Shoji S, Masaoka Y, Kurosumi M, Katoh O, Watanabe H
Department of Environment and Mutation, Division of Environmental Biology, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima 734-8553, Japan.
Oncol Rep. 1998 Sep-Oct;5(5):1175-8. doi: 10.3892/or.5.5.1175.
Experiments were conducted to determine whether following genetic damage at germ cell stages induced by paternal exposure to 252Cf fission neutron could lead to tumorigenesis in the offspring. Seven-week-old C3H/HeNCrj male mice were irradiated with 252Cf fission neutrons, at doses of 0 and 12.5 cGy and were mated with nine-week-old C57BL/6NCrj females two weeks after the exposure. Three weeks later, it was found that the proportion of abnormal sperm in the 12.5 cGy-irradiated males was higher than that of 0 cGy-irradiated group. Embryo lethality among the F1 offspring was also found to be higher in the 12.5 cGy group than in the 0 cGy group, while the incidence of liver tumors among the F1 offspring increased in males only. These results suggest that the paternal 12. 5 cGy radiation exposure may have caused genetic transmission of liver tumor-associated traits, which is in line with findings that show steep increase in incidence of tumorigenesis in B6C3F1.
开展实验以确定父本暴露于252Cf裂变中子诱导生殖细胞阶段的遗传损伤后是否会导致子代肿瘤发生。对7周龄的C3H/HeNCrj雄性小鼠用252Cf裂变中子进行照射，剂量分别为0和12.5 cGy，并在照射后两周与9周龄的C57BL/6NCrj雌性小鼠交配。三周后，发现接受12.5 cGy照射的雄性小鼠中异常精子的比例高于接受0 cGy照射的组。还发现12.5 cGy组F1代子代的胚胎致死率高于0 cGy组，而F1代子代中肝脏肿瘤的发生率仅在雄性中增加。这些结果表明，父本接受12.5 cGy辐射暴露可能导致了肝脏肿瘤相关性状的遗传传递，这与B6C3F1肿瘤发生率急剧增加的研究结果一致。
