Lloyd D, Kristensen B
J Gen Microbiol. 1985 Apr;131(4):849-53. doi: 10.1099/00221287-131-4-849.
H2 production by the human protozoan parasite Trichomonas vaginalis was monitored continuously under a mobile gas phase using a membrane-inlet mass spectrometer. Simultaneous and continuous measurement of dissolved H2, O2 and CO2 indicated that H2 evolution was inhibited at levels of O2 (less than 0.25 microM) undetectable by the technique, whereas CO2 production was stimulated. Respiration was not stimulated by admitting H2 to the gas phase. Metronidazole inhibited both H2 and CO2 production. Values of K1 for inhibition of H2 formation in strain ATCC 30001 (metronidazole sensitive) of 0.16 mM and in strain 85 (metronidazole resistant) of 1.0 mM were obtained. These data suggest that metronidazole not only competes with protons as electron acceptor but that the drug itself or a product of reduction actively inhibits some hydrogenosomal enzyme or electron carrier involved in H2 production. Under these conditions metronidazole inhibition leads to irreversible loss of cell motility.
利用膜进样质谱仪在流动气相条件下连续监测人体原生动物寄生虫阴道毛滴虫产生氢气的情况。对溶解的氢气、氧气和二氧化碳进行同步连续测量表明,在该技术无法检测到的氧气水平(低于0.25微摩尔)下,氢气的释放受到抑制,而二氧化碳的产生则受到刺激。向气相中通入氢气并不会刺激呼吸作用。甲硝唑抑制氢气和二氧化碳的产生。在ATCC 30001菌株(对甲硝唑敏感)中抑制氢气形成的K1值为0.16毫摩尔,在85菌株(对甲硝唑耐药)中为1.0毫摩尔。这些数据表明,甲硝唑不仅作为电子受体与质子竞争,而且该药物本身或还原产物会积极抑制参与氢气产生的某些氢化酶或电子载体。在这些条件下,甲硝唑抑制会导致细胞运动性不可逆转地丧失。