Longevity and the genetic determination of collagen glycoxidation kinetics in mammalian senescence
Longevity and the genetic determination of collagen glycoxidation kinetics in mammalian senescence
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DOI：
10.1073/pnas.93.1.485
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发表时间：
1996-01-09
影响因子：
11.1
通讯作者：
Monnier, VM
中科院分区：
文献类型：
--
作者：
Sell, DR;Lane, MA;Monnier, VM
衰老的基础生物学中的一个基本问题是是否存在普遍的衰老过程。如果确实存在这样的过程，人们会期望它在短寿命物种与长寿命物种中以更高的速率发展，我们已经定量了pentosidine，作为年龄函数的八种哺乳动物皮肤胶原蛋白中糖氧化应激的标志物。所有物种的曲线增长，增长率与最大寿命呈负相关。饮食限制是一种与寿命延长相关的有效干预措施，可显著抑制啮齿动物的糖氧化率。假设胶原蛋白周转率主要受糖基化引起的交联的影响，这些结果表明，控制胶原蛋白糖基化速率的过程存在与年龄相关的进行性恶化，因此，承受糖基化和美拉德反应引起的损伤的能力可能受遗传控制。
A fundamental question in the basic biology of aging is whether there is a universal aging process. If indeed such a process exists, one would expect that it develops at a higher rate in short- versus long-lived species, We have quantitated pentosidine, a marker of glycoxidative stress in skin collagen from eight mammalian species as a function of age. A curvilinear increase was modeled for all species, and the rate of increase correlated inversely with maximum life-span. Dietary restriction, a potent intervention associated with increased life-span, markedly inhibited glycoxidation rate in the rodent. On the assumption that collagen turnover rate is primarily influenced by the crosslinking due to glycoxidation, these results suggest that there is a progressive age-related deterioration of the process that controls the collagen glycoxidation rate, Thus, the ability to withstand damage due to glycoxidation and the Maillard reaction may be under genetic control.