Document Detail


The nature and mechanism of superoxide production by the electron transport chain: Its relevance to aging.
MedLine Citation:
PMID:  23604868     Owner:  NLM     Status:  PubMed-not-MEDLINE    
Abstract/OtherAbstract:
Most biogerontologists agree that oxygen (and nitrogen) free radicals play a 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 been reported 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 (as 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 of the 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.
Authors:
F Muller
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Journal of the American Aging Association     Volume:  23     ISSN:  2152-4041     ISO Abbreviation:  J Am Aging Assoc     Publication Date:  2000 Oct 
Date Detail:
Created Date:  2013-04-22     Completed Date:  2013-04-23     Revised Date:  2013-04-29    
Medline Journal Info:
Nlm Unique ID:  100964172     Medline TA:  J Am Aging Assoc     Country:  United States    
Other Details:
Languages:  eng     Pagination:  227-53     Citation Subset:  -    
Affiliation:
Laboratory of David M. Kramer, Institute of Biological Chemistry, Washington State University, Pullman, WA 99164 USA.
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