Enteral vitamin E supplementation inhibits the cytokine response to endotoxin.

OBJECTIVE: To evaluate the effect of short-term, high-dose enteral supplementation of 3 different vitamin E derivatives: free alpha-tocopherol (VE), alpha-tocopherol succinate (VES), and alpha-tocopherol acetate (VEA) on macrophage and monocyte activation. DESIGN: Sprague-Dawley rats (weight, 150-200 g) were assigned to 1 of 5 experimental groups: saline (control), ethanol (control), VES (100 mg/kg), VEA (100 mg/kg), or VE (100 mg/kg). Rats underwent oral gavage once per day for 5 days with 0.5 mL of their assigned solution. All vitamin E derivatives were diluted in 75% ethanol. Rats were then killed and whole-blood and peritoneal macrophages were harvested and stimulated with lipopolysaccharide (10 microg/mL) in vitro. Tumor necrosis factor (TNF) production was measured by enzyme-linked immunosorbent assay. Additional serum samples were analyzed for alpha-tocopherol concentration by high-performance lipid chromatography. RESULTS: Whole-blood TNF production was maximal in the control groups after 3 hours of incubation and began to decline by 6 hours. Supplementation with all 3 vitamin E derivatives resulted in suppression of lipopolysaccharide-induced TNF production at both time points when compared with both ethanol and saline controls (P<.05, analysis of variance [ANOVA]). All 3 vitamin E derivatives also resulted in significant inhibition of lipopolysaccharide-induced TNF production by peritoneal macrophages when compared with their ethanol-carrier control but not with the saline control (P<.05, ANOVA). The degree of TNF suppression correlated directly with serum alpha-tocopherol levels. CONCLUSIONS: Our data demonstrate that a short-term, high-dose enteral supplementation of vitamin E can modulate the monocyte and macrophage response to endotoxin. These data, along with other animal studies showing a protective effect of vitamin E treatment in sepsis and ischemia-reperfusion injury, suggest a potential role for vitamin E supplementation in patients at risk of the systemic inflammatory response syndrome.