Dulak L, Chiang G, Gunnison A F
Food Chem Toxicol. 1984 Aug;22(8):599-607. doi: 10.1016/0278-6915(84)90268-0.
The reproductive toxicology of sulphite was investigated in female rats with induced deficiencies of sulphite oxidase. Induction of sulphite oxidase deficiency was accomplished by administration of a diet with a high tungsten to molybdenum ratio. This animal model was chosen because it enables exposure of tissues to high systemic sulphite concentrations without debilitating side effects. The reproductive performance of female sulphite oxidase-deficient rats, exposed continuously to sulphite from about 3 wk before mating until the experiment was terminated on day 20 of gestation, was compared to that of unexposed rats with normal sulphite oxidase activity. There was no treatment-related trend in any of the parameters observed, including mating and pregnancy rates, gestational weight gain, pre-implantation loss, resorbed and dead foetuses, litter size, foetal weight and malformations. Of the spectrum of malformations observed in control and treated animals, only anophthalmia may have been treatment related. From these experiments, performed in an animal model that is a conservative metabolic analogue for man, we have concluded that there is no evidence to indicate that exposure of females to sulphite poses a significant reproductive hazard.
在亚硫酸盐氧化酶诱导缺乏的雌性大鼠中研究了亚硫酸盐的生殖毒性。通过给予高钨钼比的饮食来诱导亚硫酸盐氧化酶缺乏。选择这种动物模型是因为它能够使组织暴露于高全身性亚硫酸盐浓度而无有害的副作用。将从交配前约3周开始持续暴露于亚硫酸盐直至妊娠第20天实验结束的雌性亚硫酸盐氧化酶缺乏大鼠的生殖性能与具有正常亚硫酸盐氧化酶活性的未暴露大鼠进行比较。在所观察的任何参数中，包括交配和妊娠率、妊娠期体重增加、着床前损失、吸收和死亡胎儿、窝仔数、胎儿体重和畸形，均未发现与治疗相关的趋势。在对照动物和受试动物中观察到的一系列畸形中，只有无眼畸形可能与治疗有关。在一种对人类来说是保守的代谢类似物的动物模型中进行的这些实验得出结论，没有证据表明雌性暴露于亚硫酸盐会造成重大的生殖危害。
