Literature DB >> 21960140

Relationship of human paraoxonase-1 serum activity and genotype with atherosclerosis in individuals from the Deep South.

R Hunter Coombes1, J Allen Crow1, MaryBeth Dail1, Howard W Chambers2, Robert W Wills1, Janice E Chambers1.   

Abstract

OBJECTIVE: Paraoxonase-1 (PON1) is synthesized in the liver and is bound to high-density lipoprotein particles in blood. PON1 protects against the development of atherosclerosis by metabolizing proatherogenic-oxidized lipids. The Southeastern USA (excluding Florida) has the country's highest age-adjusted mortality rate of cardiovascular disease. This study determines the association of PON1 status with atherosclerosis in individuals from the Southeastern USA.
METHODS: Eighty African Americans (40 men, 40 women) and 120 Caucasians (60 men, 60 women) were enrolled from a cardiology practice in Northeastern Mississippi. Serum PON1 activities were determined using diazoxon, paraoxon, and phenyl acetate (PhAc) as substrates. The PON1(192) genotype of each individual was also determined. A multivariable logistic regression model was developed to identify the associations of clinical characteristics, serum PON1 activity, and PON1(192) genotype of the study population with atherosclerosis.
RESULTS: A core model consisting of age, sex, history of smoking, hypertension, and low-density lipoprotein-cholesterol group was constructed. The maximum-rescaled generalized r(2) value for the core model was 0.35. Addition of PON1 activity assessed by PhAc hydrolysis was the only measure of PON1 enzymatic activity to add significant information to the core model (P=0.0317) with the maximum-rescaled generalized r(2) value increasing to 0.37. Increasing PON1 activity was associated with decreased odds of atherosclerosis. The PON1(192) genotype was not significantly associated with atherosclerosis.
CONCLUSION: Increasing PON1 activity assessed by the hydrolysis of PhAc is associated with decreased odds of atherosclerosis in a group of African American and Caucasian Southerners.

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Year:  2011        PMID: 21960140      PMCID: PMC4817270          DOI: 10.1097/FPC.0b013e32834cebc6

Source DB:  PubMed          Journal:  Pharmacogenet Genomics        ISSN: 1744-6872            Impact factor:   2.089


  34 in total

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