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PMID: 7599204 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S. Review

Mitochondrial decay in aging.

Biochimica et biophysica acta ·Vol. 1271 ·No. 1 ·1995-05-24 ·Pages 165-70

Ames BN, Shigenaga MK, Hagen TM

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.

MeSH Terms
Aging/metabolism Animals Brain/growth & development,metabolism DNA Damage DNA, Mitochondrial/genetics,metabolism Humans Lipid Metabolism Liver/growth & development Male Mitochondria/metabolism,physiology Mitochondria, Liver/metabolism Mutation Proteins/metabolism Rats Rats, Inbred F344
Chemicals
DNA, Mitochondrial Proteins
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Ames B N
Division of Biochemistry and Molecular Biology, University of California, Berkeley, CA 94720-3202, USA.
Shigenaga M K
Hagen T M
Article Info
Journal
Biochimica et biophysica acta
Abbr.
Biochim Biophys Acta
ISSN
0006-3002
Published
1995-05-24
Pages
165-70
Language
English
Region
Netherlands
NLM ID
0217513
Subset
IM
Grants
NCI NIH HHS · CA39910 · United States
NIEHS NIH HHS · ESO1896 · United States
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