Erythrocyte Antioxidant Defenses Against Cigarette Smoking in Ischemic Heart Disease

Cigarette smoke promotes atherogenesis by producing oxygen-derived free radicals.

The present study was conducted to determine the effect of cigarette smoking on lipid peroxidation and erythrocyte antioxidant status in ischemic heart disease (IHD).

A total of 327 male subjects were enrolled for this study, divided into two groups consisting of 200 patients, who were consecutively admitted for IHD in the intensive cardiac care unit (ICCU) of a Government Hospital and 127 age matched male healthy subjects. Both the groups were subsequently categorised into smokers and non smokers sub groups depending upon the smoking history {>/= 20 pack years of smoking; (20 cigarettes per day for one year constitutes one pack year)}. All 327 subjects were investigated for lipid profile, malondialdehyde (MDA) levels and the antioxidant enzymes catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPX).

The differences in the parameters between the groups were tested for significance by one way ANOVA using the SPSS software version 19. A p-value of < 0.001 was considered to be significant statistically. Multiple comparisons were made between all the four groups by Post Hoc Tukey test.

There was highly significant difference (p<0.001) observed in GPX activity, in comparison to CAT and SOD (p=0.032, p=0.009) between smokers vs non smokers in control group as well as patient group. The plasma MDA levels were found to be increased significantly (p<0.001) in IHD patients, who smoked as compared to those who did not.

Chronic smoking enhances erythrocyte lipid peroxidation in IHD patients with concomitant failure of both plasma and erythrocyte antioxidant defense mechanisms. Along with conventional lipid markers and plasma MDA levels, the erythrocyte GPX activity was observed to be a better marker of oxidative stress, in chronic smokers, who are at risk of developing IHD.