Moreno S N, Docampo R
Environ Health Perspect. 1985 Dec;64:199-208. doi: 10.1289/ehp.8564199.
The mechanism of the trichomonicidal activity of metronidazole and other 5-nitroimidazoles appears to depend on the ferredoxin-mediated reduction of their nitro group, with generation of a reactive metabolite or metabolites which interact with DNA leading to a subsequent inhibition of nucleic acid and protein synthesis. Redox cycling of these compounds under aerobic conditions appears to be a detoxification reaction by inhibiting net reduction of the drugs, thereby inhibiting their uptake. On the other hand, redox cycling of nitrofurans or other compounds with more positive reduction potential results in formation of high steady-state concentrations of oxygen-derived metabolites that might be of toxicological significance. It seems likely that reduced metabolites of nitroimidazoles (perhaps through covalent binding to tissue macromolecules and/or thiols depletion) are also involved in the nitroimidazoles' toxic effects to animal tissues and in their mutagenic and carcinogenic action.
甲硝唑和其他5-硝基咪唑的杀滴虫活性机制似乎取决于铁氧化还原蛋白介导的硝基还原，生成一种或多种活性代谢产物，这些代谢产物与DNA相互作用，随后导致核酸和蛋白质合成受到抑制。在有氧条件下，这些化合物的氧化还原循环似乎是一种解毒反应，通过抑制药物的净还原，从而抑制其摄取。另一方面，呋喃妥因或其他具有更正还原电位的化合物的氧化还原循环会导致形成高稳态浓度的氧衍生代谢产物，这可能具有毒理学意义。硝基咪唑的还原代谢产物（可能通过与组织大分子的共价结合和/或巯基耗竭）似乎也参与了硝基咪唑对动物组织的毒性作用及其诱变和致癌作用。
