Effect of glucose-6-phosphate dehydrogenase deficiency on neutrophil function.

The bactericidal activity of neutrophils depends primarily on free oxygen radicals released by the activation of NADPH oxidase when neutrophils are stimulated by microorganisms. Severe glucose-6-phosphate dehydrogenase (G6PD) deficiency is associated with decreased NADPH production. Increased susceptibility to recurrent bacterial infections in children with severe neutrophil G6PD deficiency as a consequence of decreased NADPH production has been reported earlier. In this study, the in vitro activity of neutrophils from normal and G6PD-deficient individuals was assessed by measuring the [14C]CO2 released via the hexose monophosphate shunt from radiolabeled [1-14C]-glucose and the nitroblue tetrazolium (NBT) dye reduction test. Our results show that the G6PD activity of neutrophils from 48 individuals, identified as severely erythrocyte (RBC) G6PD deficient (< 2 U/10(12) RBC) was 23% of the enzyme activity of neutrophils from 53 individuals with normal RBC G6PD levels (98.8 U/10(12) RBC). However, the results of functional assays of neutrophils as measured by hexose monophosphate shunt and the NBT test were comparable in G6PD-deficient and normal individuals, suggesting that a reduced activity of G6PD to as low as 23% of normal does not affect neutrophil function.