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目的 研究致癌物氨基甲酸己酯作用下 ,持续低剂量率γ射线照射 (PLDRR)对两代小鼠肺肿瘤形成的干预作用和肿瘤细胞增殖、p5 3抗癌基因表达的调节。方法 2 0 μGy min× 42d1 3 7Csγ射线照射两代昆明种小鼠 ,化学致癌物单次腹部皮下注射量为 :2 0 0 0mg kg ,观察肺肿瘤的形成 ,免疫组化分析肺肿瘤组织PCNA和p5 3抗癌基因。结果 PLDRR并未明显干预化学致癌物对肺肿瘤的形成 ,实验组与对照组肺肿瘤发生率分别为 94%和 95 83 % ,差异无显著性 (P >0 0 5 χ2 =0 0 0 4) ,但在PLDRR下受精、怀孕及出生后仍在该环境中生长发育的仔代小鼠肺肿瘤发生率仅为 5 6 6 0 % ,明显低于祖代小鼠肺肿瘤发生率 (P <0 0 1χ2 =2 0 81) ,瘤体直径和平均发瘤数也低于祖代小鼠。仔鼠突变型p5 3蛋白产物和PCNA的表达显著下降。结论 PLDRR可诱发仔代小鼠对肺肿瘤的“适应性反应” ,仔代小鼠肿瘤细胞增殖能力降低。
Objective To study the effect of continuous administration of carcinogenic hexyl carbamate and low-dose-rate γ-irradiation (PLDRR) on the lung tumor formation in two generations of mice and the regulation of tumor cell proliferation and p53 anti-oncogene expression. METHODS: Two generations of Kunming mice were irradiated with 20 μg y min×42d1 3 7Cs γ-rays. The number of chemical carcinogens injected into the abdominal cavity was 200 mg kg/kg. The formation of lung tumors was observed. The lung cancer tissue PCNA was evaluated by immunohistochemistry. P5 3 anti-oncogene. Results PLDRR did not significantly interfere with the formation of lung tumors by chemical carcinogens. The incidence of lung tumors in the experimental and control groups was 94% and 958.3%, respectively, with no significant difference (P > 0 0 5 χ 2 =0 0 4). However, the incidence of lung tumors in the young mice that were fertilized, pregnant, and still growing in the environment after PLDRR was only 56.6%, which was significantly lower than the incidence of lung tumors in the progeny mice (P < 0 0 1 χ 2 = 2 0 81), the tumor diameter and the average number of tumors were also lower than in the ancestral mice. The expression of p53 mutant protein and PCNA was significantly decreased in the pups. Conclusion PLDRR can induce an “adaptive response” to lung tumors in the offspring mice.