Margison G P, Bresil H, Margison J M, Montensano R
Cancer Lett. 1976 Nov;2(2):79-85. doi: 10.1016/s0304-3835(76)80015-8.
Rats were exposed chronically to unlabelled N,N-dimethylnitrosamine (25 ppm in the drinking water) then given a single dose of N-[3H]methyl-N-nitrosourea (10 mg/kg body weight). The rates of loss of tritium-labeled 7-methylguanine, O6-methylguanine and 3-methyladenine from the liver DNA in control and dimethylnitrosamine-treated rats were found not to be significantly different. Thus, under the conditions used, inhibition of the O6-methylguanine excision repair system does not seem to be a factor in the induction of liver tumours by chronic DMN application.
将大鼠长期暴露于未标记的N,N-二甲基亚硝胺(饮用水中浓度为25 ppm),然后给予单剂量的N-[³H]甲基-N-亚硝基脲(10 mg/kg体重)。结果发现,对照组和经二甲基亚硝胺处理的大鼠肝脏DNA中氚标记的7-甲基鸟嘌呤、O⁶-甲基鸟嘌呤和3-甲基腺嘌呤的丢失速率没有显著差异。因此,在所使用的条件下,O⁶-甲基鸟嘌呤切除修复系统的抑制似乎不是慢性应用二甲基亚硝胺诱导肝脏肿瘤的一个因素。