In Vivo Lability of Red Cell Phosphofructokinase in Term Infants: The Possible Molecular Basis of the Relative Phosphofructokinase Deficiency in Neonatal Red Cells

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Abstract
Summary: Cord blood erythrocytes from nine term infants were separated rated by density gradient centrifugation into cohorts of intact cells of progressively increasing density and compared with red cells treated in a similar manner from four healthy adults. Pyruvate kinase (PK), an age-dependent enzyme, progressively decreased in activity from the lightest to the heaviest fractions, in both neonatal and adult red cells, indicating that red cells from newborn infants exhibit the same relationship between red cell age and density that had previously been demonstrated in red cells from adults. The rate of decline of red cell PK activity was essentially the same in neonates and adults, whereas phosphofructokinase (PFK) activity in cord erythrocytes decreased at a significantly faster rate when compared to adults. These data suggest that PFK has an accelerated rate of in vivo decay in neonatal red cells and is an unstable enzyme in the newborn. Speculation: The finding that PFK from cord blood has an accelerated rate of in vivo decay suggests that the relative PFK deficiency that exists in neonatal red cells is secondary to normal synthesis of an unstable enzyme, and leads to the speculation that red cell PFK in newborn infants is an isozyme (a “fetal” PFK).