Abstract

Introduction

Materials & Methods

Results

Discussion & Conclusion

References

Discussion
Board

We have previously demonstrated the existence of a multivalent-metal inducible, ATP-independent, transferrin receptor (TFR)-independent mechanism whereby myeloid cells can acquire iron from small molecular weight (smw) chelates. We postulated that this process could allow phagocytes to rapidly sequester cytotoxic iron. We now report that this iron acquisition process is present in other cell types. Hepatocytes, erythroid, epithelial, and endothelial cells each possess a multivalent-metal (e.g. gallium)inducible means of iron acquisition from smw chelates. Multivalent metals changed both KM and Vmax with myeloid cell lines, but for non-myeloid cells there was only a change in Vmax. Since most extracellular iron is chelated to transferrin or lactoferrin, we determined if this same iron acquisition mechanism contributes to iron acquisition from transferrin or lactoferrin by myeloid cells. ATP-independent acquisition of iron from transferrin and lactoferrin whose rate is markedly increased by multivalent metals was demonstrated using the HL-60 cell line. These metals increased binding of transferrin and lactoferrin to the cells but did not change TFR expression. These data suggests that many cell types share a metal-inducible pathway for iron acquisition from smw chelates. This mechanism may also contribute to cellular acquisition of iron from transferrin and lactoferrin.

Back to the top.
Presentation Number SAolakanmi0238
Keywords: iron, transferrin, lactoferrin, gallium, phagocyte