Abnormal erythropoiesis in vitamin E-deficient monkeys

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Abstract
Vitamin E deficiency was induced in sexually immature rhesus monkeys by feeding a purified diet for 24 months or longer. Control monkeys received the same diet but were supplemented with 100 mg of d-α-tocopheryl acetate 3 times weekly. Ferrokinetics, the evolution of spontaneous anemia, and the erythropoietic response to phlebotomy were studied. All deficient monkeys developed erythroid hyperplasia and multinuclearity of erythrocyte precursors, and 5 became anemic without phlebotomy, packed cell volume < 35%. Plasma iron turnover was greater in the deficient group, 2.6 versus 1.2 mg/dl whole blood per day; utilization of radioiron for the production of circulating hemoglobin was less in the deficient group, 43 versus 64%; and erythrocyte survival was shortened in the deficient group, 10.1 versus 13.6 days (T1/2 of 51Cr-tagged erythrocytes). After treatment of two deficient monkeys with d-α-tocopheryl acetate, reticulocyte counts increased, reaching peak values of 7 and 26%, anemia remitted (packed cell volume 31 → 45% and 22 → 42%), plasma iron turnover and radioiron utilization returned to normal, and erythrocyte survival returned to normal. Anemia induced by phlebotomy raised serum erythropoietin to equivalent levels in both deficient and supplemented monkeys. Nevertheless, the peripheral reticulocyte peak in response to induced anemia was less in deficient than in supplemented monkeys. These results indicate that ineffective erythropoiesis contributes significantly to the anemia of vitamin E deficiency in rhesus monkeys.