Red cell metabolism in iron-deficiency anemia

Abstract

Iron-deficiency anemia is characterized by diminished synthesis of hemoglobin andthe presence of small, misshapen red cells. Alterations in cell morphology usually denote some derangement in cell metabolism. Studies of red cell metabolism in 37 children with nutritional iron-deficiency anemia revealed an increase in reduced glutathione concentration and increased enzymatic activity in both the Embden-Meyerhof pathway (hexokinase and lactate dehydrogenase) and hexosemonophosphate shunt (glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase). The activity of acetylcholinesterase (a membrane enzyme) was normal. Glycolysis by iron-deficient cells was also increased. No correlation could be demonstrated between increased metabolic activity and the presence of reticulocytes. Both enzyme activity and glycolysis returned to normal after correction of the anemia by iron therapy. The reasons for this altered metabolic activity and its relationship to cell viability are discussed. It is suggested that the increased energy and redox potential of iron deficient cells may represent a compensatory mechanism secondary to defective synthesis of hemoglobin and stroma.