MODIFICATION OF MALE RAT REPRODUCTIVE TRACT DEVELOPMENT BY A SINGLE INJECTION OF TESTOSTERONE PROPIONATE SHORTLY AFTER BIRTH

1965 ◽  
Vol 50 (2) ◽  
pp. 310-316 ◽  
Author(s):  
H. E. Swanson ◽  
J. J. van der Werff ten Bosch

ABSTRACT Administration of 500 μg testosterone propionate (TP) to male rats within a few days of birth was followed by a reduced rate of growth of the testes and, after initial stimulation, of the seminal vesicles and ventral prostate. While the testes and accessory organs remained permanently smaller in TP-treated rats than in controls, their growth rates showed pubertal accelerations which coincided with those in the controls. On the basis of these criteria, as well as the criterion of spermatogenesis, the time of puberty was not altered by early TP-administration. The weights of the accessory organs considered in relation to the weights of the testes were identical in TP-treated and control rats; testis tubule diameters in TP-treated rats were normal for the age. It is concluded that early TP-administration caused a reduction in the volume of testicular tissue, which involved both tubules and Leydig cells. There were no indications that TP had caused any qualitative changes in the testes: the timing and the pattern of pubertal development (spermatogenesis and androgenic activity) appeared to be normal.

1979 ◽  
Vol 180 (2) ◽  
pp. 313-318 ◽  
Author(s):  
Coral A. Lamartiniere ◽  
Cindy S. Dieringer ◽  
Etsuko Kita ◽  
George W. Lucier

The hepatic microsomal enzyme UDP-glucuronyltransferase undergoes a complex developmental pattern in which enzyme activity is first detectable on the 18th day of gestation in rats. Prepubertal activities are similar for males and females. However, postpubertal sexual differentiation of enzyme activity occurs in which male activities are twice those of females. Neonatal administration of testosterone propionate or diethylstilboestrol to intact animals resulted in lowered UDP-glucuronyltransferase activity in liver microsomal fractions of adult male rats, whereas no changes were observed in the adult females and prepubertal male and female animals. Neonatal administration of testosterone propionate and diethylstilboestrol adversely affected male reproductive-tract development as evidenced by decreased weights of testes, seminal vesicles and ventral prostate. Diethylstilboestrol also markedly decreased spermatogenesis. Hypophysectomy of adult male rats resulted in negative modulation of microsomal UDP-glucuronyltransferase and prevented the sexual differentiation of enzyme activity. In contrast hypophysectomy had no effect on female UDP-glucuronyltransferase activity. A pituitary transplant under the kidney capsule was not capable of reversing the enzyme effects of hypophysectomy, therefore suggesting that the male pituitary factor(s) responsible for positive modulation of UDP-glucuronyltransferase might be under hypothalamic control in the form of a releasing factor. Neonatal testosterone propionate and diethylstilboestrol administration apparently interfered with the normal sequence of postpubertal UDP-glucuronyltransferase sexual differentiation.


1975 ◽  
Vol 53 (5) ◽  
pp. 839-844 ◽  
Author(s):  
William H. Moger

The ability of testosterone, androsterone, 5α-androstane-3α,17β-diol, and 5α-androstane-3β,17β-diol to prevent the castration-induced rise in serum gonadotropin levels was investigated in immature male rats. Rats castrated at 30 days of age were treated once per day by subcutaneous injection of 12.5–100 μg of the steroid per 100 g body weight per day for 3 days, beginning on the day of castration. The animals were sacrificed 24 h after the last injection. Testosterone propionate, androsterone propionate, and 5α-androstane-3α,17β-diol dipropionate were also tested at the approximate molar equivalent of 100 μg of the free alcohol form per 100 g body weight per day.Testosterone propionate and 5α-androstane-3α,17β-diol were the only compounds tested that prevented the castration induced rise in luteinizing hormone (LH) concentrations. Testosterone propionate also inhibited the rise in follicle stimulating hormone (FSH) concentrations whereas 5α-androstane-3α,17β-diol inhibited the rise in FSH in one but not in another experiment. These were the only compounds tested that affected serum FSH concentrations.The lower doses of testosterone tested significantly increased serum LH, but not FSH concentrations compared to castrate control animals. The highest dose tested partially inhibited the rise in serum LH concentrations.Both androsterone and androsterone propionate maintained ventral prostate weights. Although neither compound prevented the castration induced rise in serum LH, two groups receiving androsterone had serum LH concentrations significantly lower than the castrate control group.5α-Androstane-3β,17β-diol and 5α-androstane-3α,17β-diol dipropionate failed to maintain ventral prostate weights or prevent the rise in serum gonadotropin levels.These results indicate that 5α-androstane-3α,17β-diol is capable of preventing the castration induced rise in serum LH concentrations in the immature male rat and thus may participate in the regulation of LH secretion in these animals.


1974 ◽  
Vol 77 (4) ◽  
pp. 636-642 ◽  
Author(s):  
H. L. Verjans ◽  
F. H. de Jong ◽  
B. A. Cooke ◽  
H. J. van der Molen ◽  
K. B. Eik-Nes

ABSTRACT The effects of subcutaneous administration of oestradiol benzoate (EB) on the weights of sex organs and on levels of testosterone and gonadotrophins in normal adult male rats have been studied. Doses of EB varied from 0.01 to 100 μg and were administered daily for seven days. Administration of 100 μg EB resulted in suppression of pituitary LH, while serum LH levels were already decreased after treatment with EB ≧ 1 μg. Pituitary and serum FSH levels were suppressed after administration of 100 and 10 μg EB respectively. Testicular tissue and serum levels of testosterone decreased after treatment with amounts of EB ≧ 1 μg. These decreased androgen levels were also reflected in a concomitant decrease in the weights of the ventral prostate and seminal vesicles. A decrease in the weight of the testes was obtained following a dose of EB ≧ 10 μg.


1972 ◽  
Vol 69 (2) ◽  
pp. 359-368 ◽  
Author(s):  
Lars-Eric Tisell

ABSTRACT The weight and histology of the ventral and dorsolateral prostate, the coagulating glands and the seminal vesicles were studied in castrated non-adrenalectomized male rats after sixteen days of daily injections of testosterone propionate and in castrated adrenalectomized rats after daily injections of testosterone propionate alone or in combination with cortisone. Testosterone propionate was given in daily doses of 0.020 mg and cortisone in daily doses of 1 mg, 3 mg or 9 mg. Testosterone alone induced a less pronounced growth of the dorsolateral prostate, the coagulating glands and the seminal vesicles in castrated non-adrenalectomized than in castrated adrenalectomized rats, suggesting an inhibitory effect of adrenal steroids on the action of testosterone. Cortisone which has a weak androgenic effect when given alone, partially counteracted the testosterone induced growth of the accessory reproductive organs in castrated adrenalectomized rats.


1989 ◽  
Vol 121 (3) ◽  
pp. 409-417 ◽  
Author(s):  
M. Bergendahl ◽  
A. Perheentupa ◽  
I. Huhtaniemi

ABSTRACT The effects of 4–6 days of food deprivation on the pituitary-testicular function of adult male rats were studied. Fasting decreased body weights on average by 23% (P<0·01) and those of seminal vesicles by 55% (P<0·01) in 4 days. No consistent changes were found in testicular and ventral prostate weights. The pituitary levels of gonadotrophin-releasing hormone (GnRH) receptors decreased by 50% (P<0·01). Serum and pituitary levels of LH, FSH and prolactin decreased by 25–50% (P<0·01 for all). Testicular and serum levels of testosterone decreased by 70–80%, testicular LH receptors by 26%, those of prolactin by 50% (P<0·01 for all), but those of FSH remained unaffected. Acute (2 h) stimulation by a GnRH agonist (buserelin, 10 μg/kg i.m.) resulted in similar LH, FSH and testosterone responses in the fasted and control animals, and human chorionic gonadotrophin (hCG) stimulation (30 IU/kg i.m.) in similar increases in testosterone. A 42% decrease was found in pituitary content of mRNA of the common α subunit (P<0·05), but the mRNAs of the LH- and FSH-β chains and prolactin were unaffected by fasting for 4 days. When the same mRNAs were measured after 6 days of fasting, the decrease of the mRNA of FSH-β also became significant (50%, P<0·01). In contrast, the mRNA of LH-β was increased twofold (P<0·01) at this time and serum LH levels were similar in control and starved animals. It is concluded that during short-term starvation of male rats: (1) the decrease in gonadotrophin and prolactin synthesis and secretion is first noticed on the level of translation (protein synthesis), and the mRNA levels of these hormones may respond more slowly to starvation, (2) decreased pituitary GnRH receptors indicate decreased GnRH release from the hypothalamus, (3)the gonadotrophin and prolactin loss results secondarily in decreased testicular androgen synthesis and LH and prolactin receptor levels, (4) no decrease occurs during starvation in acute gonadotrophin response to GnRH, or testicular testosterone response to hCG, (5) the primary response to starvation in male rat pituitary-testicular function is the loss of normal hypothalamic support of gonadotrophin and prolactin secretion, rather than direct nutritional effects on the pituitary and testis, and (6) when starvation is continued beyond 4 days, a recovery is seen in pituitary mRNA on the LH-β chain and in serum LH, most probably because the starvation-associated decrease serum testosterone is a more potent positive stimulus of LH synthesis than the direct hypothalamic-pituitary inhibition. Journal of Endocrinology (1989) 121, 409–417


2020 ◽  
Vol 10 ◽  
Author(s):  
Neveen Asmet Farag ◽  
Ayman S Mohamed ◽  
Hanan Farag El Sayed ◽  
Eman Y. Salah EL-Din ◽  
Abdel Rahman A. Tawfik

Background:: Infertility is the first-rate public health trouble affecting one in five married couples globally, male causes embody a significant proportion. Natural products could be an alternative or complementary inexpensive treatment for such matters. Echinochrome (Ech) is a natural quinone pigment obtained from sea urchin, and it was confirmed to possess many pharmacological properties due to its chemical activity. Objective:: The current research paper was targeted to evaluate the potential effects of Ech on male fertility, and to highlight the possible involved mechanisms. Methods:: Eighteen adult male rats were randomly distributed into three groups: control (1 ml of 2% DMSO, p.o.), low dose Ech (0.1 mg/kg, p.o.), and high dose Ech (1 mg/kg p.o.). Results:: The high dose Ech caused a significant decline in the levels of glucose, ALT, AST, ALP, urea, Cr, uric acid, TG, TC and LDL-C and testicular tissue MDA, while it caused a significant rise in the levels of albumin, TP, HDL-C, FSH, LH, testosterone and testicular tissue GSH activity. Moreover, it showed a significant positive effect on the testis weight, caudal epididymis weight, sperm count, sperm motility, sperm morphology, fructose concentration, and α-glucosidase activity. However, no significant changes were observed in histological examination of testicular tissue among all groups. Conclusion:: High dose Ech improved male rat-fertility either directly by activating the pituitary gonadal axis, and or indirectly via enhancing: the renal and hepatic functions, the lipid profile and or the antioxidant pathways.


1978 ◽  
Vol 76 (2) ◽  
pp. 241-249 ◽  
Author(s):  
P. SÖDERSTEN

Male rats were treated daily with 100 μg of the anti-oestrogen ethamoxytriphetol (MER-25) or oil during the first 10 days of life and tested for lordosis behaviour and mounting behaviour as intact adults, after castration and after castration and oestradiol benzoate or testosterone propionate treatment. The MER-25-treated rats showed higher levels of lordosis behaviour than oil-treated rats in all four treatment groups. Under each of these endocrine conditions, except after castration alone, the MER-25-treated rats showed a reduced capacity to ejaculate. Treatment of the neonatal rat with MER-25 reduced body weight in adulthood but did not change the weight of the accessory sexual glands, the testes, the number of cornified papillae on the glans penis or plasma testosterone concentrations during development. The response of the accessory sexual glands and cornified papillae on the glans penis to treatment with oestradiol benzoate or testosterone propionate after castration in adulthood was unaffected by treatment with MER-25. It is suggested that formation of oestrogen in the neonatal male rat brain from testosterone in the circulation inhibits the capacity to show lordosis behaviour and facilitates the capacity to ejaculate in response to gonadal hormone treatment in adulthood.


1996 ◽  
Vol 12 (3-4) ◽  
pp. 515-531 ◽  
Author(s):  
L. Earl Gray ◽  
William R. Kelce

In humans and rodents, exposure to hormonally active chemicals during sex differentiation can produce morphological pseudohermaphrodism (Schardein, 1993; Gray, 1992). For example, hormonally active drugs like DES (estrogenic), Danazol (androgenic), and progestins cause urogenital malformations in the reproductive tracts of humans and rodents. The current discussion will present new information on the effects of toxic chemicals and pesticides that act on reproductive development via novel mechanisms, including germ cell toxicity, antiandrogenicity, and Ah-receptor binding. Information will be presented that describes how exposure during critical stages of life to synthetic chemicals present in our environment, such as benzidine- based dyes, antiandrogenic fungicides, 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD), and PCB congener 169, result in abnormal rodent sex differentiation. In rodents, perinatal exposure to fetal germ cell toxicants reduced the reproductive potential of female, and permanently reduced sperm production in male progeny. Phenotypic sex differentiation, however, was unaffected by these germ cell toxicants. In contrast, antiandrogenic drugs and fungicides induced profound alterations in phenotypic sex differentiation. Effects such as hypospadias, ectopic testes, vaginal pouches, agenesis of the ventral prostate, and nipple retention in male rats were observed commonly. Although these antiandrogens induced no permanent effects in female progeny, another class of chemicals, the Ah-receptor mediated toxicants, did reduce fertility in both male and female rat offspring. Cauda epididymal sperm numbers were reduced permanently in TCDD-exposed male rat and hamster progeny, and female progeny displayed malformations of the external genitalia. Other toxicants produced dramatic alterations of sex differentiation (uterus unicornis, agenesis of the vas and epididymis, and undescended testes), via mechanisms that have not been characterized yet. Since these adult/pubertal alterations resulted from gestational and/or neonatal exposures, future studies should include a comprehensive assessment of reproductive function after perinatal exposure because the developing animal is extremely sensitive to toxicants during sex differentiation, and many of the effects are difficult to detect until late in life.


1978 ◽  
Vol 234 (3) ◽  
pp. E262
Author(s):  
B E Piacsek ◽  
N J Statham ◽  
M P Goodspeed

Male rats were raised from birth in either continuous light (LL) or in 14 h light/10 h dark per day (LD) at 22 +/- 1 degree C. Food and water were administered ad libitum. Groups of rats were killed by decapitation at 14, 20, 25, 35, 41, 45, 51, 55, 58, 63, and 79 days of age. Testicular (TW), ventral prostate (VPW), and seminal vesicle (SVW) weights were measured. Serum concentrations of follicle stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL), and androgens were quantified by radioimmunoassay. Results indicate no significant change in TW or spermatogenesis. Spermatozoa were first seen in the lumen of 10% of seminiferous tubules at 35 days of age in both LD and LL rats and by 42 days of age, 80% of tubules from both LD and LL rats contained spermatozoa in the lumen. A highly significant depression in accessory structure development (VPW, SVW) was observed as a result of LL exposure. Serum FSH levels in LL rats were depressed on days 45, 51, 55, and 58 but elevated at 79. Serum PRL concentrations were elevated in LL rats on days 41, 55, 58, 63, and 79, whereas serum androgen levels were depressed on days 58, 63, and 79. Results suggest that exposure to LL results in delayed maturation of the accessory structures in the reproductive system of the male rat possibly as a result of reduced FSH or elevated PRL levels, which in turn may modify the rate and pattern of LH and/or androgen secretion.


1964 ◽  
Vol 47 (1) ◽  
pp. 37-50 ◽  
Author(s):  
H. E. Swanson ◽  
J. J. van der Werff ten Bosch

ABSTRACT The interaction between dose and time of administration of testosterone propionate (TP) on the development of sexual function was studied by giving a single dose of 5, 10, 50 or 500 μg TP to young rats of both sexes on the day of birth (day 1) or on day 2, 4 or 5. The effectiveness of androgen administration before birth was studied by giving a single injection of 2500 μg TP to pregnant rats on day 19 to 22 after conception. Pre-natal administration had no effect on the function of the ovaries of female offspring, although the dose was sufficient to cause masculinization of the external genitalia. The weight of the testes and accessories of the male offspring were not affected. The effects of post-natal TP administration on ovarian function varied with the dose and with the time of administration. Threshold doses (5 and 10 μg) were more effective the earlier they were given after birth. With these small doses, most of the rats had normal luteinized ovaries at 10 weeks and were able to bear and suckle normal litters. Some time later ovulations ceased so that at 21 weeks they were no longer fertile; at 27 weeks there were no more corpora lutea in the ovaries. In males, a dose of 50 μg of TP or more resulted in permanently reduced weight of testes, seminal vesicles and prostate. The earlier the treatment, the more marked was the depression of weight. From these results and others reported in the literature the following deductions can be made: (1) the critical period of brain sensitivity to physiological amounts of androgen probably lies between days 4 and 6 (day of birth counted as day 1); (2) a rough estimate of the amount of androgen secreted by the newborn male rat during the critical period would seem to be the equivalent of a single injection of 5–50 μg TP; (3) after the physiological critical period has elapsed a female rat can still be »masculinized« if a high dose of TP is given, up to a period of between 10–20 days after birth.


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