Abstract
Rats have been subjected to treatment with oestrogenic hormone and their testes examined after 1 month, 2 months, 4 months and 6 months. The general sequence of events occurring in the seminiferous tubules is an obvious decline in the number of spermatids accompanied by a more gradual reduction in the spermatocyte population until finally all that remains are spermatogonia, comparatively few primary spermatocytes which fail to complete prophase, and Sertoli cells. The spermatogonia are the least affected by oestrogenic hormone while spermatocytes appear to be the most sensitive. It is the differential sensitivity of the germ cells when exhibited in segments of tubules in different stages of the cycle of the seminiferous epithelium which is responsible for a marked variation in damage observed mainly after 1 and 2 months' treatment. After this period the variation becomes less because a more extreme condition is reached generally. Highly purified preparations of follicle stimulating hormone (F.S.H.) and luteinizing hormone (L.H.) have also been administered to rats while under prolonged treatment with oestrogenic hormone and in which spermatogenesis was suppressed. Injections of L.H. daily for 2 weeks produced no obvious change in the appearance of the seminiferous tubules. After a similar treatment with F.S.H. there was a rather dramatic return to essentially normal conditions. This helps to establish that the effect of oestrogens on the seminiferous tubules is an indirect one due to a deficiency of F.S.H. With the aid of electron microscopy it has been shown that the degenerating germ cells, which occur as a result of oestrogen treatment, are phagocytosed by the Sertoli cells. This is accompanied by a considerable increase in the lipid content (visible as droplets) of the Sertoli cells. After 1 month the presence of unsaturated sterols can be demonstrated histo-chemically in some of the droplets; by the end of 2 months practically all of the lipid contains sterols. When F.S.H. is administered the amount of lipid is reduced to normal levels and the sterol content diminished as spermatogenesis is restored. This appears to be the first demonstration of the metabolism of sterols by the Sertoli cells coincident with marked spermatogenetic activity. While the interstitium was not studied in detail, oestrogenic hormone does not produce any apparent increase in its lipid content or produce marked hyperplasia.