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本文将与年龄相关的蛋白质改变和DNA氧化称为“生物性衰老的公共机制”。氧化修饰的蛋白质和DNA随增龄而加剧,这一结论已在啮齿类动物中得到证实。通过调养可使老年动物蛋白质半衰期延长,DNA修复活动下降。在动物晚年限制饮食,可将蛋白质半衰期缩短降至年轻时的水平,从而降低老年动物体内变异蛋白质的水平。有规律的锻炼能减少大脑中氧化修饰的蛋白质,改善认知功能;还能缓解肝脏的氧化应激:改善NF-κB活性,增加还原型谷胱甘肽,并降低细胞核和线粒体DNA中的氧化鸟嘌呤。研究结果表明,有规律的运动对降低氧化应激有全身效应。因此,饮食控制和锻炼等生活方式能够扩大健康的范围,通过调节整体的抗氧能力(包括蛋白质转换和DNA修复),从而减少促使生理和病理性衰老的潜在受损蛋白质和DNA。
This article refers to age-related protein changes and DNA oxidation as a “public mechanism of biological aging.” Oxidatively modified proteins and DNA exacerbate as they age, a finding that has been confirmed in rodents. By nursed back to aging animal protein half-life extension, decreased DNA repair activity. Restricting diet in later life in animals can shorten the half-life of protein to a young age, thereby reducing the level of mutant proteins in older animals. Regular exercise reduces the oxidatively modified proteins in the brain and improves cognitive function. It also relieves oxidative stress in the liver: improves NF-κB activity, increases reduced glutathione, and reduces oxidation in the nucleus and mitochondrial DNA Guanine. The results show that regular exercise has a systemic effect on reducing oxidative stress. As a result, lifestyles such as dietary control and exercise can extend the reach of health by reducing the overall number of potentially damaging proteins and DNA that promote physiological and pathological aging by modulating the overall antioxidant capacity, including protein turnover and DNA repair.