Failure of high-dose vitamin E to correct ceruloplasmin ferroxidase deficiency in cigarette smokers

Cigarette smokers have a biochemical defect in the ferroxidase activity of their serum ceruloplasmin. Ceruloplasmin is one of the main serum antioxidants, and this defect in ferroxidase activity most likely accounts for the previously observed decrease in smoker serum antioxidant activity. This defect may be related to oxidation of ceruloplasmin in the lung. We hypothesized that vitamin E might be able to reverse the decrease in smoker ferroxidase activity and thus restore serum antioxidant activity. To test this hypothesis, we administered high-dose vitamin E to a group of young asymptomatic cigarette smokers (n = 8). Although serum levels of vitamin E significantly increased (8.7 +/- 0.8 to 20.6 +/- 3.1 micrograms/ml, p = 0.01), the ferroxidase activity of smoker serum (0.139 +/- 0.02 (0.139 +/- 0.02 to 0.144 +/- 0.03 U/ml, p = 0.824), and the antioxidant activity of serum (45.8 +/- 7.2 to 51.6 +/- 8.4%, p = 0.587) remained unchanged. Thus, at the current dose and duration of supplementation, vitamin E was unable to reverse the defect in smoker serum ferroxidase activity and thus unable to augment the antioxidant capacity of the serum.