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衰老过程中的线粒体衰退

Mitochondrial decay in aging.

作者信息

Ames B N, Shigenaga M K, Hagen T M

机构信息

Division of Biochemistry and Molecular Biology, University of California, Berkeley, CA 94720-3202, USA.

出版信息

Biochim Biophys Acta. 1995 May 24;1271(1):165-70. doi: 10.1016/0925-4439(95)00024-x.

DOI:10.1016/0925-4439(95)00024-x
PMID:7599204
Abstract

Several mitochondrial functions decline with age. The contributing factors include, the intrinsic rate of proton leakage across the inner mitochondrial membrane (a correlate of oxidant formation), decreased membrane fluidity, and decreased levels and function of cardiolipin, which supports the function of many of the proteins of the inner mitochondrial membrane. Oxidants generated by mitochondria appear to be the major source of the oxidative lesions that accumulate with age. Evidence supports the suggestion that age-associated accumulation of mitochondrial deficits due to oxidative damage is likely to be a major contributor to cellular, tissue, and organismal aging.

摘要

随着年龄增长,多种线粒体功能会衰退。促成因素包括:质子跨线粒体内膜泄漏的固有速率(与氧化剂形成相关)、膜流动性降低、心磷脂水平及功能下降,心磷脂可支持线粒体内膜许多蛋白质的功能。线粒体产生的氧化剂似乎是随年龄积累的氧化损伤的主要来源。有证据支持以下观点:由于氧化损伤导致的与年龄相关的线粒体缺陷积累很可能是细胞、组织和机体衰老的主要原因。

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