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(Received for publication, August 22, 1996, and in revised form, October 24, 1996)
From the Research Service, VA Medical Center, Iowa City, Iowa 52246 and Department of Internal Medicine, The University of Iowa College
of Medicine, Iowa City, Iowa 52242
The trivalent metals iron, aluminum, and gallium
greatly increase the rate of iron acquisition from low molecular weight
chelates by human myeloid cells. The present study explores the
mechanism responsible. Gallium-induced iron acquisition was shown to
lead to stable cellular association of iron, the magnitude of which varied with the chelate to which the iron was bound. The majority of
this iron initially associated with the plasma membrane. Cellular depletion of ATP did not affect the response to gallium nor did it
require the continued presence of extracellular gallium. However, continued cell association of gallium was needed as subsequent cellular
exposure to metal chelators resulted in a rapid loss of the
"induced" phenotype. Other trivalent metals (lanthanum and
gadolinium) and tetravalent metals (tin and zirconium) but not divalent
metals also induced iron acquisition. Neither enhanced iron reduction
nor protein kinase C or tyrosine kinases appeared involved in
gallium-mediated induction of iron acquisition. Exposure of HL-60 cells
to polyvalent cationic metals results in a dramatic and sustained
increase in the rate of iron acquisition from low molecular weight
chelating agents. This could be important for the rapid clearance of
iron by phagocytes from the extracellular environment at sites of local
tissue damage.
Volume 272, Number 5,
Issue of January 31, 1997
pp. 2599-2606
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.
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