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, 91 (23), 10771-8

Oxidative Damage and Mitochondrial Decay in Aging


Oxidative Damage and Mitochondrial Decay in Aging

M K Shigenaga et al. Proc Natl Acad Sci U S A.


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.

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    1. Ann N Y Acad Sci. 1989;568:225-33 - PubMed
    1. Brain Res. 1984 May 21;300(1):41-8 - PubMed
    1. FEBS Lett. 1990 Apr 9;263(1):73-6 - PubMed
    1. J Biol Chem. 1976 Nov 10;251(21):6683-91 - PubMed
    1. Biochemistry. 1993 May 11;32(18):4962-7 - PubMed

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