Copper deficiency is known to result in a microcytic,
hypochromic anemia. Red cells of
copper-deficient animals have less
hemoglobin than their
copper-adequate counterparts. The objective of this work was to determine what role
copper plays in maintaining
hemoglobin levels. It was hypothesized that the primary defect lies in intracellular
iron metabolism. The influence of
copper supplementation on
iron uptake and storage was examined in a cell line capable of
hemoglobin synthesis. The results demonstrated that
copper supplementation of human K562 cells was associated with higher cytosolic
iron levels and
ferritin levels.
Copper supplementation of the cell culture altered the initial rate of
iron uptake from
transferrin and enhanced
iron uptake in noninduced cells; however, in
hemin-induced K562 cells, which express fewer
transferrin receptors on the cell surface,
copper appeared to reduce
iron uptake. Subsequent studies showed that the cells were able to take up the same amount of
iron from
transferrin when incubated over a longer period of time (24 hr). In the noninduced (non-
hemoglobin synthesizing) cells, proportionally more
iron was associated with the
ferritin. We concluded from these studies that
copper affects both uptake and storage of
iron and that
copper supplementation reduces cellular
iron turnover.