Objective: To investigate the role of NADPH in the development of neonatal jaundice with G6PD deficiency.
Methods: The enzyme activities of G6PD, catalse (Cat) and glutathione peroxidase (GSH-px) were measured by quantitative determination of enzyme activity. The level of MDA was analyzed with alpha-thiobarbituric acid and the level of NADPH was determined with modified Nisselbaum JS's. Comparisons of these markers between G6PD normal and deficient erythrocytes were made before and during the incubation of the erythrocytes with H2O2.
Results: The level of MDA, which was 36 +/- 8n-mol.L-1.gHb-1, was increased and that of NADPH, which was 1792 +/- 106mumol.L-1.gHb-1, was decreased in jaundiced neonates with G6PD deficiency compared with those with normal G6PD activity. When the cells were incubated with H2O2, the level of NADPH and the activities of Cat and GSHpx in erythrocytes with normal G6PD activity increased at first, and then turned to decrease as the incubation lasted longer than 30 minutes. But in G6PD-deficient erythrocytes all these markers decreased continuously as the cells were incubated with H2O2.
Conclusions: The diminished capability of generation of NADPH in G6PD-deficient erythrocytes may contribute directly to the more extensive peroxidation of the cells. The defect capacity of generation of NADPH, which resulted in the weakened capability of antiperoxidation and finally the lysis of erythrocytes, was one of the important mechanisms in the development of jaundice in G6PD-deficient neonates.