Linked Life Data

8224243

Source:http://linkedlifedata.com/resource/pubmed/id/8224243

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1993-12-16
pubmed:abstractText
The effects of nitric oxide (.NO) and nitrovasodilators on the oxidation of low-density lipoprotein (LDL) have been studied. S-Nitroso-N-acetylpenicillamine (SNAP) and sodium nitroprusside (SNP) inhibited Cu(2+)- and 2,2'-azobis-2-amidinopropane hydrochloride-dependent oxidation of LDL as monitored by oxygen consumption and the formation of thiobarbituric acid-reactive substances, conjugated dienes, and lipid hydroperoxides. In the case of SNP, inhibition of LDL oxidation occurred only when the incubation mixture was irradiated with visible light. SNAP, however, exerted a dose-dependent inhibition of Cu(2+)-catalyzed oxidation of LDL even in the dark. Addition of .NO dissolved in deoxygenated buffer also inhibited the progression of LDL oxidation. Mouse peritoneal macrophages were less able to degrade LDL that had been oxidized in the presence of SNAP. Using an .NO electrode, it was estimated that a continuous production of .NO (< or = 760 nM/min) could retard the progression of LDL oxidation. We propose that .NO can inhibit LDL oxidation by acting as a chain-breaking antioxidant that is capable of scavenging carbon-centered and peroxyl radicals. Biological implications of this novel .NO antioxidant property are discussed in relation to atherogenesis and contrasted to the prooxidant property of .NO when generated in the presence of superoxide.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0014-5793
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
334
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
170-4
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Inhibition of low-density lipoprotein oxidation by nitric oxide. Potential role in atherogenesis.
pubmed:affiliation
Biophysics Research Institute, Medical College of Wisconsin, Milwaukee 53226.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.