Abstract

This study aims to investigate the effect of cigarette smoking on paraoxonase1 (PON1) activity according to PON1 L55M and PON1 Q192R gene polymorphisms. Our sample included 300 voluntary subjects: 138 nonsmokers and 162 current smokers aged 38.47±21.91 and 35.55±16.03years, respectively. PON1 activity was determined by kinetic methods. L55M and Q192R gene polymorphisms of PON1 were determined by multiplex polymerase chain reaction (PCR) restriction fragment length polymorphism (RFLP). We found in smokers a significant decrease of PON1 activity before and after adjustment. We noted a significant association between smoking status and lower PON1 activity [odds ratio (OR)=3.03, confidence interval 95%=1.5-5.9, p=0.001]. In smokers, there was significant association between PON1 activity and PON1 L55M polymorphisms (p=0.01). Also, the 55MM genotype presented the lowest paraoxonase activity, while the 55LL genotype showed the highest one. After adjustment for confounding variables, smokers with PON1 L55M polymorphism had the highest risk for lower PON1 activity; however, PON1 Q192R genotype might protect smokers from decrease in PON1 activity. We found significant interaction between the effect of cigarette smoking and both PON1 L55M and PON1 Q192R polymorphisms on lower PON1 activity. Cigarette smoking was significantly associated with decrease in PON1 activity. Moreover, PON1 L55M polymorphism predisposes smokers to decreased PON1 activity in contrast to PON1 Q192R genotype.

Highlights

  • Smoking is firmly established as 1 of the principal cardiovascular risk factors

  • Objective This study aims to investigate the effect of cigarette smoking on paraoxonase 1 (PON1) activity according to PON1 L55M and PON1 Q192R gene polymorphisms

  • We found significant interaction between the effect of cigarette smoking and both PON1 L55M and PON1 Q192R polymorphisms on lower PON1 activity

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Summary

Introduction

In Tunisia, literature suggests that smoking prevalence is very high, especially among young people. Among health professionals and medical students, this prevalence is the same as in the general population [1]. Oxidative stress is considered to be the major pathological mechanism associated with smoking, leading notably to lipid peroxidation [2]. Several studies have demonstrated increased susceptibility of low-density lipoprotein (LDL) to oxidation and higher levels of oxidized LDL in smokers. This would provide an important causal mechanism that links smoking with vascular disease, given the numerous pathological effects of oxidized LDL. Smoking may enhance oxidative stress through production of reactive oxygen radicals in smoke and through weakening of antioxidant defense mechanisms.

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