Rose G P, Taylor J M
Toxicology. 1985 Jan;34(1):43-56. doi: 10.1016/0300-483x(85)90077-0.
This study evaluates a major metabolite of misonidazole, desmethylmisonidazole, for its potential to induce peripheral nerve damage using the lysosomal enzyme correlates of neuropathological change, namely beta-glucuronidase and beta-galactosidase. The results showed that desmethylmisonidazole like misonidazole had a similar potential for inducing peripheral nerve damage as measured biochemically, but the dosing regimen had to be maintained for 10 consecutive days as opposed to the 7 days required for misonidazole.
本研究利用神经病理变化的溶酶体酶相关指标,即β-葡萄糖醛酸酶和β-半乳糖苷酶,评估米索硝唑的主要代谢产物去甲基米索硝唑诱导周围神经损伤的可能性。结果显示,去甲基米索硝唑与米索硝唑一样,经生化检测具有相似的诱导周围神经损伤的可能性,但给药方案必须连续维持10天,而米索硝唑只需7天。