Initial Depletion and Subsequent Recovery of Spermatogonia of the Mouse after 20 R of Gamma Rays and 100, 300, and 600 R of X-Rays

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Abstract
Experiments with both 100 and 300 r confirm our earlier conclusion that killing of cells is the primary factor in radiation-induced depletion of spermatogonia following acute exposure to X- and gamma-rays. The peak incidence of degeneration occurs 12 to 15 hours after irradiation. Furthermore, a return to the low normal incidence of necrotic cells occurs by 24 hours after 20 r, 3 days after 100 r, 7 days after 300 r, and 10 days after 600 r. The data support the conclusion that radiation-induced mitotic inhibition in spermatogonia is similar to that observed in other mitotically dividing cells and is not a major factor in depletion of the seminiferous epithelium. Division of surviving spermatogonia begins before degeneration of damaged cells has been completed. Accordingly, it is difficult to obtain exact estimates of the minimum number of surviving cells. As the radiation dose is increased from 20 to 600 r, the time of occurrence of the minimum number of type A spermatogonia is increased from 24 hours to 7 days as a result of the concurrent interaction of degenerative and repair processes. Both the testis as a whole and the individual tubules shrink markedly in size as the spermatocytes and spermatids present at the time of irradiation complete their development and are discharged from the tubule as mature sperm. As a result, the spatial relationships and relative areas occupied by remaining cells are greatly altered. Owing to their radiation resistance and spatial distribution, the number of Sertoli cells affords an excellent means for correcting counts of spermatogonia per tubule cross section. With doses of 300 r or less, no correction is required 0 to 10 days after irradiation. At intervals of 16 days or more, the experimental/control ratios for spermatogonia are consistently too high unless the correction is applied. The exactness with which cell stages can be identified and developmental sequences followed make the mouse testis a unique mammalian test system for study of the effects of irradiation. Not only are certain spermatogonial stages extremely sensitive to radiation, but their subsequent developmental sequences can be accurately timed and observations made at intervals which will reveal the response of any selected cell stage. Although certain of the responses described here may be specific for the testis, it is even more probable that the initial response and eventual recovery of type A spermatogonia is similar to that occurring in other germinative tissues. Extension of these techniques to other species and, particularly, studies on the description and duration of normal spermatogenesis would remove most of the ambiguities and confusion which have existed in the literature on radiation damage to the testis.