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Protective Effect of Dinitrosyl Iron Complexes with Glutathione in Red Blood Cell Lysis Induced by Hypochlorous Acid

机译:谷胱甘肽与二亚硝基铁配合物对次氯酸诱导的红细胞裂解的保护作用

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摘要

Hypochlorous acid (HOCl), one of the major precursors of free radicals in body cells and tissues, is endowed with strong prooxidant activity. In living systems, dinitrosyl iron complexes (DNIC) with glutathione ligands play the role of nitric oxide donors and possess a broad range of biological activities. At micromolar concentrations, DNIC effectively inhibit HOCl-induced lysis of red blood cells (RBCs) and manifest an ability to scavenge alkoxyl and alkylperoxyl radicals generated in the reaction of HOCl with tert-butyl hydroperoxide. DNIC proved to be more effective cytoprotective agents and organic free radical scavengers in comparison with reduced glutathione (GSH). At the same time, the kinetics of HOCl-induced oxidation of glutathione ligands in DNIC is slower than in the case of GSH. HOCl-induced oxidative conversions of thiolate ligands cause modification of DNIC, which manifests itself in inclusion of other ligands. It is suggested that the strong inhibiting effect of DNIC with glutathione on HOCl-induced lysis of RBCs is determined by their antioxidant and regulatory properties.
机译:次氯酸(HOCl)是人体细胞和组织中自由基的主要前体之一,具有强大的抗氧化剂活性。在生物系统中,具有谷胱甘肽配体的二亚硝基铁络合物(DNIC)发挥一氧化氮供体的作用,并具有广泛的生物学活性。在微摩尔浓度下,DNIC有效抑制HOCl诱导的红细胞(RBC)裂解,并表现出清除HOCl与叔丁基过氧化氢反应中生成的烷氧基和烷基过氧基的能力。与还原型谷胱甘肽(GSH)相比,DNIC被证明是更有效的细胞保护剂和有机自由基清除剂。同时,与GSH相比,DNIC中HOCl诱导的谷胱甘肽配体氧化的动力学要慢。 HOCl诱导的硫醇盐配体的氧化转化导致DNIC的修饰,这表明其自身包含其他配体。提示谷胱甘肽对DNIC的强抑制作用是由HOCl诱导的RBC裂解所决定的,这取决于其抗氧化剂和调节特性。

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