Three weeks' dietary supplementation with a moderate dose of vitamin E (45 IU DL-alpha-tocopherol acetate daily), in eight healthy volunteers significantly increased the serum vitamin E level from 12.3 +/- 3.3 to 16.2 +/- 3.7 mg/L (means +/- SD) and significantly decreased neutrophil chemotaxis from 15 +/- 3 to 4 +/- 1 micron/h (means +/- standard error of the means). Generation of leukotriene B4 was not influenced by vitamin E, suggesting that the decrease in neutrophil chemotaxis was not due to blockage of the lipoxygenase pathway. Neither was the plasma malondialdehyde concentration influenced by vitamin E, contradicting the possibility of an antioxidant effect of vitamin E. As one early event in neutrophil chemotaxis is an increase in intracellular calcium concentration resulting from increased membrane permeability, it is possible that vitamin E influenced chemotaxis by a stabilizing effect on the neutrophil membrane, rather than by its antioxidant effect. Vitamin E supplementation could thus be beneficial in pathological conditions with activated neutrophils, such as ischaemic heart disease.