Mitochondrial decay in aging.
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.
Ames
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Division of Biochemistry and Molecular Biology, University of California, Berkeley, CA 94720-3202, USA.
Shigenaga
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MK
Hagen
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D000375:Aging / Q000378:metabolism*; D000818:Animals; D001921:Brain / Q000254:growth & development / Q000378:metabolism; D004249:DNA Damage; D004272:DNA, Mitochondrial / Q000235:genetics* / Q000378:metabolism; D006801:Humans; D050356:Lipid Metabolism; D008099:Liver / Q000254:growth & development; D008297:Male; D008928:Mitochondria / Q000378:metabolism* / Q000502:physiology; D008930:Mitochondria, Liver / Q000378:metabolism; D009154:Mutation; D011506:Proteins / Q000378:metabolism; D051381:Rats; D011916:Rats, Inbred F344
D004272:DNA, Mitochondrial; D011506:Proteins