[en] Mice were irradiated with 36, 216, and 504 rad at the stages of spermatozoa (1 - 7 days before mating), spermatids (15 - 21 days), spermatogonia (64 - 80 days), and oocytes (1 - 7 days before ovulation). Their offspring (F₁) were examined in terms of dominant lethality and anomalies. Approximately 90 % of induced tumors occurred in the lung. There was no significant difference in tumorigenesis following either rapid or fractionated exposure to spermatozoa and spermatids. Fractionated exposure to spermatogonia induced no tumors, suggesting their repair ability. Rapid exposure to oocytes also indicated an evidence of repair ability. Abnormalities scarcely occurred in F₁ of mice irradiated at the stage of spermatogonia. However, dose-response relationships were seen in F₁ of mice irradiated at the stage of oocytes, and the frequency of anomalies was extremely higher than that in the other three sperm cells. Radiation-induced mutations were very similar to radiation-induced tumors. The pattern of inheritance was that of a dominant with about 40 % penetrance. The frequency of tumors was independent of whether or not F₁ mice had x-ray-induced translocations. When mice was treated with urethane combined with x-rays, the penetrance rate increased. The frequency of tumors per rad was approximately 10 times higher than that of dominant mutations affecting the skeleton and 100 times higher than that of site-directed reccessive mutations. (Namekawa, K.)