The discrepancy between these two weights can be explained by radiation-induced cell death of Sertoli cells in the young monkeys. In the adult testis, the Sertoli cells are terminally differentiated, nondividing cells, but at the time of irradiation, these cells were still proliferating and, hence, radiosensitive. In recent years, it has become clear that the number of Sertoli cells determines the amount of seminiferous epithelium and, thereby, the potential testicular weight. Apparently, no mechanism regulates the numbers of Sertoli cells by enhanced or prolonged proliferation when their numbers are low or by less proliferation or apoptosis when their numbers are high. Hence, irradiation before terminal differentiation of the Sertoli cells in the monkey, as in the rat, causes loss of Sertoli cells and, thereby, decreases the potential adult testicular weight. From this, it follows that, when testes are irradiated before adulthood, the killing of spermatogonial stem cells cannot be studied by establishing the degree of repopulation or testicular weight. The RI will be relatively too high, because the surviving stem cells will sooner repopulate the shorter tubules that are present, and testicular weight will be too low because of Sertoli cell loss.
In most testes of irradiated monkeys, varying numbers of tubules were found that were dilated. Serial sections were made of some testes in which these dilated tubules were common to see whether these tubules were obstructed at some point. This was never found to be the case, and several of these tubules were observed to connect to the rete testis while still dilated, suggesting that the obstruction was present in the rete testis or further up, in the efferent ducts or the epididymis. However, serial sections also did not reveal an obstruction or other abnormalities in these tissues. Probably, at some earlier time after irradiation, a transient problem with drainage of the tubular fluid from the testis took place, causing swelling and irreversible damage in some tubules. In this respect, an interesting comparison can be made with the morphology of the testes of estrogen receptor а-deficient mice, in which a mixture of relatively normal and dilated seminiferous tubules was also seen, caused by inappropriate fluid resorption in the efferent ductules.