Whiteman Matthew, Rose Peter, Halliwell Barry
Department of Biochemistry, Faculty of Medicine, National University of Singapore, Singapore.
Biochem Biophys Res Commun. 2003 Apr 18;303(4):1217-24. doi: 10.1016/s0006-291x(03)00503-5.
Acute and chronic inflammation result in increased nitrogen monoxide (z.rad;NO) formation and the accumulation of nitrite (NO(2)(-)). Neutrophils stimulated by various inflammatory mediators release myeloperoxidase to produce the cytotoxic agent hypochlorous acid (HOCl). At physiologically attainable concentrations, we found that NO(2)(-) significantly inhibits HOCl-mediated DNA strand breakage and ascorbate depletion. HOCl-mediated inactivation of pure alpha(1)-antiproteinase or of the elastase inhibitory capacity of human plasma was inhibited by the addition of NO(2)(-). NO(2)(-) was more effective than ascorbate, GSH, and urate at inhibiting HOCl-mediated toxicity to human HepG2 cells in culture. These data suggest that NO(2)(-) may act in an antioxidant manner by removing HOCl at sites of inflammation where both HOCl and z.rad;NO are overproduced.
急性和慢性炎症会导致一氧化氮（·NO）生成增加以及亚硝酸盐（NO₂⁻）积累。受各种炎症介质刺激的中性粒细胞会释放髓过氧化物酶以产生细胞毒性剂次氯酸（HOCl）。在生理可达到的浓度下，我们发现NO₂⁻能显著抑制HOCl介导的DNA链断裂和抗坏血酸消耗。添加NO₂⁻可抑制HOCl介导的纯α₁-抗蛋白酶失活或人血浆弹性蛋白酶抑制能力。在抑制HOCl对培养的人HepG2细胞的毒性方面，NO₂⁻比抗坏血酸、谷胱甘肽和尿酸更有效。这些数据表明，在HOCl和·NO均过度产生的炎症部位，NO₂⁻可能通过清除HOCl以抗氧化方式发挥作用。
