Kitchin K T, Brown J L
Environmental Toxicology Division, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711.
Cancer Lett. 1990 Aug;53(1):67-71. doi: 10.1016/0304-3835(90)90012-m.
Female Sprague-Dawley rats were given 0, 168, 840, 2550 or 4200 mg/kg of 1,4-dioxane 21 and 4 h before sacrifice. Hepatic DNA damage (by the alkaline elution technique), ornithine decarboxylase activity (ODC), reduced glutathione content, cytochrome P-450 content and serum alanine aminotransferase activity (ALT) were determined. Treatment with 1,4-dioxane increased hepatic DNA damage and cytochrome P-450 content at doses of 2550 and 4200 mg/kg. Large increases in the activity of hepatic ODC were observed at 840, 2550 and 4200 mg/kg of 1,4-dioxane. Thus the data suggest that 1,4-dioxane is a weak genotoxic carcinogen in addition to being a strong promoter of carcinogenesis (a non-genotoxic carcinogen).
在处死前21小时和4小时，给雌性斯普拉格-道利大鼠分别灌胃0、168、840、2550或4200mg/kg的1,4-二氧六环。测定肝脏DNA损伤（采用碱性洗脱技术）、鸟氨酸脱羧酶活性（ODC）、还原型谷胱甘肽含量、细胞色素P-450含量和血清丙氨酸转氨酶活性（ALT）。给予2550和4200mg/kg剂量的1,4-二氧六环处理后，肝脏DNA损伤和细胞色素P-450含量增加。给予840、2550和4200mg/kg剂量的1,4-二氧六环后，肝脏ODC活性大幅增加。因此，数据表明，1,4-二氧六环除了是一种强大的致癌促进剂（非遗传毒性致癌物）外，还是一种弱遗传毒性致癌物。
