Linked Life Data

7599204

Source:http://linkedlifedata.com/resource/pubmed/id/7599204

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1995-8-7
pubmed:abstractText
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0006-3002
pubmed:author
pubmed:issnType
Print
pubmed:day
24
pubmed:volume
1271
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
165-70
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Mitochondrial decay in aging.
pubmed:affiliation
Division of Biochemistry and Molecular Biology, University of California, Berkeley, CA 94720-3202, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review