Smoking, Tissue Antioxidant Levels, and Coronary Heart Disease

It is well established that smokers are at increased risk for developing atherosclerosis and ischemic heart disease. The exact mechanism(s) that links smoking to an increased risk for the development of accelerated atherosclerosis is not fully understood. In recent years, evidence has mounted that a pro-oxidant/antioxidant imbalance plays a significant role in promoting the atherogenic process. Cigarette smoke contains large amounts of pro-oxidants that can directly initiate the process of lipid peroxidation as well as deplete the body of nutrient antioxidants. Additionally, smoking elevates plasma and low-density lipoprotein (LDL) levels of peroxidation, and favors LDL oxidation in vivo. Antioxidants like vitamins C and E are responsible for counteracting free radical-mediated oxidative stress.

Numerous studies have shown that chronic, marginal deficiencies of vitamins C and E cause atherosclerosis-like lesions in numerous animal models, and that supplements of vitamin C or E reduces the number of these lesions. Most studies of this relationship in humans have examined levels of vitamins C and E in the plasma, often with equivocal results. A recent study has attempted to more accurately look at the relationship between antioxidant vitamin status, smoking, and coronary heart disease by examining not only the plasma vitamin levels, but also the antioxidant capacity and vitamin levels of arterial wall tissue taken from smokers and nonsmokers undergoing cardiac bypass surgery.

This study confirmed earlier results showing that smoking lowers the plasma level of vitamin C, but not vitamin E. Additionally, smokers had significantly higher plasma concentrations of lipid peroxides. However, for the first time this research demonstrated that, in smokers, a pro-oxidant/antioxidant imbalance can be found in the arterial wall tissue. In this tissue, significant decreases in vitamin E and C levels were found, along with a significant increase in tissue lipid peroxides. The integrated function between vitamins C and E in the arterial wall appears to be crucial for controlling oxidation and protecting LDL from oxidation. In fact, some researchers have suggested that both vitamins must be supplemented together to lower peroxidation. In smokers, the lowered tissue antioxidant capacity was associated with a lower content of vitamin C and higher lipid peroxidation in plasma, whereas plasma vitamin E levels were not significantly different from nonsmokers. The authors note that cigarette smoke has been shown to rapidly deplete vitamin C in plasma, which is quickly followed by lipid peroxidation. The lower vitamin C levels found in smokers is considered to be a direct consequence of vitamin C utilization as an antioxidant due to the smoke-related pro-oxidant load.

It was also found in the study that there is a direct relationship between plasma and tissue vitamin levels. In smokers, decreased plasma vitamin C appears to lower tissue vitamin C levels. This probably results in a decrease in tissue vitamin E levels, despite normal serum levels, because vitamin C acts as an antioxidant reservoir by sparing and regenerating vitamin E.

 It has been shown that plasma lipid peroxidation begins when vitamin C is depleted, while lipid peroxidation in tissue systems initiates only when vitamin E falls below a critical level. Accordingly, in this study the plasma levels of lipid peroxides was inversely and significantly related to the vitamin C level, whereas in arterial tissue the lipid peroxidation products were significantly and inversely related to the vitamin E content. In both smokers and nonsmokers, only tissue vitamin E and tissue lipid peroxidation products were significantly correlated with the degree of coronary atherosclerosis. This suggests that tissue vitamin E levels are crucial in protecting vessels from atherosclerosis, and that low serum vitamin C decreases tissue levels of both vitamin C and vitamin E. Because tissue levels of vitamin E can be significantly reduced despite normal serum levels, this study calls into question the absolute value of serum antioxidant measurements in both smokers and nonsmokers. It seems likely that a pro-oxidant/antioxidant imbalance operating in the arterial tissue is crucial to promoting atherosclerosis, due to the correlation between the severity of atherosclerotic lesions and the content of vitamins and lipid peroxide products in arterial tissue.

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© Vitamin Research Products Inc. 2001

A. Mazzetti, D. Lapenna, S.D. Pierdomenico, et al, Atherosclerosis 1995; 112: 91-99.

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