Robb Ellen L, Page Melissa M, Stuart Jeffrey A
Department of Biological Sciences, Brock University, St. Catharines, Ontario, L2S 3A1, Canada.
Curr Aging Sci. 2009 Mar;2(1):12-27. doi: 10.2174/1874609810902010012.
The causes of aging and determinants of maximum lifespan in animal species are multifaceted and complex. However, a wealth of experimental data suggests that mitochondria are involved both in the aging process and in regulating lifespan. Here we outline a somatic cell depletion (SCD) model to account for correlations between: (1) mitochondrial reactive oxygen species and lifespan; (2) mitochondrial antioxidant enzymes and lifespan; (3) mitochondrial DNA mutation and lifespan and (4) cellular stress resistance and lifespan. We examine the available data from within the framework of the SCD model, in which mitochondrial dysfunction leading to cell death and gradual loss of essential somatic cells eventually contributes to the decline in physiological performance that limits lifespan. This model is useful in explaining many of the mitochondrial manipulations that alter maximum lifespan in a variety of animal species; however, there are a number of caveats and critical experiments outstanding, and these are outlined in this review.
动物物种衰老的原因及最大寿命的决定因素是多方面且复杂的。然而，大量实验数据表明，线粒体既参与衰老过程，也参与寿命调节。在此，我们概述一种体细胞耗竭（SCD）模型，以解释以下几方面之间的相关性：（1）线粒体活性氧与寿命；（2）线粒体抗氧化酶与寿命；（3）线粒体DNA突变与寿命；（4）细胞应激抗性与寿命。我们在SCD模型的框架内审视现有数据，在该模型中，线粒体功能障碍导致细胞死亡以及必需体细胞的逐渐丧失，最终导致生理机能下降，从而限制寿命。该模型有助于解释许多改变多种动物物种最大寿命的线粒体操作；然而，仍存在一些需要注意的问题和尚未完成的关键实验，本综述将对这些内容进行概述。
