The effect of phenylhydrazine on the adenosine triphosphate content of normal and glucose-6-phosphate dehydrogenase-deficient human blood.

The erythrocytes of certain individuals are peculiarly sensitive to the hemolytic effects of primaquine and a number of related compounds. A variety of biochemical abnormalities has been uncovered in such erythrocytes, principally related to deficiency of glucose-6-phosphate dehydrogenase (G6PD) (1-3) but the mechanisms responsible for the drug-induced hemolysis have not been clearly defined. Adenosine triphosphate (ATP) is an important compound in the metabolism of the erythrocyte, and it is known that a decrease in the concentration of ATP in erythrocytes correlates wellwith decreased survival of these cells as they age in vitro (4, 5) and in vivo (6, 7). It therefore seems possible that a fall in the level of ATP might be associated with the decreased erythrocyte survival that occurs in drug-induced hemolytic anemia. In order to obtain evidence bearing on this point phenylhydrazine hemolysis was chosen as a model. The effect of phenylhydrazine on the ATP of whole blood from normal subjects and from individuals with G6PD deficiency was determined under a variety of in vitro experimental conditions. Herein are presented data from experiments which demonstrate that phenylhydrazine induces a marked fall in the ATP level