ROS induced DNA damage and checkpoint responses Influences on aging?
ROS induced DNA damage and checkpoint responses Influences on aging?
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DOI：
10.4161/cc.9.20.13577
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发表时间：
2010-10-15
期刊：
影响因子：
4.3
通讯作者：
Rudolph, K. Lenhard
中科院分区：
文献类型：
--
作者：
Guachalla, Luis Miguel;Rudolph, K. Lenhard
衰老的自由基理论支持活性氧（ROS）诱导细胞损伤限制生物体适应性，但实验数据并不明确支持这一假设。小鼠模型表明，ROS代谢的严重改变可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，并且大多数关于人类抗氧化剂治疗的临床研究未能显示出明确的有益效果。对端粒功能障碍小鼠的研究也不能揭示ROS和端粒功能障碍在加速衰老中的协同作用。总之，ROS水平的轻度增加似乎不会显著影响自然衰老率。甚至有一些证据表明，ROS诱导需要介导热量限制和体育锻炼对有机体健康和长寿的积极影响。
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 on telomere dysfunctional mice could also not reveal cooperating effects of ROS and telomere 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.