The Mechanism of Endotoxin-Induced Hypoferraemia

Abstract

The effect of endotoxin [etox] on the processing of erythrocyte Fe by RES cells of the liver and spleen was studied in rats using heat-damaged erythrocytes labeled with 59Fe. Etox did not alter the uptake of the damaged cells but markedly inhibited the subsequent early phase of Fe release from the RES cells. The inhibition was apparently due to a decreased rate of labeled heme destruction and an increased incorporation of radio-Fe into ferritin. Although early Fe release was decreased 0-2 h after etox administration, the diversion of Fe into ferritin was more marked when etox was given 18 h before. The block in Fe release was partially overcome in animals that were kept on an Fe-free diet or were phlebotomized. In these animals, the decreased rate of heme catabolism remained unaltered but less Fe was diverted into ferritin.