Life History Trade-offs within the Context of Mitochondrial Hormesis

Life History Trade-offs within the Context of Mitochondrial Hormesis
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DOI:
10.1093/icb/icy073
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发表时间:
2018-09-01
影响因子:
2.6
通讯作者:
Kavazis, A. N.
Kavazis, A. N.
中科院分区:
生物学2区
文献类型:
--
作者:
Hood, W. R.;Zhang, Y.;Kavazis, A. N.

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近一个世纪以来,进化生物学家一直对生活史特征之间的负面相互作用感兴趣,但造成这种负面相互作用的机制仍然知之甚少。氧化应激是生殖努力与寿命之间可能存在联系的一个变量。具体来说,有人提出,繁殖会产生自由基,自由基会引起氧化应激,反过来,氧化应激会损害细胞成分并加速衰老。我们认为该假说的支持有限,因为活性氧(ROS),即与氧化损伤有关的自由基,并不总是有害的。通过这篇综述,我们定义了线粒体对 ROS 的毒物兴奋反应,称为线粒体毒物兴奋作用,并描述了如何测试线粒体毒物兴奋反应。我们使用我们的模型解释现有数据,并提出实验操作将进一步提高我们对这种反应的了解。最后,我们假设线粒体激素反应曲线如何应用于动物性能和寿命的变化。
Evolutionary biologists have been interested in the negative interactions among life history traits for nearly a century, but the mechanisms that would create this negative interaction remain poorly understood. One variable that has emerged as a likely link between reproductive effort and longevity is oxidative stress. Specifically, it has been proposed that reproduction generates free radicals that cause oxidative stress and, in turn, oxidative stress damages cellular components and accelerates senescence. We propose that there is limited support for the hypothesis because reactive oxygen species (ROS), the free radicals implicated in oxidative damage, are not consistently harmful. With this review, we define the hormetic response of mitochondria to ROS, termed mitochondrial hormesis, and describe how to test for a mitohormetic response. We interpret existing data using our model and propose that experimental manipulations will further improve our knowledge of this response. Finally, we postulate how the mitohormetic response curve applies to variation in animal performance and longevity.