Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1982-1-28
pubmed:abstractText
Isolated rabbit heart mitochondria were incubated with varying amounts of inorganic pyrophosphate in 250 mM sucrose to specifically decrease the pool size of endogenous adenine nucleotides. The endogenous adenine nucleotide content decreased by as much as 80% as a result of this treatment. Phosphorylating respiration (state 3) declined from about 340 to 180 nAtoms O . min-1 . mg protein-1 over the full range of intramitochondrial adenine nucleotides measured (approx 7.5-1.5 nmol/mg protein). Uncoupled and nonphosphorylating (state 4) rates of respiration were not greatly affected by adenine nucleotide depletion. Respiratory activity of the adenine nucleotide-depleted mitochondria was enhanced by addition of exogenous adenosine 5'-triphosphate (ATP). Partial depletion (approx 40%) of the intramitochondrial adenine nucleotides resulted in an impaired ability of heart mitochondria to retain Ca2+. Premature Ca2+ efflux was associated with organelle swelling and altered energy coupling. Exogenous ATP or adenosine 5'-diphosphate (ADP) added prior to Ca2+ efflux restored Ca2+ retention in these mitochondria. Atractyloside inhibited the restoration of Ca2+ retention. This study indicates a significant role for endogenous adenine nucleotides in maintaining oxidative phosphorylation and Ca2+ transport in heart mitochondria. The results are discussed with regard to significance in ischemic heart damage.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
241
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H672-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1981
pubmed:articleTitle
Intramitochondrial adenine nucleotides and energy-linked functions of heart mitochondria.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.