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Objective To investigate the correlation between large artery atherosclerotic stroke and paraoxonase 1 (PON1) Q192R polymorphism.Methods Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to detect the PON1 Q192R polymorphism of 120 patients with large artery atherosclerotic stroke (case group) and 117 healthy subjects (control group).Results There was significant difference in the genotype distribution of PON1 Q192R (x2 =18.727,P＜0.001) and the allele frequency distribution (x2 =16.427,P ＜0.001) between the case group and the control group.Multivariate logistic regression analysis showed that RR genotype was an independent risk factor for large artery atherosclerotic stroke (odds ratio 1.377,95％ confidence interval 1.032-2.185; P =0.026).Conclusions The allelic gene mutation rate of PON1 Q192R in patients with large artery atherosclerotic stroke was significantly higher than that in the healthy population.RR genotype is an independent risk factor for large artery atherosclerotic stroke.
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Background: Polymorphisms in paraoxonase 1 (PON1) coding for PON1 enzyme have been studied as genetic markers of coronary artery disease (CAD). PON1 Q192R and PON1 L55M polymorphisms have been analyzed extensively, but data on association and role of these polymorphisms in the etiology of CAD are conflicting. In this study, we tested the genetic association between PON1 Q192R and PON1 L55M polymorphisms and CAD among north Indians. Materials and Methods: Two hundred eighty-five angiographically proven patients with coronary artery disease and 200 sex-matched and ethnically matched controls were genotyped for 2 PON1 polymorphisms by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. Genotype/ allele frequencies were compared in patients and controls using the chi-square test. Results: At PON1-192 locus, there were significant differences between patients and controls (P< 0.05), leading to significant odds ratios for RR genotype (OR= 1.92, CI: 1.19-3.10) and *R allele (OR= 1.30, CI: 1.00-1.70). These odds ratios were higher in the sub-sample of smokers (2.84 and 1.45, respectively). Binary logistic regression analysis also confirmed that *R allele carriers (QR and RR) have a higher risk of CAD (OR= 3.54, CI: 1.67-5.53). PON1-55 locus did not show significant differences between patients and controls, but LL genotype and *L allele were significant risk factors in the nonsmoker group. RL haplotype was also significantly associated with CAD risk (OR= 1.44, CI: 1.08-1.93). Conclusions: PON1-192R allele and RR genotype are significantly associated with CAD patients from the north Indian population (Uttar Pradesh). This association was stronger in smokers, supporting the conclusion that an interaction between PON1 activity and smoking augments CAD risk. Further studies with larger sample size are warranted to confirm these associations in different Indian populations.