Abstract

An imbalance between pro-oxidants and antioxidants is operative in atherosclerosis. Cigarette smoke is a major risk factor of atherosclerosis and has been reported to contain large amounts of oxidants. We assessed arterial (internal mammary artery) and plasma levels of vitamins E and C and lipid peroxides in 48 male patients, 24 smokers and 24 non-smokers, undergoing coronary bypass surgery. Lipid peroxidation was studied using fluorescent products of lipid peroxidation (FPLs). Tissue vitamins E and C levels were significantly lower and FPLs significantly higher in smokers than in non-smokers ( P < 0.0006, 0.0005 and 0.0005, respectively). This pattern was associated with lower vitamin C and higher lipid peroxide plasma levels in smokers than in non-smokers ( P < 0.0002 and 0.0005, respectively). Vitamins E and C plasma levels were strongly related to their tissue content both in smokers ( r = 0.60, P < 0.005 and r = 0.57, P < 0.01) and in non-smokers ( r = 0.42, P < 0.05 and r = 0.46, P < 0.05). Moreover, vitamin E content was significantly related to that of vitamin C only in the arterial tissue of both groups, pointing to the existence of a functional interaction between these antioxidants. In both groups, FPLs were significantly and inversely related to vitamin C in plasma and to vitamin E in tissue, suggesting the antioxidant primacy of vitamin C and vitamin E in the plasma and arterial tissue compartments, respectively. The severity of coronary atherosclerotic lesions was inversely and directly correlated to the arterial levels of vitamin E and of fluorescent products of lipid peroxidation in both smokers ( r = −0.57, P < 0.006 and r = 0.59, P < 0.005) and non-smokers ( r = −0.42, P < 0.05 and r = 0.48, P < 0.025); on the other hand, no correlation was observed between the severity of atherosclerotic lesions and the content of vitamins and FPLs in plasma. This suggests that a prooxidant/antioxidant imbalance essentially operative in the arterial tissue is crucial in conditioning atherogenic processes in humans.

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