Linked Life Data

7109706

Source:http://linkedlifedata.com/resource/pubmed/id/7109706

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1982-10-21
pubmed:abstractText
Both the rate of uptake of Ca2+ into isolated rat heart mitochondria and the rate of release of Ca2+ by a separate, Na+-dependent, pathway were shown to be diminished in senescence (24-month relative to 6-month animal). These processes were studied at lower concentrations of Ca2+ and loads of Ca2+ per mg of mitochondrial protein than those generally employed, and it is argued that these are more appropriate physiologically. In addition, Ca2+ release was characterized in terms of the sum of the added Ca2+ and the endogenous Ca2+ of the mitochondrial preparation; the endogenous Ca2+ content was found to be unchanged with age. The decrements in rates of transport are not caused by altered rates of substrate oxidation and are inferred to reflect decreased carrier-protein content or activity. The buffering of extramitochondrial free Ca2+ concentration by heart mitochondria was studied and found to be less than complete at mitochondrial Ca2+ loads inferred to be physiological. No change was shown in senescence, in keeping with the essentially equal age-linked decrements in the activity of mitochondrial Ca2+ uptake and release.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0047-6374
pubmed:author
pubmed:issnType
Print
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5-13
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1982
pubmed:articleTitle
Effect of senescence on Ca2+-ion transport by heart mitochondria.
pubmed:publicationType
Journal Article, In Vitro