Oxidative damage and mitochondrial decay in aging.

M K Shigenaga, T M Hagen, B N Ames

doi:10.1073/pnas.91.23.10771

Oxidative damage and mitochondrial decay in aging.

DOI Web Site 被引用文献58件

M K Shigenaga

Division of Biochemistry and Molecular Biology, University of California, Berkeley 94720.
T M Hagen

Division of Biochemistry and Molecular Biology, University of California, Berkeley 94720.
B N Ames

Division of Biochemistry and Molecular Biology, University of California, Berkeley 94720.

抄録

<jats:p>We argue for the critical role of oxidative damage in causing the mitochondrial dysfunction of aging. Oxidants generated by mitochondria appear to be the major source of the oxidative lesions that accumulate with age. 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. Acetyl-L-carnitine, a high-energy mitochondrial substrate, appears to reverse many age-associated deficits in cellular function, in part by increasing cellular ATP production. Such 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.</jats:p>

収録刊行物

Proceedings of the National Academy of Sciences

Proceedings of the National Academy of Sciences 91 (23), 10771-10778, 1994-11-08

Proceedings of the National Academy of Sciences