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Titolo:
The nature and mechanism of superoxide production by the electron transport chain: Its relevance to aging
Autore:
Muller, F;
Indirizzi:
Washington State Univ, Inst Biol Chem, Lab David M Kramer, Pullman, WA 99164 USA Washington State Univ Pullman WA USA 99164 Kramer, Pullman, WA 99164 USA
Titolo Testata:
JOURNAL OF THE AMERICAN AGING ASSOCIATION
fascicolo: 4, volume: 23, anno: 2000,
pagine: 227 - 253
Fonte:
ISI
Lingua:
ENG
Soggetto:
FREE-RADICAL PRODUCTION; MITOCHONDRIAL RESPIRATORY-CHAIN; NADH-UBIQUINONE OXIDOREDUCTASE; CYTOCHROME BC(1) COMPLEX; MAXIMUM LIFE-SPAN; TRANSGENIC DROSOPHILA-MELANOGASTER; OXIDATION-REDUCTION POTENTIALS; HYDROGEN-PEROXIDE PRODUCTION; BOVINE HEART-MITOCHONDRIA; GENE-KNOCKOUT MICE;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
186
Recensione:
Indirizzi per estratti:
Indirizzo: Muller, F Washington State Univ, Inst Biol Chem, Lab David M Kramer, Pullman, WA 99164 USA Washington State Univ Pullman WA USA 99164 ullman, WA 99164 USA
Citazione:
F. Muller, "The nature and mechanism of superoxide production by the electron transport chain: Its relevance to aging", J AM AGING, 23(4), 2000, pp. 227-253

Abstract

Most biogerontologists agree that oxygen land nitrogen) free radicals playa major role in the process of aging. The evidence strongly suggests that the electron transport chain, located in the inner mitochondrial membrane, is the major source of reactive oxygen species in animal cells. It has beenreported that there exists an inverse correlation between the rate of superoxide/hydrogen peroxide production by mitochondria and the maximum longevity of mammalian species. However, no correlation or most frequently an inverse correlation exists between the amount of antioxidant enzymes and maximum longevity. Although overexpression of the antioxidant enzymes SOD1 and CAT las well as SOD1 alone) have been successful at extending maximum lifespan in. Drosophila, this has not been the case in mice. Several labs have overexpressed SOD1 and failed to see a positive effect on longevity. An explanation for this failure is that there is some level of superoxide damage that is not preventable by SOD, such as that initiated by the hydroperoxyl radical inside the lipid bilayer, and that accumulation of this damage is responsible for aging. I therefore suggest an alternative approach to testing the free radical theory of aging in mammals. Instead of trying to increase the amount of antioxidant enzymes, I suggest using molecular biology/transgenics to decrease the rate of superoxide production, which in the context ofthe free radical theory of aging would be expected to increase longevity. This paper aims to summarize what is known about the nature and mechanisms of superoxide production and what genes are involved in controlling the rate of superoxide production.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 15:18:04