Linked Life Data

11978493

Source:http://linkedlifedata.com/resource/pubmed/id/11978493

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2002-4-29
pubmed:abstractText
Transition metals such as iron and copper potentiate the postischemic reperfusion (I/R) injury induced by oxygen-derived radical and nonradical toxic species (ROS). Various natural and synthetic antioxidants have been previously tested to ameliorate such injury, yet the limitations of the common antioxidants are well known. An alternative strategy for combating oxidative damage is presented wherein cell-permeable, nitroxide stable radicals, which act as SOD-mimics and oxidize reduced metals thus prompting the Fenton-like chemistry, are investigated for utility in ameliorating I/R injury. Our study concentrates on the early effect of nitroxide on the myocardial I/R injury. Isolated rat hearts in the Langendorff configuration were equilibrated with Krebs-Henseleit buffer and then subjected to 18 min of normothermic global ischemia followed by 20 min reperfusion. Iron administered as Fe(III)-citrate (10 microM) did not affect the cardiac function under normoxia but did potentiate I/R injury and decreased the recovery during reperfusion. The iron-induced damage was manifested by further deterioration of the cardiac hemodynamic function and the energy status as reflected by decreased tissue level of phosphorylated nucleotides. Nitroxide at 200 microM protected against the iron-potentiated I/R injury by improving the recovery of the hemodynamic function and the cardiac energy status. Exogenously added iron requires bioreduction to form deleterious Fe(II) bound to critical cellular sites. The nitroxide, which enters the cell and oxidizes the reduced metal instantaneously, provided protection even when administered 2 or 3.5, but not 5 min, after the onset of reperfusion. Thus, its narrow therapeutic time window provides insight into the schedule of the I/R injurious process.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0891-5849
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
32
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
912-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11978493-Animals, pubmed-meshheading:11978493-Antioxidants, pubmed-meshheading:11978493-Chromatography, High Pressure Liquid, pubmed-meshheading:11978493-Cyclic N-Oxides, pubmed-meshheading:11978493-Drug Synergism, pubmed-meshheading:11978493-Ferric Compounds, pubmed-meshheading:11978493-Free Radical Scavengers, pubmed-meshheading:11978493-Heart, pubmed-meshheading:11978493-Male, pubmed-meshheading:11978493-Myocardial Reperfusion Injury, pubmed-meshheading:11978493-Myocardium, pubmed-meshheading:11978493-Nitrogen Oxides, pubmed-meshheading:11978493-Oxidation-Reduction, pubmed-meshheading:11978493-Oxidative Stress, pubmed-meshheading:11978493-Rats, pubmed-meshheading:11978493-Rats, Sprague-Dawley, pubmed-meshheading:11978493-Reactive Oxygen Species, pubmed-meshheading:11978493-Spin Labels, pubmed-meshheading:11978493-Time Factors
pubmed:year
2002
pubmed:articleTitle
Time window of nitroxide effect on myocardial ischemic-reperfusion injury potentiated by iron.
pubmed:affiliation
The Department of Cellular Biochemistry, The Hebrew University, Hadassah Medical School, Jerusalem, Israel.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't