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  Vol. 132 No. 12, December 1997 TABLE OF CONTENTS
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Enteral Vitamin E Supplementation Inhibits the Cytokine Response to Endotoxin

Eileen M. Bulger, MD; W. Scott Helton, MD; Camille M. Clinton; Richard P. Roque; Iris Garcia; Ronald V. Maier, MD

Arch Surg. 1997;132(12):1337-1341.


Abstract



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 µg/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.

Arch Surg. 1997;132:1337-1341



Author Affiliations



From the Department of Surgery, University of Washington, Seattle.



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THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Final Report on the Safety Assessment of Tocopherol, Tocopheryl Acetate, Tocopheryl Linoleate, Tocopheryl Linoleate/Oleate, Tocopheryl Nicotinate, Tocopheryl Succinate, Dioleyl Tocopheryl Methylsilanol, Potassium Ascorbyl Tocopheryl Phosphate, and Tocophersolan
International Journal of Toxicology 2002;21:51-116.
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Antioxidants in Critical Illness
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Arch Surg 2001;136:1201-1207.
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Antioxidants, Cytokines, and Influenza Infection in Aged Mice and Elderly Humans
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The Journal of Infectious Disease 2000;182:S74-S80.
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Pretreatment of Young Pigs with Vitamin E Attenuates the Elevation in Plasma Interleukin-6 and Cortisol Caused by a Challenge Dose of Lipopolysaccharide
Webel et al.
J. Nutr. 1998;128:1657-1660.
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