Biemond P, van Eijk H G, Swaak A J, Koster J F
J Clin Invest. 1984 Jun;73(6):1576-9. doi: 10.1172/JCI111364.
During inflammation, the superoxide anion (O-2) and hydrogen peroxide (H2O2) are produced by stimulated polymorphonuclear leukocytes and macrophages. The toxic effects of these reactive oxygen intermediates increase when traces of iron are present, because iron catalyzes the formation of the hydroxyl radical (OH.). Partially saturated iron-binding proteins, such as transferrin and ferritin, are unable to catalyze OH. formation in vitro. Mobilization of iron from these proteins is necessary for iron stimulation of OH. formation. This paper reports that stimulated polymorphonuclear leukocytes mobilize iron from human and horse ferritin, but not from human transferrin. Iron release from ferritin depends on O-2 because it can be prevented by the addition of superoxide dismutase. Catalase and dimethylsulfoxide have no inhibitory effect on iron mobilization. The efficiency of the iron release increases at low levels of O-2 production. Only O-2 produced by granulocytes is sufficient for iron mobilization, because solid potassium superoxide is also able to release iron from ferritin. We propose that this reaction may potentiate the formation of the OH. radical in inflammatory states.
在炎症过程中，受刺激的多形核白细胞和巨噬细胞会产生超氧阴离子（O₂⁻）和过氧化氢（H₂O₂）。当存在微量铁时，这些活性氧中间体的毒性作用会增强，因为铁会催化羟基自由基（OH·）的形成。部分饱和的铁结合蛋白，如转铁蛋白和铁蛋白，在体外无法催化OH·的形成。从这些蛋白质中动员铁对于铁刺激OH·的形成是必要的。本文报道，受刺激的多形核白细胞可从人及马的铁蛋白中动员铁，但不能从人转铁蛋白中动员铁。铁从铁蛋白中的释放依赖于O₂⁻，因为添加超氧化物歧化酶可阻止这种释放。过氧化氢酶和二甲基亚砜对铁的动员没有抑制作用。在低水平的O₂⁻产生时，铁释放的效率会增加。只有粒细胞产生的O₂⁻足以实现铁的动员，因为固体超氧化钾也能够从铁蛋白中释放铁。我们认为，这种反应可能会在炎症状态下增强OH·自由基的形成。
