Floyd R A, West M, Hensley K
Free Radical Biology and Aging Research Program, Oklahoma Medical Research Foundation, 825 NE 13th Street, Oklahoma City, OK 73104, USA.
Exp Gerontol. 2001 Apr;36(4-6):619-40. doi: 10.1016/s0531-5565(00)00231-x.
Clues as to why long-lived species live so much longer than short-lived species may reside in the amount of reactive oxygen species (ROS) produced and their effect on damaging cell components (especially proteins) and alterations of crucial cellular processes. Rigorous evaluation of these concepts required critical comparisons of oxidative damage markers and/or parameters with assess difference in ROS flux and the critical age-modifying processes they influence. The limited experimental comparative results available implicate that ROS production per unit weight of total oxygen consumed is much less in the longer-lived species than in shorter-lived species. Mitochondria are the major site of ROS production. They are also the functional nexus for intracellular signaling thus modulating stress and growth factor mediated cellular survival, proliferation and apoptotic processes. Mitochondrial DNA mutations, perhaps caused by ROS, increase with age. Mutant mitochondria possess comparative replicative advantage, which leads to age-specific intracellular swarms. General inflammatory stress tends to increase with age. Disruption in coordinated cell-to-cell signaling triggered by alterations in intracellular signaling may be the basis of the age-related increases in tissue inflammation, which may explain some of the differences between long-lived species and short-lived species.
关于长寿物种为何比短寿物种寿命长得多的线索，可能在于活性氧（ROS）的产生量及其对细胞成分（尤其是蛋白质）的损伤作用以及关键细胞过程的改变。对这些概念进行严格评估需要对氧化损伤标志物和/或参数进行关键比较，以评估ROS通量的差异以及它们所影响的关键年龄修饰过程。现有的有限实验比较结果表明，长寿物种每消耗单位重量总氧气所产生的ROS比短寿物种少得多。线粒体是ROS产生的主要部位。它们也是细胞内信号传导的功能枢纽，从而调节应激和生长因子介导的细胞存活、增殖和凋亡过程。线粒体DNA突变（可能由ROS引起）随年龄增长而增加。突变的线粒体具有相对复制优势，这导致特定年龄的细胞内群体形成。一般炎症应激往往随年龄增长而增加。细胞内信号改变引发的细胞间信号协调破坏可能是与年龄相关的组织炎症增加的基础，这可能解释了长寿物种和短寿物种之间的一些差异。
