Linked Life Data

11809774

Source:http://linkedlifedata.com/resource/pubmed/id/11809774

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
14
pubmed:dateCreated
2002-4-1
pubmed:abstractText
Complete lecithin:cholesterol acyltransferase (LCAT) deficiency is a rare cause of severe hypoalphalipoproteinemia, but the affected subjects are surprisingly not particularly prone to premature coronary heart disease. We studied oxidative stress in lcat-/- mice and their cross-breed with apolipoprotein-E knockout mice (apoE-/-xlcat-/-) by measuring vascular ring superoxide production and plasma phospholipid (PL)-bound F2-isoprostane levels and their relationship with aortic atherosclerosis. Compared with wild type control (lcat+/+), lcat-/- and lcat+/- mice showed a 4.9- (p = 0.003) and a 2.1-fold (p = 0.04) increase in plasma PL-F2-isoprostane levels, respectively. There was also a 3.6- (p < 0.0001) and 2.9-fold (p = 0.003) increase in the area under the curve for the aortic ring superoxide excursion by lucigenin-derived chemiluminescence. A comparison of apoE-/-xlcat+/+ mice with wild type control mice showed a more modest 2.1- (p = 0.04) and 2.2-fold (p < 0.00001) increase in these respective markers. Surprisingly, the apoE-/-xlcat-/- mice showed a paradoxical normalization in both oxidation markers. Furthermore, by fast protein liquid chromatography separation, we observed an associated retention and redistribution of serum paraoxonase activities to the non-high density lipoprotein fractions in both the apoE-/-xlcat-/- and apoE-/-xlcat+/- mice. Aortic atherosclerotic lesions in male apoE-/-xlcat-/- and apoE-/-xlcat+/- mice were reduced by 52 (p = 0.02) and 24% (p = 0.46), respectively. Our data suggest that LCAT-deficient mice are associated with an increased oxidative stress that is paradoxically reversed in a hyperlipidemic background, possibly due to the redistribution of paraoxonase. This modulation of oxidative stress may in part contribute to the reduced atherosclerosis seen in the apoE-/- xlcat-/- mice.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
5
pubmed:volume
277
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
11715-20
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11809774-Alleles, pubmed-meshheading:11809774-Animals, pubmed-meshheading:11809774-Aorta, pubmed-meshheading:11809774-Apolipoproteins E, pubmed-meshheading:11809774-Area Under Curve, pubmed-meshheading:11809774-Arteriosclerosis, pubmed-meshheading:11809774-Aryldialkylphosphatase, pubmed-meshheading:11809774-Chromatography, Liquid, pubmed-meshheading:11809774-Esterases, pubmed-meshheading:11809774-Genotype, pubmed-meshheading:11809774-Isoprostanes, pubmed-meshheading:11809774-Lecithin Acyltransferase Deficiency, pubmed-meshheading:11809774-Lipids, pubmed-meshheading:11809774-Mice, pubmed-meshheading:11809774-Mice, Knockout, pubmed-meshheading:11809774-Oxidative Stress, pubmed-meshheading:11809774-Phosphatidylcholine-Sterol O-Acyltransferase, pubmed-meshheading:11809774-Phosphatidylcholines, pubmed-meshheading:11809774-Superoxides, pubmed-meshheading:11809774-Time Factors
pubmed:year
2002
pubmed:articleTitle
Oxidative stress is markedly elevated in lecithin:cholesterol acyltransferase-deficient mice and is paradoxically reversed in the apolipoprotein E knockout background in association with a reduction in atherosclerosis.
pubmed:affiliation
Department of Medicine, St. Michael's Hospital, Toronto, Ontario, Canada. ngd@smh.toronto.on.ca
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't