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- W12323964 abstract "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 thatmore » copper deficiency impairs the transport of iron by transferrin into the cell.« less" @default.
- W12323964 created "2016-06-24" @default.
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- W12323964 date "1991-03-15" @default.
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- W12323964 title "Copper's influence on iron metabolism in K562 cells" @default.
- W12323964 hasPublicationYear "1991" @default.
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