Paraoxonase activity as a marker of exposure to xenobiotics in tobacco smoke.

The paraoxonase (PON) family is composed of 3 proteins (PON1, PON2, and PON3), each of which plays a crucial role in the body, displaying antioxidant, anti-inflammatory, and antiatherosclerotic properties. The activities and properties of PON proteins can be modulated by a number of environmental factors, including cigarette smoke. In the present article, a review of existing literature is employed to analyze both the direct and the indirect impact of cigarette smoking on the activity of members of the PON family. Cigarette smoking leads to direct inhibition of the hydrolytic activity of PON enzymes by modification of thiol groups, by the reactions of free radicals, or by inhibiting enzyme-active regions with heavy metals. It has been shown that cigarette smoking correlates with a decrease in high-density lipoprotein (HDL) concentration as well as with an increase in other components of the lipid profile (low-density lipoprotein (LDL), triglycerides, and total cholesterol). By decreasing HDL levels, cigarette smoking likely acts indirectly to induce a decline in PON1 activity. Inhibition of PON1 activity by smoking is a reversible process after cessation of exposure to the xenobiotics in tobacco smoke.