Linked Life Data

14555229

Source:http://linkedlifedata.com/resource/pubmed/id/14555229

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2003-10-13
pubmed:abstractText
Nitric oxide (NO) is a physiological signalling molecule, however, at high concentrations NO is cytotoxic, and has been implicated in a wide range of inflammatory, ischaemic and degenerative diseases, including heart failure. We investigated whether NO or S-nitrosothiols can induce apoptosis in perfused heart, and whether it is mediated via the mitochondrial pathway of caspase activation. We found that perfusion of rat hearts with a physiological S-nitrosothiol, S-nitrosoglutathione, at 0.4-1mM concentrations for just 10 min caused the release of cytochrome c from mitochondria into the cytosol, inhibition of mitochondrial respiration and caspase activation. Inhibited mitochondrial respiration was restored when exogenous cytochrome c was added to mitochondria, indicating that respiratory inhibition was caused by lack of cytochrome c in mitochondria. Release of cytochrome c, respiratory inhibition and caspase activation were prevented when hearts were pre-perfused with cyclosporin A, suggesting that mitochondrial permeability transition pore was involved. In contrast, perfusion of the hearts with diethylenetriamine/NO adduct releasing similar levels of NO to the S-nitrosoglutathione had no measurable effect on the heart. These data suggest that S-nitrosothiols are potent inducers of apoptosis in the heart and that S-nitrosothiol-induced apoptosis is mediated by mitochondrial permeability transition but not via NO.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0006-2952
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
66
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1513-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
S-nitrosothiol-induced rapid cytochrome c release, caspase activation and mitochondrial permeability transition in perfused heart.
pubmed:affiliation
Institute for Biomedical Research, Kaunas University of Medicine, Kaunas, Lithuania.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't