Abstract

Studies were undertaken to define further the extent of oxidant-induced injury and the degree to which it was repairable in the red cells of the newborn infant. Red cells from both infants and adults were incubated in the presence of either acetylphenhydrazine or menadione with and without glucose. Glucose deprivation produced irreversible loss of red cell hexokinase and glyceraldehyde-3-phosphate dehydrogenase activity in the cells, which lost the capacity to consume glucose at a normal rate. Menadione, even in the presence of glucose, inhibited fatty acid incorporation into the membrane of the infant's erythrocytes, but stimulated uptake in the cells of adults. The intracellular metabolic alterations produced by the oxidants were reduced by pretreatment of the cells with carbon monoxide, suggesting that hydrogen peroxide generation with inadequate detoxification was responsible for the injury observed in the erythrocytes of the neonate.

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