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Defective delivery of iron to the developing red cell of the Belgrade
laboratory rat
JA Edwards, AL Sullivan and JE Hoke
Erythroid cell iron 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 iron (21% of control at 60 min) than control cells. These
findings with b/b cells were simulated by sodium-fluoride-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 of 125I from both the b/b cells (mean 71%) and
control cells (mean 49%), but only a loss of 59Fe from the b/b cells (mean
21%). These findings suggest a defect in the delivery of iron to the b/b
reticulocyte, which is distal to the binding of transferrin to its cell
surface receptor.
Volume 55,
Issue 4,
pp. 645-648,
04/01/1980
Copyright © 1980 by The American Society of Hematology
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