Late effects of gamma radiation on the murine spermatogonia

Following irradiation, the recovery of the seminiferous epithelium could be due to regeneration of the isolated spermatogonial population or to a combination of isolated spermatogonial regeneration and compensatory mitosis of the type A₁ spermatogonial clones that precede the A₁ mitoses leading to the type A₂ spermatogonial generation. The purpose of this investigation was to determine the late effects of radiation injury to the isolated and type A₁ spermatogonia and to determine their respective roles in the repopulation of the seminiferous epithelium.

To examine these alternatives, adult male CRF 1 mice were irradiated with either 600 or 800 rad of ⁶⁰Co gamma radiation at a dose rate of 19 rad/min. . Gross testicular morphology, seminiferous tubule cross sections and seminiferous tubule whole mounts were evaluated at 4 week intervals up to 16 weeks after irradiation.

Following absorbed doses of 600 and 800 rad, testis weight was reduced to 60 and 50 percent of control respectively, at 4 weeks after irradiation. Subsequently, weight increased to 75 and 68 percent of control at 20 (600 rad) and 16 (800 rad) weeks after irradiation. Tubular cross sections containing germ cells were 70 and 45 percent of control at 4 weeks, but reached 90 (600 rad) and 75 (800 rad) percent of control within 16 weeks after irradiation.

The late effects of radiation on the isolated and A₁ spermatogonial populations were determined within the fertile regions of the seminiferous tubules. The isolated spermatogonial population remained below control levels during the 16 weeks after 600 and 800 rad doses. The mitotic activity of the isolated spermatogonia remained below control levels in stages I through VI. The clonal A₁ spermatogonial population in the tubular segments containing germ cells was below but near control levels during the entire investigation period as was the distribution of the relative clonal sizes at 16 weeks after irradiation. Therefore, an apparent compensatory increase in the A₁ population occurring between stages II and VIII was not a result of an increase in clonal size, but rather an increase in the mitotic activity of the A₁ spermatogonial clones.

The very low incidence of isolated mitoses, the high incidence of clonal mitoses and the apparent absence of isolated spermatogonia at the borders between the fertile and sterile regions suggest that increased clonal mitotic activity in the fertile regions is the mechanism by which the A₁ population is replenished. The low mitotic activity of the isolated population seen in the irradiated mice, as well as the appearance of many clones comprised of an odd number of spermatogonia, indicated that the clonal population may be a self perpetuating system in that through clonal fragmentation new clones are contributed to the proliferating A₁ population.