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高铁血红素-谷胱甘肽配合物对次氯酸诱导的红细胞溶解的保护作用。

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

机构信息

Research Center of Biotechnology of the Russian Academy of Sciences, Bach Institute of Biochemistry, Moscow 119071, Russia.

National Medical Research Centre for Cardiology, Moscow 121552, Russia.

出版信息

Oxid Med Cell Longev. 2019 Apr 8;2019:2798154. doi: 10.1155/2019/2798154. eCollection 2019.

DOI:10.1155/2019/2798154
PMID:31089406
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6476047/
Abstract

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 -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.

摘要

次氯酸(HOCl)是细胞和组织中自由基的主要前体之一,具有很强的促氧化剂活性。在活细胞系统中,具有谷胱甘肽配体的二硝酰基铁复合物(DNIC)作为一氧化氮供体发挥作用,具有广泛的生物学活性。在微摩尔浓度下,DNIC 能有效抑制 HOCl 诱导的红细胞(RBC)裂解,并能清除 HOCl 与 -丁基过氧化氢反应生成的烷氧基和烷过氧基自由基。与还原型谷胱甘肽(GSH)相比,DNIC 是更有效的细胞保护剂和有机自由基清除剂。同时,DNIC 中谷胱甘肽配体被 HOCl 诱导氧化的动力学比 GSH 慢。HOCl 诱导的硫醇配体的氧化转化导致 DNIC 的修饰,表现为包含其他配体。研究表明,DNIC 与谷胱甘肽对 HOCl 诱导的 RBC 裂解的强烈抑制作用取决于其抗氧化和调节特性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bba/6476047/76a17d388f0e/OMCL2019-2798154.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bba/6476047/f57c3d9ce023/OMCL2019-2798154.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bba/6476047/b4a62f390e73/OMCL2019-2798154.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bba/6476047/71ea621e172d/OMCL2019-2798154.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bba/6476047/88958a9f90a8/OMCL2019-2798154.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bba/6476047/5d082cb9888d/OMCL2019-2798154.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bba/6476047/5b784d959f9d/OMCL2019-2798154.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bba/6476047/76a17d388f0e/OMCL2019-2798154.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bba/6476047/f57c3d9ce023/OMCL2019-2798154.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bba/6476047/b4a62f390e73/OMCL2019-2798154.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bba/6476047/71ea621e172d/OMCL2019-2798154.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bba/6476047/88958a9f90a8/OMCL2019-2798154.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bba/6476047/5d082cb9888d/OMCL2019-2798154.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bba/6476047/5b784d959f9d/OMCL2019-2798154.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bba/6476047/76a17d388f0e/OMCL2019-2798154.007.jpg

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