Effect of iron stores on hepatic metabolism of transferrin-bound iron

Hepatic and splenic accumulation and hepatic subcellular distribution of iron from a tracer dose of purified 59Fe-labeled transferrin were studied in normal, iron-deficient, iron-loaded, and pregnant rats. Hepatic and splenic 59Fe content was determined at varying intervals and the subcellular distribution then studied. In normal rats hepatic accumulation of 59Fe was biphasic with 9-10% of the dose present in the liver in the first 2 h postinjection, followed by a plateau of 4 h and a second rise to 20-25% at 16-18 h. During iron deficiency, 5-6% of the dose accumulated in the liver in 2 h and remained at this level. Iron loading resulted in a rapid accumulation of 17% of the dose at 6 h, and the normal plateau was absent. Splenic iron accumulation was similar in the normal and iron-loaded groups with approximately 3% of the dose present in the spleen over the 7-day study. Iron deficiency resulted in a threefold increase in splenic iron content to 10% of the dose at 1 h postinjection. Hepatic and splenic iron accumulation was markedly depressed in the pregnant group. Subcellular distribution studies showed that the 59Fe moved rapidly into ferritin in all groups and was not at any time associated with either lysosomes or mitochondria. These studies present further physiological data of the effects of differing iron states on hepatic and splenic iron accumulation.