Caloric restriction or catalase inactivation extends yeast chronological lifespan by inducing H2O2 and superoxide dismutase activity
Caloric restriction or catalase inactivation extends yeast chronological lifespan by inducing H2O2 and superoxide dismutase activity
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DOI：
10.1073/pnas.1004432107
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发表时间：
2010-08-24
影响因子：
11.1
通讯作者：
Ludovico, Paula
中科院分区：
文献类型：
--
作者：
Mesquita, Ana;Weinberger, Martin;Ludovico, Paula
衰老的自由基理论假定大分子的氧化损伤是寿命的主要决定因素。最近的研究挑战了这一理论，证明在某些情况下，长寿是通过氧化应激防御的失活而增强的，或者与增加而不是减少活性氧和氧化损伤有关。在这里，我们表明，在酿酒酵母，热量限制或失活的过氧化氢酶延长时间寿命诱导水平升高的活性氧物种过氧化氢，激活超氧化物歧化酶，抑制超氧阴离子的积累。过氧化氢酶缺乏细胞中过氧化氢的增加延长了时间寿命，尽管氧化损伤平行增加。这些发现确立了过氧化氢的兴奋效应在促进寿命方面的作用，这对理解衰老和与年龄相关的疾病具有广泛的意义。
The free radical theory of aging posits oxidative damage to macromolecules as a primary determinant of lifespan. Recent studies challenge this theory by demonstrating that in some cases, longevity is enhanced by inactivation of oxidative stress defenses or is correlated with increased, rather than decreased reactive oxygen species and oxidative damage. Here we show that, in Saccharomyces cerevisiae, caloric restriction or inactivation of catalases extends chronological lifespan by inducing elevated levels of the reactive oxygen species hydrogen peroxide, which activate superoxide dismutases that inhibit the accumulation of superoxide anions. Increased hydrogen peroxide in catalase-deficient cells extends chronological lifespan despite parallel increases in oxidative damage. These findings establish a role for hormesis effects of hydrogen peroxide in promoting longevity that have broad implications for understanding aging and age-related diseases.