Blakley B R
Can J Comp Med. 1984 Jul;48(3):299-302.
Female Swiss mice were exposed to methylmercury in the drinking water for 15 weeks. The mice were administered concentrations of methylmercury ranging from 0 to 2.0 micrograms/mL mercury. After three weeks of the 15 week exposure period, the mice were administered urethan (1.5 mg/g) intraperitoneally. Pulmonary adenoma formation was evaluated 12 weeks later. Methylmercury exposures of 0.2 and 0.5 micrograms/mL did not affect the number of adenomas, but 2.0 micrograms/mL mercury caused a significant increase in adenoma production. A dose-dependent increase in the mean tumor diameter was seen at methylmercury exposures up to 0.5 micrograms/mL. No further increase in diameter was seen at higher exposures (2.0 micrograms/mL). The changes in adenoma production were seen at exposure levels of methylmercury which did not cause any clinical manifestations. Animal weight gains and water consumption were not affected. In addition, urethan-induced sleeping times which reflect the rate of urethan metabolism or excretion remained unchanged.
雌性瑞士小鼠饮用含甲基汞的水15周。给小鼠施用的甲基汞浓度范围为0至2.0微克/毫升汞。在15周暴露期的三周后,给小鼠腹腔注射乌拉坦(1.5毫克/克)。12周后评估肺腺瘤的形成情况。0.2和0.5微克/毫升的甲基汞暴露不影响腺瘤数量,但2.0微克/毫升汞导致腺瘤生成显著增加。在甲基汞暴露量高达0.5微克/毫升时,平均肿瘤直径呈剂量依赖性增加。在更高暴露量(2.0微克/毫升)时未观察到直径进一步增加。在未引起任何临床表现的甲基汞暴露水平下可见腺瘤生成的变化。动物体重增加和水消耗未受影响。此外,反映乌拉坦代谢或排泄速率的乌拉坦诱导睡眠时间保持不变。