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Copper's influence on iron metabolism in K562 cells

Conference · · FASEB Journal (Federation of American Societies for Experimental Biology); (United States)
OSTI ID:5213448
;  [1]
  1. Univ. of Florida, Gainesville, (United States)
Copper deficiency is associated with a cellular defect in iron metabolism that results in poor hemoglobin synthesis. In order to determine this mechanisms, K562 cells, a human erythroleukemic cell line, were incubated with 1 mM bethocuproine disulfonic acid (BCS) to produce a copper deficiency or were supplemented with 8 {mu}M copper. Hemoglobin was simultaneously induced in some cells by the addition of 25 {mu}M hemin to the culture medium. Incubation with BCS resulted in a 30 to 40% reduction in intracellular Cu/Zn superoxide dismutase activity while supplementation resulted in a 20 to 50% increase in activity. The authors then examined the effect of these copper manipulations on {sup 59}Fe uptake from transferrin, on ferritin levels and on hemoglobin levels. Hemoglobin was only slightly affected by the copper treatments. In both noninduced cells and induced cells, copper supplementation resulted in a greater level of intracellular iron, a greater level of immunoreactive ferritin, and an enhanced uptake of {sup 59}Fe from transferrin. In BCS-incubated cells, intracellular iron, ferritin and {sup 59}Fe uptake from transferrin were reduced by at least 50%. Because the ferritin levels were reduced, intracellular iron mobilization did not appear to be impaired in copper deficiency. The results suggest that copper deficiency impairs the transport of iron by transferrin into the cell.
OSTI ID:
5213448
Report Number(s):
CONF-9104107--
Conference Information:
Journal Name: FASEB Journal (Federation of American Societies for Experimental Biology); (United States) Journal Volume: 5:5
Country of Publication:
United States
Language:
English

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