Institute of Molecular Medicine, Max-Planck-Research-Department on Stem Cell Aging, Ulm University, Ulm, Germany.
Cell Cycle. 2010 Oct 15;9(20):4058-60. doi: 10.4161/cc.9.20.13577. Epub 2010 Oct 10.
The free radical theory of aging sustains that reactive oxygen species (ROS) induce cellular damage limiting organismal fitness but experimental data do not clearly support this hypothesis. Mouse models have shown that severe alterations of ROS metabolism can result in impairments of organ homeostasis and premature organ failure. However, partial impairments in anti-oxidants defence did not influence the aging process in laboratory mice and most clinical studies on antioxidants treatments in humans failed to show clear beneficial effects. Studies dysfunction in accelerating aging. Together, it seems that mild increases of ROS levels do not significantly influence the natural rate of aging. There is even some evidence that ROS induction is required to mediate positive effects of calorie restriction and physical exercise on organismal fitness and longevity.
衰老的自由基理论认为,活性氧(ROS)会引起细胞损伤,从而限制生物体的适应能力,但实验数据并不清楚支持这一假说。小鼠模型表明,ROS 代谢的严重改变可能导致器官稳态受损和过早的器官衰竭。然而,抗氧化剂防御的部分损伤并没有影响实验室小鼠的衰老过程,大多数关于人类抗氧化剂治疗的临床研究也未能显示出明确的有益效果。研究表明,ROS 诱导与加速衰老有关。总的来说,ROS 水平的轻微升高似乎不会显著影响自然衰老的速度。甚至有一些证据表明,ROS 的诱导是必需的,以介导热量限制和体育锻炼对生物体适应性和长寿的积极影响。