿命延长的主要决定因素之一。在本研究中，我们回顾了近期关于热量限制与长寿的报告，重点关注线粒体氧化应激以及热量受限动物寿命延长的潜在机制。
