Factors influencing relative rates of synthesis of adult and fetal hemoglobin in vitro.

What causes the gradual decrease of fetal hemoglobin in the normal maturing infant, or the persistence of fetal hemoglobin in the blood of adults with certain congenital anemias, especially thalassemia, is not known. The production of fetal hemoglobin is evidently determined by genes nonallelic with those regulating adult hemoglobin formation (1). The fact that all red cells can be sickled in sickle cell anemia patients having relatively high proportions of fetal hemoglobin indicates that the same cell can produce both an adult hemoglobin (i.e., S) and fetal hemoglobin. This in turn implies that the rate of formation of fetal hemoglobin is not dependent upon the formation of a different cell by a different gene, but reflects a metabolic adaptation by the individual young red cells of the fetus or of the abnormal adult to the cellular environment (2). The present investigation concerns the effect of cellular environment on the relative quantities of fetal and adult hemoglobin synthesized in vitro by the reticulocytes of umbilical cord blood, as determined by the rates of Fe59 incorporation into heme and of C14-leucine incorporation into globin.