An Abnormality of Circulating Erythrocytes in Untreated and in Coenzyme Q10-treated Vitamin E-deficient Monkeys

Abstract

In a study of the anemia of vitamin E deficiency and its inadequate response to oral coenzyme Q10 treatment, survival of 51Cr-labeled erythrocytes was measured. Half-times for erythrocyte survival were: 14, 14.5 and 16 days in 3 control monkeys; 21 and 23 days in two previously vitamin E-deficient monkeys treated with vitamin E; and 8, 10, 10.5 and 12 days in 4 vitamin E-deficient monkeys. Erythrocytes from vitamin E-deficient monkeys exhibited increased susceptibility to hemolysis by hydrogen peroxide, but a cause and effect relationship between a low environmental capacity to protect erythrocytes from oxidative destruction and shortened erythrocyte survival was not demonstrated. In fact, in experiments in which labeled erythrocytes were transfused into recipients other than the donor, erythrocytes from vitamin E-deficient monkeys had no improvement in survival when transfused into the vitamin E-replete environment of control monkeys, and erythrocytes from a control monkey survived normally when transfused into a vitamin E-deficient monkey. These results indicate that there is an intrinsic defect in the erythrocyte of the vitamin E-deficient monkey. Exogenous coenzyme Q10 did not improve erythrocyte survival; 3 coenzyme Q10-treated, vitamin E-deficient monkeys had erythrocyte survival half-times of 5, 6 and 6 days. This persistence of shortened erythrocyte survival explains the reticulocytosis without an increase in hemoglobin concentration which occurred in these monkeys. Inadequate intracellular accumulation of the intact coenzyme Q10 molecule is proposed to explain the inadequate response of vitamin E-deficient monkeys to exogenous coenzyme Q10.