氧化应激、线粒体与线粒体DNA突变小鼠
Oxidative stress, mitochondria and mtDNA-mutator mice.
作者信息
Thompson LaDora V
机构信息
Department of Physical Medicine and Rehabilitation, University of Minnesota, 420 Delaware Street, S.E., Minneapolis, MN 55455, USA.
出版信息
Exp Gerontol. 2006 Dec;41(12):1220-2. doi: 10.1016/j.exger.2006.10.018. Epub 2006 Nov 28.
The oxidative stress theory of aging, an expansion of the mitochondrial theory of aging, is based around the idea of a vicious cycle, in which somatic mutations of mitochondrial DNA (mtDNA) provoke respiratory chain dysfunction leading to enhanced ROS production and in turn to the accumulation of further mtDNA mutations. Mitochondrial dysfunction and mtDNA mutations are amplified during the course of aging. Recently, results obtained from mtDNA-mutator mice further strengthen the role of mitochondria in the aging process. However, lack of increased oxidative stress in the mtDNA-mutator mice raises doubts in the direct connection of mtDNA mutations with increased ROS production, challenging the oxidative stress theory of aging. The purpose of this short review is to highlight several studies that provide direct evidence that accelerated aging is linked to mtDNA mutations, without an increase in oxidative damage.
衰老的氧化应激理论是线粒体衰老理论的扩展，它基于一个恶性循环的概念，即线粒体DNA（mtDNA）的体细胞突变引发呼吸链功能障碍，导致活性氧（ROS）生成增加，进而导致更多mtDNA突变的积累。线粒体功能障碍和mtDNA突变在衰老过程中会不断放大。最近，从mtDNA突变小鼠获得的结果进一步强化了线粒体在衰老过程中的作用。然而，mtDNA突变小鼠中氧化应激并未增加，这让人对mtDNA突变与ROS生成增加之间的直接联系产生怀疑，从而对衰老的氧化应激理论提出了挑战。这篇简短综述的目的是强调几项研究，这些研究提供了直接证据，表明加速衰老与mtDNA突变有关，而氧化损伤并未增加。
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