Blumer J L, Simpson J M, Lucas S V, Webster L T
Immunopharmacology. 1979 Dec;2(1):51-61. doi: 10.1016/0162-3109(79)90020-1.
It has been suggested that the suppression of cell-mediated immune phenomena following niridazole administration is most likely due to a niridazole metabolite rather than the parent drug. This hypothesis was tested using two inbred strains of mice that manifest different rates of microsomal niridazole oxidation and reduction. DBA/2J mice were found to metabolize niridazole at a rate approximately 3-fold greater than C57BL/6J mice under both aerobic and anaerobic conditions. Niridazole was found to be more potent with respect to suppression of cutaneous delayed hypersensitivity in the former than in the latter. An immunosuppressive component was isolated from the urine fraction obtained from niridazole-treated rats. This component was found to be chromatographically pure; have a simple UV absorbance spectrum containing no 360 nm absorbing material characteristic of niridazole; to show no strain difference with respect to potency or efficacy in the ear-swelling assay for cutaneous delayed hypersensitivity; and to be 10(7) times more potent than niridazole with respect to the suppression of cutaneous delayed hypersensitivity.
有人提出，服用硝唑咪后细胞介导免疫现象的抑制很可能是由于硝唑咪的一种代谢产物，而非母体药物。使用两种表现出不同微粒体硝唑咪氧化和还原速率的近交系小鼠对这一假说进行了验证。发现在需氧和厌氧条件下，DBA/2J小鼠代谢硝唑咪的速率比C57BL/6J小鼠快约3倍。结果表明，硝唑咪对前者皮肤迟发型超敏反应的抑制作用比对后者更强。从硝唑咪处理大鼠的尿液组分中分离出一种免疫抑制成分。该成分经色谱分析为纯品；具有简单的紫外吸收光谱，不含硝唑咪特有的360nm吸收物质；在皮肤迟发型超敏反应的耳部肿胀试验中，其效力和功效没有品系差异；在抑制皮肤迟发型超敏反应方面，其效力比硝唑咪强10^7倍。
