Hypochlorous acid as a precursor of free radicals in living systems

被引:116
作者
Panasenko, O. M. [1 ,2 ]
Gorudko, I. V. [3 ]
Sokolov, A. V. [1 ,4 ]
机构
[1] Res Inst Physicochem Med, Moscow 119435, Russia
[2] Pirogov Russian Natl Res Med Univ, Moscow 117997, Russia
[3] Belarusian State Univ, Dept Biophys, Minsk 220050, BELARUS
[4] Russian Acad Med Sci, North West Branch, Inst Expt Med, St Petersburg 197376, Russia
基金
俄罗斯基础研究基金会;
关键词
myeloperoxidase; hypochlorous acid; free radicals; reactive halogen species; halogenative stress; biomarker of myeloperoxidase; inflammation; LOW-DENSITY-LIPOPROTEIN; HYDROGEN-PEROXIDE-CHLORIDE; HUMAN NEUTROPHILS EMPLOY; MYELOPEROXIDASE-CATALYZED OXIDATION; MATRIX PROTEOGLYCAN DEGRADATION; RESPIRATORY-DISTRESS-SYNDROME; BRONCHOALVEOLAR LAVAGE FLUID; EGG-YOLK PHOSPHATIDYLCHOLINE; NITROGEN-CENTERED RADICALS; TERT-BUTYL HYDROPEROXIDE;
D O I
10.1134/S0006297913130075
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Hypochlorous acid (HOCl) is produced in the human body by the family of mammalian heme peroxidases, mainly by myeloperoxidase, which is secreted by neutrophils and monocytes at sites of inflammation. This review discusses the reactions that occur between HOCl and the major classes of biologically important molecules (amino acids, proteins, nucleotides, nucleic acids, carbohydrates, lipids, and inorganic substances) to form free radicals. The generation of such free radical intermediates by HOCl and other reactive halogen species is accompanied by the development of halogenative stress, which causes a number of socially important diseases, such as cardiovascular, neurodegenerative, infectious, and other diseases usually associated with inflammatory response and characterized by the appearance of biomarkers of myeloperoxidase and halogenative stress. Investigations aimed at elucidating the mechanisms regulating the activity of enzyme systems that are responsible for the production of reactive halogen species are a crucial step in opening possibilities for control of the development of the body's inflammatory response.
引用
收藏
页码:1466 / 1489
页数:24
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