Synergistic effects between Q192R polymorphism of paraoxonase I gene and some conventional risk factors in premature coronary artery disease

被引:19
|
作者
Balcerzyk, Anna [1 ]
Zak, Iwona
Krauze, Jolanta
机构
[1] Med Univ Silesia, Dept Biochem & Med Genet, Katowice, Poland
[2] Med Univ Silesia, Dept Cardiol 1, Katowice, Poland
关键词
coronary artery disease; paraoxonase; 1; polymorphism; conventional risk factor; HIGH-DENSITY-LIPOPROTEIN; MYOCARDIAL-INFARCTION; HEART-DISEASE; CHOLESTEROL; PROTECTION; THICKNESS; OXIDATION; SMOKING; PLASMA; LDL;
D O I
10.1016/j.arcmed.2007.03.004
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Background. Genetic susceptibility to coronary artery disease (CAD) may be determined by polymorphic variants of genes encoding isoforms involved in the processes important in the pathogenesis of atherosclerosis, including lipoprotein oxidation. Participation of single polymorphic variants is relatively small; however, its significance may increase in the presence of specific environmental background. The aim of the study was an evaluation of a possible association between R192Q polymorphism of PON1 gene and CAD as well as interactions between polymorphic variants and conventional risk factors of CAD in determining the risk of the disease. Methods. We studied 358 subjects: 178 patients with angiographically confirmed CAD and 180 blood donors without history of CAD. Polymorphisms were genotyped using PCR-RFLP method. Results. We observed statistically significant differences in the frequencies of Q allele and Q allele carriers of PON1 gene between CAD and controls. We also found a strong synergistic effect between Q allele carrier state and smoking, as well as Q allele carrier state and elevated level of total cholesterol. Conclusions. The present study revealed an association between carrier state of Q allele of PON1 gene and coronary artery disease as well as synergistic effects between genotype and some conventional risk factors, mainly smoking and elevated level of total cholesterol. (c) 2007 IMSS. Published by Elsevier Inc.
引用
收藏
页码:545 / 550
页数:6
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