Cell kinetics in mouse lung following administration of carcinogens and butylated hydroxytoluene.
Cell kinetics in mouse lung following administration of carcinogens and butylated hydroxytoluene.
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施用致癌物和丁基羟基甲苯后小鼠肺部的细胞动力学。
DOI：
10.1016/0041-008x(85)90254-6
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发表时间：
1985
影响因子：
3.8
通讯作者：
Morse,CC
中科院分区：
文献类型：
--
作者：
Witschi,HP;Morse,CC
描述了一系列的实验，其目的是测试的假设，在小鼠肺，增强肿瘤的发展可能会发生独立的整体肺泡细胞增生。雄性AJ小鼠给予1000 mg/kg的氨基甲酸乙酯或10 mg/kg的3-甲基胆蒽（MCA）。给药后6周，通过持续输注[3 H]胸苷标记肺泡细胞。尿烷产生了显着增生的II型肺泡细胞群，而MCA没有这样的效果。5次重复注射300 mg/kg的丁基羟基甲苯（BHT）（一种已知可促进肺肿瘤发展的方法）仅在前2周内产生细胞增生;随后小鼠对BHT的作用产生耐药性。在BHT之前用胡椒基丁醚处理的动物中，细胞增殖被消除。BHT对肿瘤发展仍有较小但显著的增强作用。然而，观察到单独的胡椒基丁醚极大地抑制了肿瘤的发展，这一效果相形见绌。这些数据不允许排除肺泡细胞增生作为BHT介导的小鼠肺肿瘤发展增强的机制。
A series of experiments is described which was designed to test the hypothesis that, in mouse lung, enhancement of tumor development could occur independently of overall alveolar cell hyperplasia. Male A J mice were given 1000 mg/kg of urethan or 10 mg/kg of 3-methylcholanthrene (MCA). Alveolar cells were labeled through continous infusion of [3H]thymidine for 6 weeks after administration of the carcinogen. Urethan produced a significant hyperplasia of the type II alveolar cell population, whereas MCA had no such effect. Five repeated injection of 300 mg/kg of butylated hydroxytoluene (BHT), a procedure known to enhance lung tumor development, produced cell hyperplasia only during the first 2 weeks; later the mice became resistant to the action of BHT. In animals treated with piperonyl butoxide prior to BHT, cell proliferation was abolished. BHT still had a small but significant enhancing effect on tumor development. However, this effect was dwarfed by the observation that piperonyl butoxide alone greatly inhibited tumor development. The data do not allow exclusion of alveolar cell hyperplasia as a mechanism in BHT-mediated enhancement of mouse lung tumor development.