The relationship between oxidants and organismal aging was first articulated through the free radical theory of aging. One of the major predictions of the free radical theory of aging is that oxidative stress shortens organisms' lifespan because of an increased level of oxidants, which are damaging to macromolecules. However, challenging the role of oxidants in age-related diseases, there is now sufficient evidence that antioxidant supplements do not provide significant health benefits. Interestingly, in addition to an increase in oxidant-mediated macromolecules damage, there is convincing experimental data to support the role of senescent cells in the process of aging. Here, the current knowledge regarding the role of oxidants and cellular senescence in organismal aging is reviewed and it is proposed that, in addition to the role of oxidants as inducers of macromolecular damage, oxidants may also function as regulators of signaling pathways involved in the establishment of cellular senescence. If this role for oxidants is established, it may be necessary to modify the free radical theory of aging from "Organisms age because cells accumulate reactive oxygen species-dependent damage over time" to: "Organisms age because cells accumulate oxidants'-dependent damage and oxidants'-dependent senescent characteristics over time."

中文翻译：

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超出大分子损害的生物衰老和氧化剂。

氧化剂与机体衰老之间的关系首先是通过自由基衰老理论阐明的。自由基衰老理论的主要预测之一是，氧化应激会缩短生物的寿命，这是因为氧化剂的含量增加，会对大分子造成破坏。然而，挑战氧化剂在与年龄有关的疾病中的作用，现在有充分的证据表明抗氧化剂补充剂并不能提供明显的健康益处。有趣的是，除了增加氧化剂介导的大分子损伤外，还有令人信服的实验数据来支持衰老细胞在衰老过程中的作用。在此，回顾了有关氧化剂和细胞衰老在生物衰老中的作用的当前知识，并提出，除了氧化剂作为大分子损伤的诱导剂外，氧化剂还可以充当细胞衰老建立过程中信号通路的调节剂。如果确立了氧化剂的这种作用，则可能有必要将自由基的衰老理论从“有机物的衰老，因为细胞随时间积累了依赖活性氧的损伤”改为：“有机物的衰老，因为细胞在积累氧化剂的依赖时的损害，随着时间的推移，氧化剂的衰老特性将随之而来。”