Hepatocyte iron kinetics in the rat explored with an iron chelator

Abstract

The hepatocyte metabolism of 59Fe-labeled ferritin, Hb-haptoglobin and transferrin was examined in rats. All 3 forms of 59Fe became transiently available to desferrioxamine (DF) at the time they would otherwise have entered storage or alternative pathways of Fe metabolism. Differences in both the patterns of spontaneous 59Fe reutilization, by normal and Fe-deficient rats and the partition of chelate Fe excretion between bile and urine, suggested that Fe in transit within hepatocytes did not behave as a single common pool. Ferritin 59Fe, entering a pool of nonradioactive Fe the size of which is determined by liver Fe stores, was chelated predominantly into the bile. Transferrin 59Fe was distinguished by a greater reflux to the erythron in Fe-deficient rats and by excretion of a larger proportion of 59Fe chelated by DF in the urine. Hb-haptoglobin 59Fe followed a metabolic pathway which was relatively independent of both the Fe stores and DF. If the heterogeneous behavior of rat hepatocyte transit Fe has a parallel in man, alterations in the size of similar chelatable Fe pools could explain the dependence of DF-induced urine and fecal Fe excretion on both liver Fe stores and the level of erythropoiesis.