DEFECTIVE DELIVERY OF IRON TO THE DEVELOPING RED-CELL OF THE BELGRADE LABORATORY RAT

  • 1 January 1980
    • journal article
    • research article
    • Vol. 55  (4) , 645-648
Abstract
Erythroid cell Fe and transferrin uptake and release was studied in the anemia of the Belgrade laboratory rat (gene symbol, b), an autosomal recessive trait characterized by hypochromia and hyperferrinemia. When reticulocyte-rich red cells were incubated in vitro with doubly (59Fe, 125I) labeled transferrin, b/b cells demonstrated a significantly higher uptake of transferrin (164% of control at 60 min) and a significantly lower uptake of Fe (21% of control at 60 min) than control cells. These findings with b/b cells were simulated by NaF-treated control cells, but not by trypsin-treated control cells. When reticulocytes exposed to doubly labeled transferrin were incubated in normal rat plasma, there was a substantial loss of125I from the b/b cells (mean 71%) and control cells (mean 49%), but only a loss of 59Fe from the b/b cells (mean 21%). A defect in the delivery of Fe to the b/b reticulocyte, which is distal to the binding of transferrin to its cell surface receptor, was suggested.