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Effect of High Levels of Dietary Vitamin E on Hematological Indices and Biochemical Parameters in Rats¹

Division of Human Nutrition, School of Home Economics, University of British Columbia, Vancouver, B.C., Canada V6T 1W5

The effects of low, normal and high levels of dietary vitamin E on rats were assessed by feeding diets containing 0, 25, 250, 2,500, 10,000, and 25,000 IU vitamin E/kg diet for prolonged periods of 8 and 16 months. All nutrients in the basal diet except vitamin E were adequate. Excess vitamin E and vitamin E deficiency depressed body weight over a period of time. High levels of dietary vitamin E increased the relative heart weight after 8 months and relative spleen weight after 16 months. The ash content of the bones decreased with concurrent increase in plasma alkaline phosphatase activity after 16 months of treatment. The prothrombin time was reduced after 12 months, while elevated hematocrit value was observed after 16 months on high intake of dietary vitamin E. Erythrocytes from vitamin E deficient rats showed spontaneous hemolysis when incubated in saline-phosphate buffer, while cells from rats given normal or excess vitamin E did not show signs of hemolysis when incubated under identical conditions. Urinary excretion of creatine and creatinine were apparently normal in all rats with the exception of vitamin E deficient rats which had significantly higher creatine and lower creatinine levels in urine. Results of these studies clearly indicate that excess vitamin E has deleterious effects and that further investigations are urgently warranted to test the implications of these findings on the long range metabolic and physiological consequences in animal and man.

KEY WORDS: • vitamin E • hypervitaminosis E • vitamin E supplements • vitamin E toxicity

¹ First in a series of papers from this laboratory on hypervitaminosis E supported by research grants from the National Research Council of Canada and the Research Committee of the University of British Columbia.

² Postdoctoral Research Associate.

³ To whom reprint requests should be addressed.

Manuscript received 27 August 1976.

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