Cleland L G, Betts W H, Vernon-Roberts B, Bielicki J
J Rheumatol. 1982 Nov-Dec;9(6):885-92.
The production of a potent hydroxylating species, presumed to be hydroxyl radical, was studied using hydroxylation of salicylate as a detector system. Oxygen-derived free radicals (ODFR) were generated by (a) autoxidation of ferrous-EDTA chelates and (b) enzymatically (xanthine oxidase/hypoxanthine). Hydroxylation by these ODFR-generating systems was inhibited by superoxide dismutase, hydroxyl radical scavengers and singlet oxygen quenchers. Low concentrations (1 mM-10 mM) of penicillamine stimulated hydroxylation by the autoxidation system, although higher concentrations were inhibitory; all concentrations were inhibitory in the enzymatic system. The chelating agents, diethylenetriamine pentaacetic acid and bathophenanthroline sulphonate, were inhibitory in both systems, as were the long acting anti-rheumatic drugs, gold sodium thiomalate and chloroquine. The mechanisms of hydroxyl radical generation described may have relevance to the mechanisms of ODFR generation occurring in vivo at sites of inflammation.
以水杨酸的羟基化作为检测系统，对一种假定为羟基自由基的强效羟基化物质的生成进行了研究。氧衍生自由基（ODFR）通过以下方式产生：（a）亚铁 - 乙二胺四乙酸螯合物的自氧化，以及（b）酶促反应（黄嘌呤氧化酶/次黄嘌呤）。超氧化物歧化酶、羟基自由基清除剂和单线态氧猝灭剂可抑制这些产生ODFR的系统引发的羟基化反应。低浓度（1 mM - 10 mM）的青霉胺可刺激自氧化系统的羟基化反应，尽管高浓度时具有抑制作用；在酶促系统中，所有浓度均具有抑制作用。螯合剂二乙烯三胺五乙酸和bathophenanthroline sulphonate在两个系统中均具有抑制作用，长效抗风湿药物硫代苹果酸金钠和氯喹也是如此。所描述的羟基自由基生成机制可能与炎症部位体内发生的ODFR生成机制相关。
