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目的：给昆明种小鼠以2．0Gy钴60γ射线一次性照射前后，分别给予口服胸腺因子D（TFD），观察其对钴60γ射线诱发小鼠骨髓嗜多染红细胞微核的影响。方法：将小鼠随机分成5组：对照组；钴60γ射线A组；TFD预防组；钴60γ射线B组；TFD治疗组。每组16只，雌雄各半。TFD的剂量为0．625mg／kg，每日灌胃1次，连续8d。TFD预防组与射线A组于d9照射，d10处死；TFD治疗组与射线B组于d1照射，d10处死。钴60γ射线剂量为2．0Gy，全身一次照射。小鼠处死后制作骨髓片，常规染色与计数。结果表明：无论是TFD预防组还是治疗组，其微核率均比相应的钴60γ射线组下降，差异极其显著（P＜0．01）。而2个钴60γ射线组之间和2个TFD组之间，差异均不显著（P＞0．05）。结论；TFD可在短期内恢复由于钴60γ射线所造成的小鼠骨髓嗜多染红细胞微核率的上升，从遗传毒理学的角度证实了TFD抗辐射损伤的作用。
OBJECTIVE: To study the effects of oral administration of 2.0Gy Cobalt 60γ ray on the micronuclei of bone marrow-derived polychromatic erythrocytes in Kunming mice before and after irradiation with cobalt 60γ ray. Methods: The mice were randomly divided into 5 groups: control group; cobalt 60γ ray group A; TFD prevention group; cobalt 60γ ray group B; TFD treatment group. Each group of 16, male and female half. TFD dose of 0.625mg / kg, gavage once daily for 8d. The TFD group and the radiation group A were exposed to d9 and d10. The TFD treatment group and the radiation group B were d1 irradiated and d10 sacrificed. Cobalt 60 gamma ray dose 2.0Gy, a whole body irradiation. Mice were killed after the production of bone marrow tablets, conventional staining and counting. The results showed that the micronucleus rate of both the TFD prevention group and the treatment group was significantly lower than that of the corresponding cobalt 60γ-ray group (P <0.01). However, there was no significant difference between the two cobalt 60γ-ray groups and the two TFD groups (P> 0.05). Conclusion TFD can restore the increase of micronuclei in mouse bone marrow polychromatic erythrocytes caused by cobalt 60γ-ray in a short period of time, and from the perspective of genotoxicity, the anti-radiation damage of TFD is confirmed.