Source:http://linkedlifedata.com/resource/pubmed/id/11378531
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
5
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| pubmed:dateCreated |
2001-5-29
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| pubmed:abstractText |
Human serum paraoxonase (PON) is an antioxidative enzyme, which circulates on high-density lipoproteins and appears to use oxidized phospholipids as physiological substrates. PON M/L55 substitution changes the ability of PON to prevent lipid oxidation. Urinary 8-iso-PGF(2alpha) (one of F2 -isoprostanes) may represent a non-invasive in vivo index of free radical generation and we propose that PON might influence the biosynthesis of 8-iso-PGF(2alpha) in the vasculature. We studied the urinary excretion of 8-iso-PGF(2alpha) and related it to PON M/L55 genotypes in patients with type 2 diabetes mellitus (n = 55) and non-diabetic control subjects (n = 55). Urinary 8-iso-PGF(2alpha) was determined by competitive ELISA and the PON genotype by a PCR based restriction enzyme digestion method. LL homozygotes were compared to M-allele carriers (ML heterozygotes and MM homozygotes). The urinary excretion of 8-iso-PGF(2alpha) among non-diabetic non-smoking LL homozygotes was 3995.5 +/- 3352.8 ng/24-hour and among M-allele carriers 1689.8 +/- 1051.3 ng/24-hour (p = 0.017, ANCOVA; gender, hypertension, total cholesterol, triglycerides and LDL cholesterol as covariates). The excretion of 8-iso-PGF(2alpha), was increased in type 2 diabetes mellitus compared to non-diabetic control subjects. PON may thus protect against oxidative stress by destroying some biologically active lipids. Excretion of 8-iso-PGF(2alpha) is increased in type 2 diabetes, which may reflect oxidant injury.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/6-S-hexadecyl-2-methoxythioascorbic...,
http://linkedlifedata.com/resource/pubmed/chemical/8-epi-prostaglandin F2alpha,
http://linkedlifedata.com/resource/pubmed/chemical/Aryldialkylphosphatase,
http://linkedlifedata.com/resource/pubmed/chemical/Ascorbic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Dinoprost,
http://linkedlifedata.com/resource/pubmed/chemical/Esterases,
http://linkedlifedata.com/resource/pubmed/chemical/F2-Isoprostanes
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| pubmed:status |
MEDLINE
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| pubmed:month |
May
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| pubmed:issn |
1071-5762
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
34
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
477-84
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:11378531-Aryldialkylphosphatase,
pubmed-meshheading:11378531-Ascorbic Acid,
pubmed-meshheading:11378531-Case-Control Studies,
pubmed-meshheading:11378531-Diabetes Mellitus, Type 2,
pubmed-meshheading:11378531-Dinoprost,
pubmed-meshheading:11378531-Esterases,
pubmed-meshheading:11378531-F2-Isoprostanes,
pubmed-meshheading:11378531-Female,
pubmed-meshheading:11378531-Glomerular Filtration Rate,
pubmed-meshheading:11378531-Homozygote,
pubmed-meshheading:11378531-Humans,
pubmed-meshheading:11378531-Lipid Peroxidation,
pubmed-meshheading:11378531-Male,
pubmed-meshheading:11378531-Middle Aged,
pubmed-meshheading:11378531-Oxidative Stress,
pubmed-meshheading:11378531-Polymorphism, Genetic,
pubmed-meshheading:11378531-Random Allocation,
pubmed-meshheading:11378531-Reference Values,
pubmed-meshheading:11378531-Smoking
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| pubmed:year |
2001
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| pubmed:articleTitle |
Lipid peroxidation is increased in paraoxonase L55 homozygotes compared with M-allele carriers.
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| pubmed:affiliation |
Tampere University Hospital, Centre for Laboratory Medicine, Department of Clinical Chemistry and University of Tampere, Medical School; P.O. Box 2000, 33521 Tampere, Finland.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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