赤血球負荷ラット腹腔マクロファージを用いた"RE Iron Block"(網内系鉄ブロック)に関する研究

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Reticuloendothelial (RE) system plays a key role in iron metabolism. A senescent red blood cell is processed by the RE system at the end of its life span, and the iron derived from hemoglobin is returned into serum transferrin which shuttles iron to various tissues, mainly bone marrow, via the transferrin receptor. It has been well recognized that the patients with chronic inflammation develop a moderate anemia with a decreased serum iron level. Cartwright designated this anemia as the anemia of chronic disorders (ACD). The cause of the ACD has been suspected as an impaired iron release from the RE system ("RE iron block") in inflammation. However, virtually nothing is known about the mechanism involved in iron release from the RE system and no direct evidence to prove "RE iron block" has been reported. In the present paper, in vitro studies on iron release to transferrin from non-stimulated or stimulated macrophages which had phagocytosed rat red blood cells in vitro or in vivo were carried out and the following results were obtained: (1) Each macrophage phagocytosed less than 1.8 rat red blood cells, which seemed within the physiological dose for the macrophage to digest and metabolize hemoglobin. Non-stimulated or stimulated macrophages showed no significant difference in phagocytosis and digestion of red blood cells. (2) One milliliter of culture medium for erythrophagocytosed macrophages contained only 8-10 ng of iron which was low enough to enable examination of subtle changes in iron saturation of transferrin with 6 M urea PAGE. (3) Non-stimulated macrophages erythrophagocytosed in vitro or in vivo released iron actively to transferrin in the medium, within 1 hour of incubation. The released iron from macrophage bound to a-site of transferrin preferentially. (4) Contrary, peptone or methemalbumin stimulated macrophages (inflammatory macrophages) which were both erythrophagocytosed in vitro showed no iron release to transferrin in the culture medium even after 24 hours of incubation. ?(5) Increased heme oxygenase activity induced by methemalbumin seemed to have no effect on iron release to transferrin from macrophages. These experimental results proved the active iron release to transferrin in vitro from macrophages which had processed red cells, and revealed an impaired iron release from macrophages during inflammation, namely "RE iron block" in vitro. Also, the present study indicates that the mechanism for impaired "RE iron block" in inflammation is neither an increased synthesis of apoferritin nor a lactoferrin secreted by polymorphonuclear leukocytes, but rather an impaired iron release from a pre-release iron pool to transferrin itself.
札幌医科大学の論文
1985-04-01

赤血球負荷ラット腹腔マクロファージを用いた"RE Iron Block"(網内系鉄ブロック)に関する研究

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札幌医科大学 | 論文

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