Cattanach B M, Papworth D, Patrick G, Goodhead D T, Hacker T, Cobb L, Whitehill E
Medical Research Council, Didcot, Oxfordshire, UK.
Mutat Res. 1998 Jul 17;403(1-2):1-12. doi: 10.1016/s0027-5107(97)00322-9.
In series of papers Nomura has reported that parental irradiation can lead to an enhanced incidence of lung and other tumours. However, in a recent study with BALB/cJ mice, using optimum conditions as defined by Nomura, we were unable to confirm this. We have now repeated the investigation using a different inbred strain, C3H/HeH, with and without tumour promotion in the F1 by urethane, again using protocols defined by Nomura. In a series of replicate studies spanning over 2 years, males were exposed to single, acute doses of 0, 250 and 500 cGy X-rays and thereafter placed with two females each in each of two consecutive weeks. Half the offspring from each treatment group and each week of mating were given 5 mmol/kg body weight of the urethane, while the remainder remained untreated. Most of the offspring produced were killed and scored for lung tumours at 6 months of age, while the rest were examined at 12 months of age. The proportion of fertile females and litter size provided evidence of a dose-dependent mutational response to the paternal irradiation, but no trace of a radiation-enhanced lung tumour incidence was detected among the progeny, whether in the urethane or non-urethane groups at 6 or 12 months of age, and whether assessed by numbers of mice with tumours, clusters of tumours, or cluster size. As seen in the BALB/cJ study, significant differences among different replicates were found, again suggesting a cyclical or seasonal variation in tumour incidence, but the variations seen with the two strains were not the same. The need for concurrent controls for tumour work was, nevertheless, again indicated. The overall findings do not therefore accord with those of Nomura. Furthermore, they do not support the causal association between the raised incidence of childhood leukaemia and non-Hodgkins lymphoma near Sellafield and the father's recorded radiation exposure during employment in the nuclear industry, as suggested by the Gardner report.
野村在一系列论文中报告称，亲代辐射可导致肺部及其他肿瘤的发病率增加。然而，在最近一项针对BALB/cJ小鼠的研究中，我们采用野村所定义的最佳条件，却未能证实这一点。我们现在使用不同的近交系C3H/HeH重复了该研究，在F1代中通过给予氨基甲酸乙酯进行肿瘤促进或不进行肿瘤促进，同样采用野村所定义的方案。在一项为期2年的系列重复研究中，雄性小鼠接受单次急性剂量的0、250和500 cGy X射线照射，之后在连续两周的每一周中，每只雄性小鼠与两只雌性小鼠配对。每个处理组以及每周交配产生的后代中，一半给予5 mmol/kg体重的氨基甲酸乙酯，其余则不进行处理。大多数后代在6个月龄时被处死并对肺部肿瘤进行评分，其余的在12个月龄时进行检查。可育雌性的比例和窝仔数提供了亲代辐射剂量依赖性突变反应的证据，但在子代中未检测到辐射增强的肺部肿瘤发病率的迹象，无论是在6个月龄还是12个月龄时的氨基甲酸乙酯组或非氨基甲酸乙酯组，无论通过有肿瘤的小鼠数量、肿瘤簇还是簇大小来评估。正如在BALB/cJ研究中所见，不同重复实验之间存在显著差异，这再次表明肿瘤发病率存在周期性或季节性变化，但两种品系中观察到的变化并不相同。然而，再次表明肿瘤研究需要同时设置对照。因此，总体研究结果与野村的研究结果不一致。此外，它们不支持加德纳报告所暗示的，在塞拉菲尔德附近儿童白血病和非霍奇金淋巴瘤发病率升高与父亲在核工业工作期间记录的辐射暴露之间的因果关系。
