Inactivation of myeloperoxidase by benzoic acid hydrazide
نویسندگان
چکیده
منابع مشابه
Mechanism of inactivation of myeloperoxidase by 4-aminobenzoic acid hydrazide.
Hypochlorous acid is the most powerful oxidant generated by neutrophils and is likely to contribute to the damage mediated by these inflammatory cells. The haem enzyme myeloperoxidase catalyses its production from hydrogen peroxide and chloride. 4-Aminobenzoic acid hydrazide (ABAH) is a potent inhibitor of hypochlorous acid production. In this investigation we show that, in the presence of hydr...
متن کاملSecretion and inactivation of myeloperoxidase by isolated neutrophils.
Neutrophils prevent infection by ingesting and killing microorganisms but oxidants and proteases released by neutrophils damage host tissues. Our aim was to identify factors that regulate oxidant production by the enzyme myeloperoxidase (MPO) following secretion of MPO into the medium. Cells stimulated with phorbol myristate acetate (PMA) or opsonized zymosan particles secreted MPO and released...
متن کاملInhibition of myeloperoxidase by salicylhydroxamic acid.
Salicylhydroxamic acid inhibited the luminol-dependent chemiluminescence of human neutrophils stimulated by phorbol 12-myristate 13-acetate or the chemotactic peptide N-formylmethionyl-leucyl-phenylalanine (fMet-Leu-Phe). This compound had no inhibitory effect on the kinetics of O2.- generation or O2 uptake during the respiratory burst, but inhibited both the peroxidative activity of purified m...
متن کاملINHIBITION OF THE d-AMINO ACID OXIDASE BY BENZOIC ACID
Benzoic acid has been reported to inhibit the oxidation of succinic acid by muscle (l), the oxidation of butyric acid and crotonic acid by liver slices (2), and the oxidation of acetoacetic acid by kidney slices (3). It has also been reported to inhibit the oxygen uptake of liver and kidney slices, diaphragm, minced liver, kidney, and brain (4). In the present work it was found that benzoic aci...
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ژورنال
عنوان ژورنال: Archives of Biochemistry and Biophysics
سال: 2015
ISSN: 0003-9861
DOI: 10.1016/j.abb.2015.01.028