线粒体是细胞中的发电厂——能量产生单元。以前的研究发现，在人和小鼠体内，线粒体点变异在老化过程中积累。如今，研究人员在本周在线出版的《自然—遗传学》中报道说，小鼠体内大量的线粒体点变异与其老化过程没有直接关系，新发现与“线粒体点变异是老化过程诱导因素”的传统观点相矛盾。
死亡原理中的线粒体理论是一个颇有争议的理论，这个理论认为，与生命期相当的线粒体DNA变异与衰老过程中观察到的组织功能衰落有关。Lawrence Loeb和同事使用一种全新的、高度敏感的方法来确定在小鼠的正常老化过程中，线粒体DNA中以单个碱基对为基础的变异速度，以及在线粒体变异小鼠体内线粒体的点变异速度。线粒体变异小鼠线粒体点变异量是正常小鼠的500倍。
研究人员发现，随着年龄的增长，正常小鼠的线粒体点变异增加了11倍，而线粒体变异小鼠却没有表现出随着年龄增长的明显特征。
特别需要指出的是，新研究并没有排除线粒体DNA的大量剔除与老化的关系。比如，以前的研究显示，线粒体DNA中的大量剔除与老年人和帕金森氏症患者的某种神经元损害有关。
部分英文原文：
Published online: 4 March 2007; | doi:10.1038/ng1988
Mitochondrial point mutations do not limit the natural lifespan of mice
Marc Vermulst1, Jason H Bielas1, Gregory C Kujoth2, Warren C Ladiges3, Peter S Rabinovitch1, Tomas A Prolla2 & Lawrence A Loeb1
1 Department of Pathology, University of Washington, Seattle, Washington 91895, USA.
2 Departments of Genetics and Medical Genetics, University of Wisconsin, Madison, Wisconsin 53706, USA.
3 Department of Comparative Medicine, University of Washington, Seattle, Washington 98195, USA.
Correspondence should be addressed to Lawrence A Loeb laloeb@u.washington.edu
Whether mitochondrial mutations cause mammalian aging, or are merely correlated with it, is an area of intense debate1. Here, we use a new, highly sensitive assay2 to redefine the relationship between mitochondrial mutations and age. We measured the in vivo rate of change of the mitochondrial genome at a single–base pair level in mice, and we demonstrate that the mutation frequency in mouse mitochondria is more than ten times lower than previously reported. Although we observed an 11-fold increase in mitochondrial point mutations with age, we report that a mitochondrial mutator mouse3 was able to sustain a 500-fold higher mutation burden than normal mice, without any obvious features of rapidly accelerated aging. Thus, our results strongly indicate that mitochondrial mutations do not limit the lifespan of wild-type mice.
