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Multivalent Metal-Induced Iron Acquisition from Transferrin and Lactoferrin by Myeloid Cells¹

Oyebode Olakanmi^*,, George T. Rasmussen^*,, Troy S. Lewis^*, John B. Stokes^*,, John D. Kemp^, and Bradley E. Britigan^2,*,,¶

Departments of ^* Internal Medicine and Pathology, Veterans Affairs Medical Center, Iowa City, IA 52246; and Departments of Internal Medicine and Pathology, and ^¶ Free Radical Biology Program, Department of Radiation Oncology, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA 52242

We previously described a unique, high-capacity, ATP-independent mechanism through which myeloid cells acquire Fe from low-m.w. chelates. The rate of this Fe acquisition is markedly increased by cellular exposure to multivalent metal cations. Because most Fe in vivo is bound to transferrin or lactoferrin, we examined whether this mechanism also contributes to myeloid cell acquisition of Fe from transferrin and/or lactoferrin. Using HL-60 cells as a model system, we show cellular acquisition of ⁵⁹Fe from both lactoferrin and transferrin that was unaffected by conditions that depleted the cells of ATP or disrupted their cytoskeleton. Fe acquisition was dramatically increased by cell exposure to various metals including Ga³⁺, Gd³⁺, Al³⁺, Fe³⁺, La³⁺, Zr⁴⁺, Sn⁴⁺, Cu²⁺, and Zn²⁺ by a process that was reversible. Exposure to these same metals also increased binding of both transferrin and lactoferrin to the cell surface by a process that does not appear to involve the well-described plasma membrane receptor for transferrin. Approximately 60% of the Fe acquired by the cells from transferrin and lactoferrin remained cell associated 18 h later. HL-60 cells possess a high-capacity multivalent metal-inducible mechanism for Fe acquisition from transferrin and lactoferrin that bears many similarities to the process previously described that allows these and other cell types to acquire Fe from low-m.w. Fe chelates. The biologic importance of this mechanism may relate to its high Fe acquisition capacity and the speed with which it is able to rapidly adapt to the level of extracellular Fe.

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