Linked Life Data

1756028

Source:http://linkedlifedata.com/resource/pubmed/id/1756028

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1992-2-6
pubmed:abstractText
Reperfusion of the ischaemic or hypoxic heart elicits a number of oxygen dependent processes such as cell lysis and Ca2+ uptake. It is known that the energisation of mitochondria, which requires oxygen, plays a key role in these processes and that the organelle actively sequesters Ca2+ under these circumstances. In this brief review we discuss how oxidants derived from mitochondrial electron transport may perturb mitochondrial calcium handling on reoxygenation of the hypoxic myocardium. In addition we show that the immunosuppressive agent cyclosporin has little or no effect on the oxygen dependent increase in total cell Ca2+ which occurs when hypoxic myocytes are reoxygenated. This result suggests that the Ca2+ dependent mitochondrial pore, which is known to function under conditions of oxidative stress, does not play a major role in the perturbation of Ca2+ homeostasis which occurs on reoxygenation of hypoxic hearts.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0785-3890
pubmed:author
pubmed:issnType
Print
pubmed:volume
23
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
583-8
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Mitochondria, oxygen and reperfusion damage.
pubmed:affiliation
Department of Biochemical Sciences, Wellcome Research Laboratories, Beckenham, Kent U.K.
pubmed:publicationType
Journal Article, Review