Abstract
Results of these experiments are in agreement with the conclusion that depletion of spermatogenic cells following radiation results from sensitivity of spermatogonia. Depletion of spermatogonia results from killing of cells, and not from inhibition of mitosis of type A cells. Necrosis of spermatogonia occurs primarily in late interphase or early prophase of the 1st postirradiation division. A few cells may undergo one or more divisions before degenerating. In contrast to spermatogonia, damage to primary spermatocytes remains latent until meiotic metaphase, anaphase, and telophase. Many abnormal figures typical of chromosomal aberrations occur during meitoic division, and nuclei of resulting spermatids show abnormal size variation. Intermediate and type B spermatogonia show extreme sensitivity to radiation. Type A spermatogonia are of heterogeneous sensitivities dependent upon mitotic activity and stage of development. Pachytene spermatocytes are less sensitive than most type A cells; spermatids and sperm showed no visible changes with the doses used. Quantitative and qualitative differences in sensitivity are correlated with nuclear changes in spermatogenesis. The conclusion that nuclear reactions are primarily responsible for behavior of these cells is further strengthened by results obtained with more favorable cytological material, where correlation of nuclear state and sensitivity to chromosome breakage can be demonstrated.

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