SummaryMice maintained on a pyridoxine deficient diet developed a progressive anemia characterized by hypochromia, microcytosis, reticulocytosis, and erythroid hyperplasia of the marrow and spleen. Circulating siderocytes were greatly increased. Hypertransfusion of these animals with red cells obtained from pyridoxine deficient donors resulted in erythroid aplasia. The response to exogenous erythropoietin was comparable to that observed in erythropoietin treated control hypertransfused mice. These data indicate normal erythroid differentiation and maturation in pyridoxine deficient mice.The authors thank Drs. H. Baker and O. Frank of the East Orange Veterans Administration Hospital, East Orange, New Jersey for the pyridoxine assays.The erythropoietin was collected and concentrated by the Department of Physiology, University of the Northeast, Corrientes, Argentina, further processed and assayed by the Hematology Research Laboratories, Children's Hospital of Los Angeles, under Research Grant HE 10880 (Natio...