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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 well- with 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 * This work was presented in part before the Joint

THE EFFECT OF PHENYLHYDRAZINE ON THE ADENOSINE TRIPHOSPHATE CONTENT OF NORMAL AND GLUCOSE-6-PHOSPHATE DEHYDROGENASE-DEFICIENT HUMAN BLOOD*