Experimental production of siderocytes.

Abstract

Siderocytosis was observed in swine with a defect in heme synthesis induced by a deficiency of pyridoxin and rapid blood regeneration induced by phlebotomy. The siderocytes in these conditions differed in several important respects. In pyridoxin deficiency, the siderotic granules were contained mostly within nonreticulated erythrocytes. The number of circulating siderocytes was greater in splenectomized than spleen-intact animals. When the nonreticulated siderocytes were transfused into normal recipients, they disappeared more rapidly from the circulation of spleen-intact than splenectomized pigs. When the nonreticulated siderocytes were incubated in vitro no significant disappearance of granules was noted. After phlebotomy, the siderotic granules were contained within reticulocytes. The degree of siderocytosis was as great in spleen-intact as in splenectomized animals. When the reticulated siderocytes were transfused into normal recipients, they disappeared as rapidly from the circulation of splenectomized as from spleen-intact pigs. When reticulated siderocytes were incubated in vitro most of the granules disappeared within 72 hours. In the presence of a defect in heme synthesis, the sideroblast may be unable to incorporate all of the Fe into hemoglobin as the cell matures and siderocytes are released into the circulation. The granule in the siderocyte is then dispersed or removed by the spleen. When erythropoiesis is greatly increased, terminal maturation divisions of marrow normoblasts are eliminated. Hemoglobin synthesis is incomplete in these reticulocytes. The cell which carries the Fe granule, mitochondria and polysomes completes hemoglobin synthesis while circulating. This process is independent of the spleen.