Paternal Exposure to Radiation and Offspring Cancer in Mice: Reanalysis and New Evidences

• Published in: JOURNAL OF RADIATION RESEARCH 1991, Vol.32 (suppl-2), p.64-72
• Main Author: NOMURA, TAISEI
• Format: Article
• Language: English
• ISSN: 0449-3060; 1349-9157
• DOI: 10.1269/jrr.32.SUPPLEMENT2_64

Parental exposure to radiation could induce various kinds of tumors in the next generation. In ICR mice, a large and significant increase of adult types tumor was observed in the F1 offspring after X-ray exposure at spermatozoa and spermatid stages, and less clear increase was observed after spermatogonial exposure. Mature oocytes were resistant upto 1 Gy, but very sensitive to tumor induction at higher doses. While there was no difference in the tumor incidence between acute and fractionated (0. 36 Gy at 2 hr intervals) irradiation at post-gonial stages, a large reduction of tumor incidence was observed after spermatogonial and mature oocyte exposure, suggesting some repairs of X-ray damages in these germ cells. Acute lymphocytic leukemia was not induced in ICR and LT mice after spermatogonial exposure, while a large increase of adult type cancers was observed in F1 offspring. However, 1. 9-3. 2 fold and 4. 5-7. 4 fold increases of leukemia incidence were observed in ICR and LT mice, when spermatozoa stage was treated with the X-ray doses of 0. 36-5. 04 Gy and 3. 6-5. 04 Gy, respectively, indicating the large difference in the sensitivity of developing germ cells to leukemia induction by radiation in the F1 offspring. In contrast to ICR and LT mice, N5 strain developed about 10 or 18 times higher incidence of leukemia in the offspring after spermatogonial or spermatozoa exposure to 5. 04 Gy of X-rays, respectively, showing a marked difference in the sensitivity to the leukemia induction by radiation between mouse strains. These differential sensitivities between germ cell stages and also between mouse strains reconcile the difference between two population studies in Hiroshima/Nagasaki and Sellafield. However, there were large differences in the doubling doses for leukemia induction between the mouse experiments and Sellafield study in human.