Iron metabolism in the erythrophagocytosing Kupffer cell

Authors

  • Hitoshi Kondo,

    1. Departments of Physiology and Biophysics, and Medicine, Albert Einstein College of Medicine, Bronx, New York 10461
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  • Kainosuke Saito,

    1. Departments of Physiology and Biophysics, and Medicine, Albert Einstein College of Medicine, Bronx, New York 10461
    Current affiliation:
    1. Wakakusa Clinic, 4–24, Wakakusa-cho Noboribetsu, Japan
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  • Joseph P. Grasso,

    1. Departments of Physiology and Biophysics, and Medicine, Albert Einstein College of Medicine, Bronx, New York 10461
    Current affiliation:
    1. Department of Anatomy, University of Connecticut Health Center, Farmington, Connecticut 06032
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  • Philip Aisen M.D.

    Corresponding author
    1. Departments of Physiology and Biophysics, and Medicine, Albert Einstein College of Medicine, Bronx, New York 10461
    • Department of Physiology and Biophysics, Albert Einstein College of Medicine, Bronx, New York 10461
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Abstract

Like the peritoneal macrophage, the isolated Kupffer cell is capable of processing and releasing iron acquired by phagocytosis of immunosensitized homologous red blood cells. When erythrophagocytosis is restrained to levels which do not affect cell viability, or less than 1.5 red cells/macrophage (phagocytic index of 150%), over 40% of iron acquired from red cells is released within 24 hr. More active erythrophagocytosis results in greater release of iron but progressive deterioration in cell viability. Iron release is temperature-dependent, the rate at 37° C being nearly 5-fold greater than at 4° C. Inclusion of either desferrioxaminine or apotransferrin in the culture medium augments iron release by 25 to 30%, with both agents together having an almost additive effect. Despite its effect on iron release, apotransferrin is not found in sonicates of Kupffer cells, while desferrioxamine appears to chelate iron within the cells. Ascorbate also enhances iron release, but at the expense of cell viability. Neither chloroquine nor colchicine at concentrations which do not affect cell viability influence iron release. The inflammatory state, characterized by hypoferremia due to impaired processing or release of iron by the reticuloendothelial system, may be modeled in vitro when serum from rats bearing turpentine-induced abscesses is included in the culture medium. Attempts to delineate the humoral agent responsible for this effect have not been successful, iron release being insensitive to the presence of interleukin-1, γ-interferon and tumor necrosis factor.

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