Cutler R G
Proc Natl Acad Sci U S A. 1985 Jul;82(14):4798-802. doi: 10.1073/pnas.82.14.4798.
Peroxidation reactions may cause many of the dysfunctions associated with aging. Accordingly, the 30-fold differences in aging rate among the mammalian species could be determined in part by peroxidation defense processes. This possibility was tested by measuring the spontaneous autoxidation of aerobically incubated brain and kidney tissue homogenates of 24 different mammalian species as a function of their maximum lifespan potential. Results show a statistically significant inverse correlation between both the rate of autoxidation and the amount of peroxidizable substrate with maximum lifespan potential. Kinetic analysis of the data indicates that the amount of peroxidizable substrate was the major factor determining the rate of autoxidation. For human tissues, antioxidants also appear to contribute to their unusually low sensitivity to peroxidation. These results support the hypothesis that aging may be caused in part by oxygen radicals initiating peroxidation reactions and that peroxidation defense processes are involved in governing the longevity of mammalian species.
过氧化反应可能会导致许多与衰老相关的功能障碍。因此,哺乳动物物种之间30倍的衰老速度差异可能部分由过氧化防御过程决定。通过测量24种不同哺乳动物需氧培养的脑和肾组织匀浆的自发自氧化作用,并将其作为最大寿命潜能的函数,对这一可能性进行了测试。结果表明,自氧化速率和具有最大寿命潜能的可过氧化底物量之间存在统计学上显著的负相关。对数据的动力学分析表明,可过氧化底物的量是决定自氧化速率的主要因素。对于人体组织,抗氧化剂似乎也有助于其对过氧化的异常低敏感性。这些结果支持了这样一种假说,即衰老可能部分是由引发过氧化反应的氧自由基引起的,并且过氧化防御过程参与了控制哺乳动物物种的寿命。