The iron concentration within enterocytes varies directly with the body s requirement for iron. Absorptive cells in iron-deficient humans and animals contain little stainable iron, whereas this is increased significantly in subjects who are replete in iron. Untreated phenotypic hemochromatosis creates little stainable iron in the enterocyte, similar to iron deficiency. In contrast to findings in iron deficiency, enhanced erythropoiesis, or hypoxia, endotoxin rapidly diminishes iron absorption without altering enterocyte iron concentration. This suggests that endotoxin and, perhaps, cytokines alter iron absorption by a different mechanism.
Most iron delivered to nonintestinal cells is bound to transferrin.
Otherwise, the nonsaturability of transferrin binding to cells cannot be explained. In the classical transferrin pathway, the transferrin iron complex enters the cell within an endosome. Acidification of the endosome releases the iron from transferrin so that it can enter the cell. The apotransferrin is delivered by the endosome to the plasma for reutilization. The method by which the transferrin receptor independent pathway delivers iron to the cell is not known.