Linked Life Data

16831573

Source:http://linkedlifedata.com/resource/pubmed/id/16831573

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2006-10-2
pubmed:abstractText
This review addresses the data that support the presence and contribution of decreased mitochondrial oxidative phosphorylation during aging to impaired cellular metabolism. Aging impairs substrate oxidation, decreases cellular energy production and increases the production of reactive intermediates that are toxic to the cell. First, the basic principles of mitochondrial oxidative physiology are briefly reviewed. Second, the focus on the relationship of altered mitochondrial respiration to the increased production of reactive oxygen species that are employed by the "rate of living" and the "uncoupling to survive" theories of aging are discussed. Third, the impairment of function of respiration in aging is reviewed using an organ-based approach in mammalian systems. Fourth, the current state of knowledge regarding aging-induced alterations in the composition and function of key mitochondrial constituents is addressed. Model organisms, including C. elegans and D. melanogaster are included where pertinent. Fifth, these defects are related to knowledge regarding the production of reactive oxygen species from specific sites of the electron transport chain.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1568-1637
pubmed:author
pubmed:issnType
Print
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
402-33
pubmed:dateRevised
2008-9-3
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Oxidative phosphorylation and aging.
pubmed:affiliation
Department of Medicine, Division of Cardiology, Case Western Reserve University, Cleveland, OH, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Review, Research Support, N.I.H., Extramural