EFFECTS OF VITAMIN-E SUPPLEMENTATION ON ERYTHROCYTE ANTIOXIDANT DEFENSE-MECHANISMS OF SMOKING AND NONSMOKING MEN

1. During all aerobic metabolism, free radicals generated by the parti al reduction of oxygen are potentially injurious to cells. Highly effi cient antioxidant defence systems exist to inhibit oxidative damage to cellular lipids and proteins. Specific enzymes have a crucial role in these antioxidant defences, and their activity may be induced by regu latory mechanisms that respond to oxygen metabolite concentration. 2. To assess whether smoking induces an additional adaptive response, we compared antioxidant defence systems in erythrocytes from smokers and nonsmokers and assessed whether a high intake of vitamin E (280 mg/day ), a major lipophilic free-radical-scavenging antioxidant, affects the activity of antioxidant enzymes. 3. A total of 100 men, 50 smokers an d 50 nonsmokers, were allocated to four treatment groups in a 2 x 2 fa ctorial design (smokers versus non-smokers and placebo versus vitamin E). For 10 weeks each subject took one capsule per day of either 280 m g dl-alpha-tocopherol acetate or a visually identical placebo (hydroge nated coconut oil with negligible vitamin E content). 4. Despite incre ased erythrocyte cytosolic antioxidant enzyme activities in smokers co mpared with nonsmokers, erythrocytes from smokers were more susceptibl e to hydrogen peroxide-induced lipid peroxidation in vitro. 5. Vitamin E supplementation further increased erythrocyte catalase (EC 1.11.1.6 ) activity in both smokers and non-smokers (P<0.001) and erythrocyte g lutathione peroxidase (EC 1.11.1.9) and glutathione reductase (EC 1.6. 4.2) activities in non-smokers (P<0.001). After supplementation with v itamin E there was a concomitant fall in erythrocyte superoxide dismut ase (EC 1.15.1.1) activity (P<0.001) and total glutathione concentrati on (P<0.01). Furthermore, in both smokers and non-smokers there was a significant decrease in the susceptibility of erythrocytes to peroxida tion (P<0.001). 6. Various endogenous and exogenous factors exert cont rol over cellular protection against reactive oxygen species, and our data suggest that one such factor is the supply of vitamin E.