Linked Life Data

3123331

Source:http://linkedlifedata.com/resource/pubmed/id/3123331

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1988-2-26
pubmed:abstractText
Chelation by citrate was found to promote the autoxidation of Fe2+, measured as the disappearance of 1,10-phenanthroline-chelatable Fe2+. The autoxidation of citrate-Fe2+ could in turn promote the peroxidation of microsomal phospholipid liposomes, as judged by malondialdehyde formation. At low citrate-Fe2+ ratios the autoxidation of Fe2+ was slow and the formation of malondialdehyde was preceded by a lag phase. The lag phase was eliminated by increasing the citrate-Fe2+ ratio, which also increased the rate of Fe2+ autoxidation. The Fe2+ autoxidation product required for the initiation of lipid peroxidation was characterized as being Fe3+. As direct evidence of this, linear initial rates of lipid peroxidation were obtained via the combination of citrate-Fe2+ and citrate-Fe3+, optimum activity occurring at a Fe3+-Fe2+ ratio of 1:1. Evidence is also presented to suggest that the superoxide and the hydrogen peroxide that are formed during the autoxidation of citrate-Fe2+ can either stimulate or inhibit lipid peroxidation by affecting the yield of citrate-Fe3+ from citrate-Fe2+. No evidence was obtained for the participation of the hydroxyl radical in the initiation of lipid peroxidation by citrate-Fe2+.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0891-5849
pubmed:author
pubmed:issnType
Print
pubmed:volume
3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
379-87
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1987
pubmed:articleTitle
An investigation into the mechanism of citrate-Fe2+-dependent lipid peroxidation.
pubmed:affiliation
Department of Biochemistry, Michigan State University, East Lansing 48824-1319.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't