Primaquine is an antimalarial that imposes heavy oxidative stress on circulating red cells. Erythrocytes cannot make new proteins or use mitochondria, so their only shield against oxidant damage is reduced glutathione, and keeping glutathione in its reduced form depends on a steady supply of NADPH. The single source of NADPH in the red cell is the pentose phosphate pathway, and the gatekeeper of that pathway is glucose-6-phosphate dehydrogenase. When this enzyme is deficient, the cell runs short of NADPH, glutathione cannot be regenerated, and an oxidant drug such as primaquine causes hemoglobin to precipitate as Heinz bodies, leading to acute intravascular hemolysis. The other listed defects do not fit: glucose-6-phosphatase deficiency is a glycogen storage disorder, alpha-ketoglutarate dehydrogenase belongs to the citric acid cycle, and pyruvate kinase deficiency produces a chronic hemolysis unrelated to oxidant drug exposure. The drug-induced hemolysis therefore points to G6PD deficiency. \[\boxed{\text{Glucose-6-phosphate dehydrogenase deficiency}}\]