Document Detail


Hyperhomocysteinemia, paraoxonase activity and risk of coronary artery disease.
MedLine Citation:
PMID:  16875684     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVES: Paraoxonase-1 (PON1) detoxifies homocysteine thiolactone (HcyT) in human blood and could thus delay the development of atherosclerosis. We investigated (a) PON1 activity and polymorphisms, and (b) the relationship between PON1 activity, homocysteine (Hcy) and the severity of CAD patients in Tunisian population. DESIGN AND METHODS: We used PCR-RFLP analysis to detect the Q192R and L55M variants of the PON1 gene in 100 patients with CAD and in 120 healthy controls. Paraoxonase activity was measured spectrophotometrically using phenylacetate as a substrate. Total plasma homocysteine concentrations were determined by direct chemiluminescence assay. RESULTS: We found an increased Hcy level in CAD patients compared to the control group (15.86+/-8.63 vs. 11.9+/-3.25 micromol/L respectively, P<0.001), and a decrease in PON1 activity in CAD patients as compared to the control group (117+/-56 vs. 181+/-73 U/mL respectively, P<0.001). PON1 Q192R and L55M polymorphisms were not associated with the presence of CAD (P=0.592, P=0.294, respectively). However, we found that PON1 activity is lower with the PON1 192RR than with PON1 192QQ genotypes in the study population. Furthermore, there were no association between PON1 L55M polymorphism and PON1 activity. We showed a significant decrease in PON1 activity in CAD patients presenting 0- to 3-vessel stenosis (155+/-39; 135+/-36; 103+/-22; 77+/-24 U/mL, respectively; P<0.001). CONCLUSION: In this study, we showed that low PON1 activity is associated with the PON1 192RR genotypes and associated with the severity of CAD in the Tunisian population. We hypothesize that high level of Hcy together with low PON1 activity results in an increased plasma HcyT plasma concentration leading to protein N-homocysteinylation and the development and progression of atherosclerosis.
Authors:
Mohsen Kerkeni; Faouzi Addad; Maryline Chauffert; Laurence Chuniaud; Abdelhedi Miled; François Trivin; Khira Maaroufi
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Publication Detail:
Type:  Journal Article     Date:  2006-06-07
Journal Detail:
Title:  Clinical biochemistry     Volume:  39     ISSN:  0009-9120     ISO Abbreviation:  Clin. Biochem.     Publication Date:  2006 Aug 
Date Detail:
Created Date:  2006-08-17     Completed Date:  2006-10-25     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0133660     Medline TA:  Clin Biochem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  821-5     Citation Subset:  IM    
Affiliation:
Research Unit 03/UR/08-14, Faculty of Pharmacy, Monastir, Tunisia, and Department of Biochemistry, Hospital Saint-Joseph, 75014 Paris, France. m.kerkeni@belgique.com
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MeSH Terms
Descriptor/Qualifier:
Adult
Aryldialkylphosphatase / blood*,  genetics
Base Sequence
Case-Control Studies
Coronary Artery Disease / complications*,  enzymology
DNA Primers
Humans
Hyperhomocysteinemia / complications*
Middle Aged
Multivariate Analysis
Polymorphism, Genetic
Risk Factors
Severity of Illness Index
Chemical
Reg. No./Substance:
0/DNA Primers; EC 3.1.8.1/Aryldialkylphosphatase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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