OXIDATIVE STRESS BIO MARKERS AND ANTIOXIDANT STATUS IN CIGARETTE SMOKERS COMPARED TO NONSMOKERS

Abstract

Oxidative stress plays an important role in the pathogenesis of some diseases such as lung cancer, chronic obstructive pulmonary disease, and atheroscleorosis. Smoking may enhance oxidative stress not only through the production of reactive oxygen radicals in smoke but also through weakening of the antioxidant defense systems. Cigarette smoke may promote atherogenesis by producing oxygen-derived free radicals that damage lipids. The present study was conducted to determine the effect of cigarette smoking on changes in lipid profile, lipid peroxidation and antioxidant status in cigarette smokers. The study population consisted of 200 male subjects divided into two groups; 100 smokers and age- and sex-matched non-smokers 100 subjects were selected. The mean systolic and diastolic blood pressure values were found to be significantly higher for smokers than for non-smokers. Biochemical parameters such as cardiac markers, lipid profile, apolipoproteins B and A1 (Apo B and A1), lipid peroxidation thiobarbituric acid reactive substances (TBARS) and antioxidants (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH), vitamin A, vitamin C and vitamin E were measured. A highly significant increase in the levels of cardiac markers was found in smokers when compared with non-smokers. Enhanced lipid peroxidation with concomitant depletion of antioxidants was observed smokers as compared to non-smokers. The levels of serum total cholesterol, triglycerides, LDL and VLDL were found to be significantly high, while HDL was significantly low in smokers compared to non-smokers. In addition, the activity of enzymatic and non-enzymatic antioxidants were more significantly altered in smokers than nonsmokers. These results suggest that the atherogenic effects of smoking are mediated in part by free radical damage to lipids and possible breakdown of antioxidant status in cigarette smoking.