Hodgkiss R J, Middleton R W
Biochem Pharmacol. 1985 Jun 15;34(12):2175-8. doi: 10.1016/0006-2952(85)90414-9.
The inhibitor of glutathione biosynthesis, buthionine sulphoximine (BSO) has been used to deplete endogenous thiols in mammalian cells in vitro. The effect of such depletion on the toxicity of nitroaromatic compounds has been investigated. Substantial enhancement of both aerobic and hypoxic toxicity of the 2-nitroimidazole, misonidazole is observed in thiol-depleted cells; the hypoxic toxicities of metronidazole, nitrofurantoin and nimorazole are also increased by thiol depletion. These data of significance for the potential combined use of BSO with nitroaromatic radiosensitizers to increase their radiosensitizing efficiency in radiotherapy, and as a potential method for enhancing the efficiency of anti-protozoal nitroaromatic drugs.
谷胱甘肽生物合成抑制剂丁硫氨酸亚砜胺（BSO）已被用于在体外耗尽哺乳动物细胞中的内源性硫醇。已经研究了这种耗尽对硝基芳族化合物毒性的影响。在硫醇耗尽的细胞中观察到2-硝基咪唑米索硝唑的需氧毒性和缺氧毒性均显著增强；甲硝唑、呋喃妥因和尼莫唑的缺氧毒性也因硫醇耗尽而增加。这些数据对于BSO与硝基芳族放射增敏剂联合使用以提高其在放射治疗中的放射增敏效率具有重要意义，并且作为提高抗原生动物硝基芳族药物效率的一种潜在方法。
