The organ distribution of intravenously injected hepatic ferritin either labelled with 59Fe or with 59Fe and 125I, was studied in pregnant guinea-pigs. At 5 h 71.2% of injected 59Fe was present in the placenta and fetus. Transfer of 59Fe to the fetus was slow, with 11.2% present at 5 h and 38.6% at 21 h. Analysis of a placental cellular lysate for 59Fe and 125I revealed that the injected iron was present as intact ferritin at 2 h but by 21 h the ferritin had been catabolized, the 125I excreted and the 59Fe incorporated into endogenous ferritin. Most of the fetal 59Fe counts were detected in the liver, with 35.3% of the transferred 59Fe in ferritin, 30.4% in haemoglobin and 10.6% in a low molecular weight pool. The uptake of labelled ferritin by the placenta was inhibited by a 300-fold molar excess of unlabelled ferritin but not by albumin, asialofetuin or by the injection of carbon particles. A nonsignificant reduction in uptake was noted after injection of mannosylated bovine serum albumin. The mannosidase inhibitor swainsonine had no effect. Iron transfer to the fetus was not affected by various microtubular inhibitors. Presaturation of endogenous transferrin with oral carbonyl iron prevented iron release from the feto-placental unit back into the maternal circulation. In consequence, marrow 59Fe uptake by the maternal marrow was reduced. The ferrous chelator 2,2'-bipyridine significantly reduced 59Fe transfer to the fetus and this occurred irrespective of whether the chelator was given prior to or after 59Fe ferritin administration. The ferric chelator desferrioxamine had no such effect. Electron microscopy of placental tissues revealed endocytosis of ferritin molecules. These results indicate that the guinea-pig placenta takes up homologous tissue ferritin and transfers the iron slowly to the fetus after reductive mobilization. The process is compatible with a receptor-mediated pathway.