Kettle A J, Winterbourn C C
Department of Pathology, Christchurch School of Medicine, Christchurch Hospital, New Zealand.
Free Radic Res Commun. 1991;12-13 Pt 1:47-52. doi: 10.3109/10715769109145766.
Human neutrophils stimulated with opsonized zymosan promoted hypochlorous acid (HOCl)-dependent loss of monochlorodimedon. Formation of HOCl was completely inhibited by catalase, and it was also inhibited up to 70% by SOD. There was no inhibition by desferal, DTPA, mannitol or dimethylsulphoxide, which excluded the involvement of .OH. Our results indicate that generation of O2- by neutrophils enables these cells to enhance their production of HOCl. Furthermore, inhibition of neutrophil processes by SOD and catalase does not necessarily implicate .OH. We propose that O2- may potentiate oxidant damage at inflammatory sites by boosting the myeloperoxidase-dependent production of HOCl.
用调理酵母聚糖刺激的人中性粒细胞促进了一氯二甲基酮依赖于次氯酸（HOCl）的损失。过氧化氢酶完全抑制了HOCl的形成，超氧化物歧化酶（SOD）也将其抑制了高达70%。去铁胺、二乙烯三胺五乙酸（DTPA）、甘露醇或二甲基亚砜均无抑制作用，这排除了羟基自由基（·OH）的参与。我们的结果表明，中性粒细胞产生超氧阴离子（O₂⁻）能使这些细胞增强HOCl的产生。此外，SOD和过氧化氢酶对中性粒细胞过程的抑制不一定意味着有·OH参与。我们提出，O₂⁻可能通过促进髓过氧化物酶依赖的HOCl产生来增强炎症部位的氧化损伤。
