Effects of Neonatal Estrogen Administration on Rat Testis Development with Particular Reference to Sertoli Cells

Abstract

An ultrastructural and morphometric study of the testes in 15-, 22-, 45-, and 90-day-old neonatally estrogenized rats was performed. At 45 days of age, the Sertoli cells appeared immature in estrogenized rats, whereas they were fully mature in the controls. This finding might be related to a deficiency in gonadotropins and androgens during the postnatal period. In 90-day-old estrogenized rats, however, Sertoli cell maturation had occurred, which might be attributed to a recovery of hormone levels. Cytoplasmic alterations, however, such as vacuolation, were present at this age. The morphometric study revealed decreased testicular and tubular volumes as well as decreased mean tubular diameters in the estrogenized animals. In contrast, the absolute tubular length increased more in these animals than in the controls during the period from 15 to 90 days of age. This lengthening process might be related to the large number of hypercurved tubules in the estrogenized rats.

Quantitative analysis of Sertoli cells in neonatally oestrogen-treated rats

“…In the present study, degenerating Sertoli cells were only occasionally found in control or oestrogen-treated rats, although a great number of degenerating germ cells was found in neonatally oestrogenized rats (Gaytan et al, 1986 (Griswold et al, 1977) and in prepubertal rats after antiandrogen treatment with flutamide (Viguier-Martinez et al, 1983). The factors regulating postnatal Sertoli cell replication remain unclear, and the contribution of the postnatal cell divisions to the adult Sertoli cell population is not well established.…”

“…Since important hormonal alterations are present in neonatally oestrogen-treated rats during the early postnatal period (Bellido et al, 1985), it is tempting to suggest that the postnatal Sertoli cell divisions are not dependent on hormonal levels, and the finding that the replication pattern of Sertoli cells was retained in organ cultures in the absence of extragonadal factors (Steinberger & Steinberger, 1971) supports this view. However, the smaller tubular volume present in oestrogen-treated rats (Gaytan et al, 1986) results in the relative numbers of Sertoli cells being greater in oestrogen-treated rats than in control ones. The pseudostratified distribution of Sertoli cell nuclei in the former seems to reflect not only a lack of cell maturation but an effect of the reduced tubular volume.…”

“…The morphological aspects of the seminiferous tubules in neonatally oestrogen-treated rats have been described elsewhere (Gaytan et al, 1986). Briefly, Sertoli cell nuclei in 22-day-old control rats were located at the periphery of the seminiferous epithelium and showed small nuclear membrane infoldings and a variable number of developing nucleoli, most of them associated with the peri¬ nuclear heterochromatin clumps (Fig.…”

“…Neonatally oestrogen-treated rats present several hormonal alterations during prepubertal development (Aguilar et al, 1984;Bellido et al, 1985), as well as an impaired maturation of various testicular cell types (Ohta & Takasugi, 1974;Gaytan et al, 1986). The (Elias & Hyde, 1980) corresponded to the nuclear diameter parallel to the basement membrane and was 4-86 ± OTOpm and 6-98 ± 016 pm for control rats at 22 and 45 days of age respectively, and 3-54 ± 0-17 pm and 5-42 ± 0-20 pm for oestrogen-treated rats at the same ages (mean ± s.e.m.…”

Progression of the Dose-Related Effects of Estrogenic Endocrine Disruptors, an Important Factor in Declining Fertility, Differs between the Hypothalamo-Pituitary Axis and Reproductive Organs of Male Mice

“…Diethylstilbestrol (DES), a synthetic non-steroidal estrogen, exhibits a high estrogenic activity by binding to the ERs, and is thus a useful model compound for evaluating the potential toxicity of a wide range of chemicals that affect or mimic estrogen activity [7]. Previous studies have shown that fetal and/or neonatal treatment of rodents with DES induces adverse changes similar to those that occur after administration of estradiol-17β [1,10,34], dichlorodiphenyl trichloroethane (DDT) and methoxychlor (an estrogenic pesticide currently used as a substitute for DDT) [14,38]. It is suggested that many of the adverse changes to the testis and reproductive tract induced by exposure to estrogens result from a combination of high estrogen and low andro-gen activity [39].…”