Hoepelman I M, Jaarsma E Y, Verhoef J, Marx J J
Department of Internal Medicine, University Hospital Utrecht, The Netherlands.
Br J Haematol. 1988 Dec;70(4):495-500. doi: 10.1111/j.1365-2141.1988.tb02523.x.
It has been shown that iron (III) impairs the function of polymorphonuclear granulocytes (PMN). We have studied the effect of iron (II), on the membrane function of PMN, by assessing the uptake of radiolabelled Staphylococcus aureus by these cells. Iron (II), significantly impaired PMN phagocytic function. Addition of ascorbic acid reduced uptake further. Ferrous ascorbate, molar ratio 1:20, impaired phagocytic capacity of PMN significantly at iron concentrations as low as 1-10 microM. The toxic effect of iron (II) was not observed when desferrioxamine or transferrin was present in the incubation medium. The oxygen-free radical scavengers thiourea, mannitol and catalase prevented toxicity mediated by ferrous ammoniumsulphate but not by ferrous ascorbate (molar ratio of 1:20). Although high concentrations of ascorbic acid inhibited the generation of .OH and also the formation of the DMPO-.OH adduct by zymosan stimulated PMN, toxicity of iron increased. Iron (II) impaired the uptake of S. aureus by PMN of a patient with chronic granulomatous disease while iron (III) did not. Iron mediated impairment of PMN function is not only a result of the generation of toxic oxygen metabolites but also of direct interaction of iron (II) or an iron (II)-oxygen intermediate with molecules of the cell membrane.
业已表明，铁（III）会损害多形核粒细胞（PMN）的功能。我们通过评估这些细胞对放射性标记的金黄色葡萄球菌的摄取，研究了铁（II）对PMN膜功能的影响。铁（II）显著损害了PMN的吞噬功能。添加抗坏血酸会进一步降低摄取量。摩尔比为1:20的抗坏血酸亚铁在低至1 - 10微摩尔的铁浓度下就会显著损害PMN的吞噬能力。当孵育培养基中存在去铁胺或转铁蛋白时，未观察到铁（II）的毒性作用。无氧自由基清除剂硫脲、甘露醇和过氧化氢酶可防止硫酸亚铁铵介导的毒性，但不能防止抗坏血酸亚铁（摩尔比为1:20）介导的毒性。尽管高浓度的抗坏血酸会抑制·OH的生成，也会抑制酵母聚糖刺激的PMN形成DMPO - ·OH加合物，但铁的毒性却增加了。铁（II）会损害慢性肉芽肿病患者的PMN对金黄色葡萄球菌的摄取，而铁（III）则不会。铁介导的PMN功能损害不仅是有毒氧代谢产物生成的结果，也是铁（II）或铁（II） - 氧中间体与细胞膜分子直接相互作用的结果。
