The effect of cigarette smoking on anti-oxidation function of HDL

Abstract

Objective: Cigarette smoking is an independent risk factor for prediction of heart disease. Much research indicates that smoking reduce the level of HDL-C simultaneously. Smoking cessation can reverse this kind of change. But the continual variation of the function of HDL in the process of smoking remains unknown. The objective of our research is to determine whether the anti-oxidation function of HDL varies in healthy candidates during smoking. Methods: 42 healthy candidates were enrolled and divided into 4 groups: non-smokers before and after smoking, smokers before and after smoking. Lipoprotein was isolated by ultracentrifugation from plasma samples. The anti-oxidation ability of HDL was tested by ultraviolet absorption spectrometry and lagging time (Tlag) and t at Vmax of the OD-t curve. Results: Pulse rate, systolic blood pressure and diastolic blood pressure are obviously higher after smoking in both non-smokers and chronic smokers. Serum amyloid A is obviously higher after smoking in non-smokers; SAA is lower in chronic smokers than non-smokers after smoking. Tlag of mixed lipoprotein is lower after smoking in both non-smokers and chronic smokers. Tlag of chronic smokers is higher than non-smokers, whatever the value before or after smoking. The margin (descending) in chronic smokers is larger than in non-smokers. T at Vmax of mixed lipoprotein of chronic smokers is higher than non-smokers, whatever the value before or after smoking. Conclusions: After once-smoking, the anti-oxidation ability of HDL decreases. The anti-oxidation ability of HDL increases in chronic smokers, which is a possible compensative mechanism of organism. But it cannot correct the chronic oxidation state by long-time cigarette smoking. The anti-oxidation ability of HDL in chronic smokers performs a more obvious descending when organism is encountering an acute stress strike.