Denk B, Filser J G, Oesterle D, Deml E, Greim H
Institut für Toxikologie, Gesellschaft für Strahlen- und Umweltforschung, Neuherberg, Federal Republic of Germany.
J Cancer Res Clin Oncol. 1988;114(1):35-8. doi: 10.1007/BF00390483.
The metabolite of E, EO, has been shown to be an extrahepatic carcinogen in rats in long-term studies. By means of a rat liver foci bioassay with 3 to 4 days old Sprague-Dawley rats, EO showed an initiating capacity in the livers of female, but not of male rats, measured as incidence of foci deficient in ATPase. After inhalation of 55 and 100 ppm EO, 8 h daily, 5 days weekly, and over 3 weeks, 1 week of pause, and another 8 weeks of promotion with polychlorinated biphenyls, foci incidence was generally low. But it was concentration dependently higher than in controls 12 weeks after starting the experiment. A linear concentration-effect relationship existed with a correlation coefficient of r = 0.991. With 33 ppm EO the number of foci was not enhanced significantly. The administration of 10,000 ppm E did not result in an enhanced foci incidence. In general the carcinogenic potential of EO, which has not been shown so far to cause hepatic tumors in rats, could be demonstrated in rat liver using a sensitive rat liver foci bioassay.
在长期研究中，环氧乙烷（EO）的代谢产物已被证明是大鼠的一种肝外致癌物。通过对3至4日龄的斯普拉格-道利大鼠进行大鼠肝灶生物测定，以缺乏ATP酶的灶发生率衡量，EO在雌性大鼠肝脏中显示出启动能力，但在雄性大鼠肝脏中未显示。每天吸入55和100 ppm的EO，每周5天，每天8小时，持续3周，暂停1周，然后用多氯联苯促进8周，灶发生率一般较低。但在实验开始12周后，其浓度依赖性地高于对照组。存在线性浓度-效应关系，相关系数r = 0.991。使用33 ppm的EO时，灶的数量没有显著增加。给予10,000 ppm的乙烯（E）并未导致灶发生率增加。总体而言，环氧乙烷的致癌潜力（迄今为止尚未显示在大鼠中引起肝肿瘤）可以通过敏感的大鼠肝灶生物测定在大鼠肝脏中得到证实。
