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The important investigations of Carson, Dern and Beutler and their co-workers (1-8) have identified an inherent deficiency of erythrocyte glucose-6-phosphate dehydrogenase as the biochemical basis for the hemolytic anemia induced in "sensitive" individuals by administration of primaquine and certain related compounds. The relationship between this enzyme deficiency and the mechanism of the hemolytic response remains to be defined. The hemolysis certainly involves disruptive changes in the red cell membrane. The possibility of a direct action of primaquine on the membrane must be seriously considered. As Rothstein (9) has pointed out, it is important to examine the effects of toxic agents on the membranes of the cells as well as their effects on intracellular metabolism, since any administered agent will, of course, first contact the cell membrane. In normal red blood cells, the studies of Beutler, Dern and Alving (5) indicate that hemolysis is produced in vitro only by concentrations of primaquine greatly in excess of pharmacologic blood levels. A prehemolytic loss of K+ is, however, induced by subhemolytic concentrations of these agents. It was the purpose of the present investigations to study these in vitro prelytic abnormalities in red cell permeability. It is accepted that the event of hemolysis occurring within a population of red cells represents an "all or none" response of individual cells, although the degree of hemolglobin loss by the individual cell varies with the lytic stimulus (10).

EFFECTS OF PRIMAQUINE AND OTHER RELATED COMPOUNDS ON THE RED BLOOD CELL MEMBRANE. I. NA+ AND K+ PERMEABILITY IN NORMAL HUMAN CELLS*