Abstract:Estradiol-17p (E2-17p) treatment induced dose-related reduction of sperm population and eventual azoospermia, atrophy of accessory organs, and suppressed serum LH and testosterone levels. In spite of all these alterations mating behavior was not affected, although the number of implantation sites paralleled the reduction of sperm population, suggesting that the primary detectable response to E2-17P treatment is related to the steroidogenic components of the testis and the hypothalamic pituitary axis. The durat… Show more
“…Moreover, complete degeneration of seminiferous tubules and depopulation of germinal cells occurred in testis of rats treated for 24 days which indicate that these effects are dependent on the duration of the treatment. Hunt et al (1979) also reported that the duration of treatment is more critical for the induction of azoospermia in the rat than the total dose of estradiol, in support of our present observations and earlier data (Rao and Chinoy, 1983). Thus, E2B manifested a direct effect on testicular steroidogenesis by inhibiting the Leydig cell function concomitant with an accumulation of protein and cholesterol and a reduction in the activities of 3ß-and 17ß-hvdroxysteroid dehydrogenases (HSDs) in steroidogenic organs in treated rats.…”
Section: Discussionsupporting
confidence: 93%
“…The suppression of 17x-hydroxylass and 17-20 desmolase activities by estrogens in testis of laboratory animals and human being have also been extensively reviewed (Dörner et al, 1975;Steinberger et al, 1977;Dufau et al, 1978). The loss of ofgan weights, significant decrease in androgenic parameters of target organs and in sperm population, loss of their motility as well as increase in abnormal spermatozoa in epididymis leading to 100% failure in fertility have also been reported as a consequence of androgen deprivation in treated rats (Hunt et al, 1979;Chinoy M. R. et al, 1984;Bao and Chinoy, 1983). However, there is a paucity of reports on the effects of estrogens on the histoarchitecture and functional integrity of reproductive tract in male rats.…”
The effects of estradiol benzoate (E2B) at a dose of 50 micrograms/rat/day for 7, 15 and 24 days on histoarchitecture, histocytometry and relative weights of reproductive organs in mature albino rats were investigated. The results revealed that the organ weights, histology of the testis, epididymis, vas deferens and seminal vesicle of treated rats were considerably affected as a consequence of the treatment. The height of germinal/secretory epithelium and tubular diameter of these organs also declined, whereas the peritubular muscle layer thickness of epididymis and accessory gland was increased. In vas deferens, in contrast, the muscle layer was reduced. The induced effects of estrogen were related to the duration of the treatment and support our earlier data that estrogens have a direct effect on the testis.
“…Moreover, complete degeneration of seminiferous tubules and depopulation of germinal cells occurred in testis of rats treated for 24 days which indicate that these effects are dependent on the duration of the treatment. Hunt et al (1979) also reported that the duration of treatment is more critical for the induction of azoospermia in the rat than the total dose of estradiol, in support of our present observations and earlier data (Rao and Chinoy, 1983). Thus, E2B manifested a direct effect on testicular steroidogenesis by inhibiting the Leydig cell function concomitant with an accumulation of protein and cholesterol and a reduction in the activities of 3ß-and 17ß-hvdroxysteroid dehydrogenases (HSDs) in steroidogenic organs in treated rats.…”
Section: Discussionsupporting
confidence: 93%
“…The suppression of 17x-hydroxylass and 17-20 desmolase activities by estrogens in testis of laboratory animals and human being have also been extensively reviewed (Dörner et al, 1975;Steinberger et al, 1977;Dufau et al, 1978). The loss of ofgan weights, significant decrease in androgenic parameters of target organs and in sperm population, loss of their motility as well as increase in abnormal spermatozoa in epididymis leading to 100% failure in fertility have also been reported as a consequence of androgen deprivation in treated rats (Hunt et al, 1979;Chinoy M. R. et al, 1984;Bao and Chinoy, 1983). However, there is a paucity of reports on the effects of estrogens on the histoarchitecture and functional integrity of reproductive tract in male rats.…”
The effects of estradiol benzoate (E2B) at a dose of 50 micrograms/rat/day for 7, 15 and 24 days on histoarchitecture, histocytometry and relative weights of reproductive organs in mature albino rats were investigated. The results revealed that the organ weights, histology of the testis, epididymis, vas deferens and seminal vesicle of treated rats were considerably affected as a consequence of the treatment. The height of germinal/secretory epithelium and tubular diameter of these organs also declined, whereas the peritubular muscle layer thickness of epididymis and accessory gland was increased. In vas deferens, in contrast, the muscle layer was reduced. The induced effects of estrogen were related to the duration of the treatment and support our earlier data that estrogens have a direct effect on the testis.
“…Testicular steroids exert a feedback action on the hypothalamus and pituitary gland to regulate gonadotrophin secretion in young (Schanbacher, 1980a) and mature rams (Schanbacher, 19806). Oestrogen-induced testicular atrophy in mature rats is considered to be secondary to inhibition of LH secretion (Swerdloff & Walsh, 1973;Verjan, de Jong, Cooke, van der Molen & Eik-Nes, 1974;de Jong, Uilenbroek & van der Molen, 1975;Hunt, Saksena & Chang, 1979). Thus, the influence of oestradiol-17ß treatment on sexual development in bulls appeared to be worthy of study.…”
An experiment was conducted to determine the importance of episodic LH secretion during pubertal development in beef bulls. Testicular growth, LH secretory patterns and serum testosterone concentrations were monitored in control bulls, and bulls implanted with one or two oestradiol-filled capsules from 26 to 38 weeks of age. Control but not oestradiol-treated bulls showed normal testicular growth and episodic LH secretory patterns. Serum LH and testosterone responses of 38-week-old control and oestradiol-treated bulls to an intravenous challenge of 5 micrograms LH releasing hormone indicated normal pituitary responsiveness, but steroidogenic responsiveness had not yet developed in oestradiol-treated bulls. Removal of the capsules at 38 weeks of age resulted in a normal episodic release pattern for LH, with concomitant growth of the underdeveloped tests up to 44 weeks of age. Serum concentrations of LH and testosterone were within the range of normal, adult values by 42 weeks of age. These results suggest that oestradiol can interfere with episodic LH secretion and normal pubertal development in beef bulls, and furthermore that episodic LH secretion is commensurate with the establishment of normal development of the bovine testis during puberty.
“…In-vitro studies have suggested that the drug has a direct effect on testicular steroidogenesis (Barbieri et al, 1977). Oestrogens also have anti-androgenic properties in the male, causing azoospermia and reduction of plasma testosterone levels (Verjans, de Jong, Cooke, van der Molen & Eik-Nes, 1974;Bartke, Williams & Dalterio, 1977;Hunt, Saksena & Chang, 1979). The present study describes the effect of danazol and oestradiol-17ß on the histochemistry of the testis and epididymis of the gerbil.…”
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