Adkins B, Van Stee E W, Simmons J E, Eustis S L
J Toxicol Environ Health. 1986;17(2-3):311-22. doi: 10.1080/15287398609530825.
Strain A/J mice were exposed by inhalation for 6 h/d, 5 d/wk, for 6 mo to carbon disulfide, 1,2-dibromoethane, ethylene oxide, naphthalene, nitrogen dioxide, or vinyl chloride. Significant increases in pulmonary adenoma formation were observed following exposure to 300 ppm carbon disulfide; 20 and 50 ppm 1,2-dibromoethane; 70 and 200 ppm ethylene oxide; 10 ppm nitrogen dioxide; and 50, 200, and 500 ppm vinyl chloride compared to control animals. Repeated studies with 1,2-dibromoethane, ethylene oxide, and vinyl chloride gave similarly significant results. Exposure of mice to 30 ppm naphthalene did not elicit a significant adenoma response. Histopathological examination of lungs from animals in these studies revealed multiple alveolar adenomas. Results from earlier studies with these chemicals, using strain A mice and Swiss mice, and bioassay information with rats and mice were compared with these data. These results provide further information for the validation of this in vivo model as a tool for predicting oncogenic potential following chemical exposure.
将A/J品系小鼠每天吸入暴露6小时，每周5天，持续6个月，暴露于二硫化碳、1,2 - 二溴乙烷、环氧乙烷、萘、二氧化氮或氯乙烯中。与对照动物相比，暴露于300 ppm二硫化碳；20 ppm和50 ppm 1,2 - 二溴乙烷；70 ppm和200 ppm环氧乙烷；10 ppm二氧化氮；以及50 ppm、200 ppm和500 ppm氯乙烯后，观察到肺腺瘤形成显著增加。对1,2 - 二溴乙烷、环氧乙烷和氯乙烯进行的重复研究也得到了类似的显著结果。将小鼠暴露于30 ppm萘未引发显著的腺瘤反应。这些研究中动物肺部的组织病理学检查显示有多个肺泡腺瘤。将这些化学物质早期使用A品系小鼠和瑞士小鼠进行的研究结果以及大鼠和小鼠的生物测定信息与这些数据进行了比较。这些结果为验证该体内模型作为预测化学物质暴露后致癌潜力的工具提供了进一步的信息。
