Roisman F R, Walz D T, Finkelstein A E
Inflammation. 1983 Dec;7(4):355-62. doi: 10.1007/BF00916300.
Superoxide radicals produced by phagocytic cells are considered to be important mediators in the rheumatoid inflammation. The effect of the gold compounds auranofin (AF) and gold sodium thiomalate (GST) on superoxide production by human leukocytes was investigated in two models of immunologic injury: immune-complex phagocytosis and frustrated phagocytosis. In both systems, AF (0.5-1.0 micrograms Au/ml) showed a potent inhibitory activity on superoxide generation, quantitated by ferricytochrome c and NBT reduction. GST showed only modest inhibition at higher concentrations (100 microM). The thiol protecting agent dithiothreitol, 1 mM, completely blocks the inhibitory effect of AF. The inhibition of the oxy radical generation by AF may play an important role in the control of rheumatoid inflammation; it is suggested that this action might be mediated through sulfhydryl-AF interaction at the cellular membrane level.
吞噬细胞产生的超氧自由基被认为是类风湿性炎症中的重要介质。在免疫损伤的两种模型中研究了金化合物金诺芬（AF）和硫代苹果酸金钠（GST）对人白细胞产生超氧的影响：免疫复合物吞噬作用和受阻吞噬作用。在这两个系统中，AF（0.5 - 1.0微克金/毫升）对超氧生成显示出强大的抑制活性，通过高铁细胞色素c和NBT还原进行定量。GST仅在较高浓度（100微摩尔）时表现出适度的抑制作用。1毫摩尔的硫醇保护剂二硫苏糖醇完全阻断了AF的抑制作用。AF对氧自由基生成的抑制可能在类风湿性炎症的控制中起重要作用；有人提出这种作用可能是通过细胞膜水平的巯基 - AF相互作用介导的。
