Ferritin distribution and synthesis in sex-linked anemia.

The ferritin concentration of duodenum, liver, and spleen and the incorporation of L-leucine-3H into immunoprecipitated duodenal and liver ferritin was measured in genotypically normal (+/Y) mice and mice with sex-linked anemia (sla/Y), an X-linked recessive trait determined by a defect in intestinal iron absorption. Liver and splenic ferritin concentration was lower in sla/Y animals than in +/Y animals. Parenteral iron administration produced an increase in the duodenal, liver, and splenic ferritin concentration in both sla/Y and +/Y animals that was most striking in the case of the liver. Duodenal ferritin synthesis, both in vivo and in vitro, was increased in iron-deficient sla/Y animals and decreased in iron-deficient +/Y animals. In contrast, liver ferritin synthesis was decreased in both sla/Y and +/Y iron-deficient animals. In sla/Y animals fed an iron-deficient diet, duodenal ferritin synthesis decreased to near normal levels. These results indicating a high level of duodenal ferritin synthesis in standard-fed mice with sex-linked anemia suggest that the primary genetic defect is more likely a disorder of intramucosal iron transport than a primary disturbance of ferritin metabolism.