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首页> 外文期刊>Nature >Formation of nitric oxide-derived inflammatory oxidants by myeloperoxidase in neutrophils.
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Formation of nitric oxide-derived inflammatory oxidants by myeloperoxidase in neutrophils.

机译：嗜中性粒细胞中的髓过氧化物酶形成一氧化氮衍生的炎性氧化剂。

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摘要

Nitric oxide (.NO) plays a central role in the pathogenesis of diverse inflammatory and infectious disorders. The toxicity of .NO is thought to be engendered, in part, by its reaction with superoxide (O2.-), yielding the potent oxidant peroxynitrite (ONOO-). However, evidence for a role of ONOO- in vivo is based largely upon detection of 3-nitrotyrosine in injured tissues. We have recently demonstrated that nitrite (NO2-), a major end-product of .NO metabolism, readily promotes tyrosine nitration through formation of nitryl chloride (NO2Cl) and nitrogen dioxide (.NO2) by reaction with the inflammatory mediators hypochlorous acid (HOCl) or myeloperoxidase. We now show that activated human polymorphonuclear neutrophils convert NO2- into NO2Cl and .NO2 through myeloperoxidase-dependent pathways. Polymorphonuclear neutrophil-mediated nitration and chlorination of tyrosine residues or 4-hydroxyphenylacetic acid is enhanced by addition of NO2- or by fluxes of .NO. Addition of 15NO2- led to 15N enrichment of nitrated phenolic substrates, confirming its role in polymorphonuclear neutrophil-mediated nitration reactions. Polymorphonuclear neutrophil-mediated inactivation of endothelial cell angiotensin-converting enzyme was exacerbated by NO2-, illustrating the physiological significance of these reaction pathways to cellular dysfunction. Our data reveal that NO2- may regulate inflammatory processes through oxidative mechanisms, perhaps by contributing to the tyrosine nitration and chlorination observed in vivo.
机译：一氧化氮（.NO）在多种炎症和感染性疾病的发病机理中起着核心作用。人们认为.NO的毒性部分是由于其与超氧化物（O2.-）反应而产生的，是强氧化剂过氧亚硝酸盐（ONOO-）。然而，ONOO-体内作用的证据主要基于在受伤组织中检测到3-硝基酪氨酸。我们最近证明，.NO代谢的主要最终产物亚硝酸盐（NO2-）通过与炎性介质次氯酸（HOCl）反应，通过形成亚硝酰氯（NO2Cl）和二氧化氮（.NO2）来促进酪氨酸硝化）或髓过氧化物酶。我们现在显示，活化的人类多形核中性粒细胞通过髓过氧化物酶依赖性途径将NO2-转化为NO2Cl和.NO2。通过添加NO2-或通入.NO，可增强多形核中性粒细胞介导的酪氨酸残基或4-羟苯基乙酸的硝化和氯化作用。 15NO2-的添加导致硝化酚醛底物的15N富集，证实了其在多形核中性粒细胞介导的硝化反应中的作用。 NO2-加剧了多形核中性粒细胞介导的内皮细胞血管紧张素转化酶的失活，说明了这些反应途径对细胞功能障碍的生理意义。我们的数据表明，NO2-可能通过氧化机制调节炎症过程，可能是通过促进体内观察到的酪氨酸硝化和氯化作用来实现的。

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