Department of Experimental Medicine, University of Lleida-IRBLleida, Lleida, 25008, Spain.
Biogerontology. 2011 Oct;12(5):409-35. doi: 10.1007/s10522-011-9348-1. Epub 2011 Jul 14.
Key mechanisms relating oxidative stress to longevity from an interespecies comparative approach are reviewed. Long-lived animal species show low rates of reactive oxygen species (ROS) generation and oxidative damage at their mitochondria. Comparative physiology also shows that the specific compositional pattern of tissue macromolecules (proteins, lipids and nucleic acids) in long-lived animal species gives them an intrinsically high resistance to modification that likely contributes to their superior longevity. This is obtained in the case of lipids by decreasing the degree of fatty acid unsaturation, and in the case of proteins by lowering their methionine content. These findings are also substantiated from a phylogenomic approach. Nutritional or/and pharmacological interventions focused to modify some of these molecular traits were translated with modifications in animal longevity. It is proposed that natural selection tends to decrease the mitochondrial ROS generation and to increase the molecular resistance to the oxidative damage in long-lived species.
从种间比较的角度综述了与长寿相关的氧化应激的关键机制。长寿动物的线粒体产生的活性氧（ROS）和氧化损伤的速率较低。比较生理学还表明，长寿动物组织大分子（蛋白质、脂质和核酸）的特定组成模式使它们具有内在的高抗修饰性，这可能有助于它们的卓越长寿。在脂质的情况下，这是通过降低脂肪酸不饱和程度来实现的，而在蛋白质的情况下，这是通过降低其蛋氨酸含量来实现的。这些发现也从系统基因组学的角度得到了证实。营养或/和药理学干预的重点是改变这些分子特征中的一些，这些干预措施已在动物的寿命上得到了修正。有人提出，自然选择倾向于降低线粒体 ROS 的产生，并增加长寿物种对氧化损伤的分子抵抗力。
