Neonatal growth of testosterone propionate-treated embryos.
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Effect of testosterone on neuronal refractory periods, sexual behaviour and luteinizing hormone: a comparison of time-courses.
Measurements of the refractory period of stria terminalis neurones that are sensitive to testosterone propionate, of sexual behaviour and of plasma levels of LH were taken in castrated rats at various times after initiation of treatment with testosterone propionate. Levels of LH dropped within 24 h, before there was any change in neuronal refractory periods. The period of latency to mounting, however, was reduced to its shortest only after 7-8 days and ejaculations first occurred at the same time; these sexual responses correlated in time with reduction of the neuronal refractory period to its lowest level.
Amygdala↗
Topical treatment of vulvar dystrophies with progesterone.
The Authors have studied the topical use of progesterone gel in the treatment of vulvar dystrophies. The results compared with those obtained previously with testosterone propionate pointed out the positive effects even of the progesterone, which has to be the first therapeutical approach for all the types of vulvar dystrophies, reserving to serious and resistants cases the treatment with testosterone propionate.
Administration, Topical↗
Possible involvement of androgen in increased norepinephrine synthesis in blood vessels of spontaneously hypertensive rats.
We investigated the effects of castration and testosterone propionate on sympathetic nervous systems in spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY). Four-week-old male rats were castrated. For replacement of androgen, testosterone propionate (500 micrograms/rat) was administered subcutaneously 2 times a week to castrated rats after their 14th week. The systolic blood pressure of the castrated SHR (44 weeks) was significantly lower than those of intact SHR and testosterone-replaced SHR. The norepinephrine (NE) levels and the tyrosine hydroxylase (TH) activities in the abdominal aorta and mesenteric artery of castrated SHR (45-50 weeks) were significantly lower than those of intact SHR. The NE levels and the TH activities in these blood vessels of testosterone-replaced SHR recovered to the levels obtained in those of intact SHR. As well as the systolic blood pressure, the NE levels and TH activities in blood vessels of WKY were significantly lower than those of intact SHR and showed no significant difference among the three groups. These results suggest that androgen may contribute to the development of hypertension in SHR via sustained enhancement of TH activity in blood vessels leading to increased NE level.
Androgens↗
Effects of testosterone, pregnenolone, progesterone and cortisol on pituitary and testicular function in male golden hamsters with gonadal atrophy induced by short photoperiods.
Testicular regression was induced in adult golden hamsters by exposure to a short photoperiod (5 h light:19 h darkness). The response of these animals to exogenous steroids (ten injections each of 5 mg testosterone, testosterone propionate, pregnenolone, progesterone or cortisol administered s.c. three times/week) was evaluated from weight changes in testes and seminal vesicles, from plasma levels of LH, FSH and testosterone, and from testicular human chorionic gonadotrophin (HCG) binding and testosterone levels. Administration of testosterone or testosterone propionate produced a decrease in plasma gonadotrophins and a three- to fourfold increase in weights of testes and seminal vesicles, thus indicating that the seminiferous tubules, similarly to accessory reproductive glands, retained the ability to respond to androgenic stimulation. Binding of HCG by testicular tissue was dramatically reduced by treatment with testosterone, probably reflecting atrophy of the Leydig cells. Treatment with pregnenolone or progesterone failed to increase testicular weight, seminal vesicle weight or concentrations of in the testes. This suggests that the atrophic testes of these animals may have a limited capacity to produce biologically significant amounts of androgens from C21 steroids. Administration of cortisol did not alter any of the parameters of reproductive function that were examined.
Animals↗
Susceptibility of Lobund-Wistar x Copenhagen hybrid rats to autochthonous prostate carcinogenesis.
BACKGROUND: Transplantation of the Dunning R-3327 prostate tumor cell line is a common model of prostate cancer, though the rat strain (Copenhagen) from which the cell line was derived is resistant to spontaneous and chemically induced prostate cancer. METHODS: To determine if susceptibility to chemically induced prostate carcinogenesis can be transferred from the susceptible Lobund-Wistar (LW) rat strain to the resistant Copenhagen (COP) strain, male COP rats and LW x COP hybrids were administered an intravenous dose (30 mg/kg) of methylnitrosourea (MNU) and implanted three times with silastic capsules containing testosterone propionate (25 mg each) at a 2-month interval. Serum was sampled at 3, 6, 9, and 12 months of age and assayed for testosterone. RESULTS: Serum testosterone was significantly but transiently elevated following implantation of capsules with testosterone propionate, but then decreased by 12 months of age to a level which was significantly less (P < or = 0.001) than in LW rats but not significantly different from COP rats. Prostate cancer did not develop in COP rats, but 36% of LW x COP hybrids developed prostate-seminal vesicle tumors which expanded into the dorsolateral lobes within 10 months of MNU administration; this compares to 90% of LW rats which develop such tumors following this same induction protocol. CONCLUSIONS: COP rats lack inherent susceptibility to development of prostate cancer; susceptibility may be transferred from LW rats, or resistance from COP rats, to LW x COP hybrids and is present in the haploid state, consistent with the two-mutation event hypothesis of Knudson which holds that two mutations are required at a genetic locus for development of some cancers.
Adenocarcinoma↗
Prostate carcinomas developing in transgenic rats with SV40 T antigen expression under probasin promoter control are strictly androgen dependent.
We have generated a transgenic rat with the SV40 T antigen under probasin promoter control, allowing prostate-specific gene expression. Males demonstrate atypical epithelial cell proliferation in the prostate from 4 weeks of age and develop prostate carcinomas at 100% incidence before they are 15 weeks old. Castration at 5 weeks of age was found to inhibit the prostate tumor formation completely, whereas testosterone propionate administration induced marked cell proliferation as well as microinvasion in prostate carcinomas. Castration at 20 weeks of age, after tumor development, even with testosterone propionate treatment, induced complete tumor involution within 5 weeks. To investigate the underling processes, sequential histological changes were monitored 1, 2, 3, 7, 14, and 21 days after castration. At days 1-3, many apoptotic bodies and inflammatory cells, including foam cells, were observed, and clear glandular structures were no longer evident in the tumors. Seven days after castration, most glands were involved, and nuclei of the cells did not show atypia. After 14 and 21 days, only atrophic glands were observed. During this process, expression of caspase 3, caspase 6, BAX, bcl-x, TRPM-2, and MMP7 genes was apparently increased. Comparison of the gene expression profile between a prostate carcinoma in a transgenic animal and a normal prostate of a wild-type rat by a cDNA array technique was also conducted. The results suggested that our model is suitable to investigate mechanisms of carcinogenesis, including androgen dependence, involution, and apoptosis.
Androgen-Binding Protein↗
Testicular regulation of epididymal protein secretion.
The effects of different androgen and testicular fluid levels on the protein synthesis and secretion of the epididymis of mice and rats were examined. In mice, the in vitro protein synthesis and secretion of five epididymal segments were measured from 3 days up to 8 weeks after efferent duct ligation. During the entire period, alterations in the rate of protein secretion per milligram tissue were small. At 8 weeks, the mean rate of protein synthesis per milligram ligated epididymal tissue was 80% of that of the control side. As a consequence of the weight loss of the ligated epididymis, however, the protein secretion per organ can be estimated to be reduced by 50%. Changes in the protein profile were only found in the proximal segment, where a 40-kd protein appeared and a 29-kd protein disappeared. In rats, the effects of efferent duct ligation were studied in vivo for up to 8 months. Structural changes were present both in the proximal and in the distal epididymis. The most conspicuous change in the protein profile of secretory proteins was the disappearance of a 27-kd protein from the proximal segment. In the distal epididymis, a 32-kd protein was no longer secreted. In mice, the effects of castration on the profile of secreted proteins demonstrated that, without androgen stimulation, some proteins are still secreted 6 weeks after castration. Administering low or high doses of testosterone propionate to castrated mice resulted in almost similar profiles of secretory proteins. However one protein secreted in the proximal epididymis was preferentially stimulated by the high dose of testosterone propionate.
Animals↗
Strain-dependent gonadal effects upon adrenal cholesterol ester concentration and composition in C57BL/10J and DBA/2J mice.
The effects of gonadectomy and sex hormone administration on the concentrations of the individual cholesterol esters in the adrenals of C57BL/10J and DBA/2J mice are described. The methyl esters of the fatty acids derived from the cholesterol ester fraction have been analyzed by gas-liquid chromatography. In both strains the females have a higher total adrenal cholesterol ester concentration than the males. However, different gonadal effects operate in the two strains. In the C57 strain the presence of the ovary or the administration of estradiol benzoate to the ovariectomized female increases the concentrations of all adrenal cholesterol esters. This effect does not occur in the DBA strain. In the DBA strain the presence of the testes or the administration of testosterone propionate to the castrate male lowers the concentration of all adrenal cholesterol esters. This effect does not occur in the C57 strain. The response to testosterone propionate in the castrate male of the DBA strain is significantly greater than that of ovariectomized female. This finding suggests that sexual differentiation influences the magnitude of the response. In both strains cholesteryl adrenate (C22:4) shows these gonadal effects to a greater degree than the other adrenal cholesterol esters. Thus, there are at least two types of gonadal control of adrenal cholesterol esters. One of these affects all the esters in general while the other affects adrenic acid metabolism specifically.
Adrenal Glands↗
Dissociation of increases in plasma insulin-like growth factor I and testosterone during the onset of puberty in bulls.
The present study was conducted to examine the relationship between plasma concentrations of testosterone, insulin-like growth factor I (IGF-I) and IGF-binding proteins (IGFBPs) during puberty, in male calves treated with GnRH or testosterone propionate. Twelve male Holstein calves (10 weeks old) were assigned to the control group (n = 6), the GnRH-treated group (n = 3) or the testosterone-treated group (n = 3). For 8 weeks, the GnRH-treated group received a single i.v. injection of GnRH (0.5 microgram kg-1 body mass) each day while the testosterone-treated group received an i.m. injection of testosterone propionate (0.5 mg kg-1 body mass) twice a day. The calves were studied until they were 200 days old. Hormone treatments were stopped one month after puberty was reached in the control group. Blood samples were collected every 30 min for 8 h every third day. Hormone concentrations were determined by radioimmunoassay. Western ligand blotting and immunoblotting, using monoclonal antibodies against IGFBP-2 and IGFBP-3, were used to characterize the IGF-binding proteins. In the control group, puberty occurred at about 120 days of age and was associated with an increase in concentrations of testosterone, IGF-I and IGFBP-3 and a decrease in concentration of IGFBP-2. In the GnRH-treated group, plasma testosterone remained low until 8 weeks after establishment of puberty in the control group (4 weeks after the end of treatment). In the testosterone-treated group, testosterone was high during the treatment period and then decreased to prepubertal values when treatment was stopped. Testosterone values increased again to reach postpubertal values 5 weeks after the end of hormone treatment. Nevertheless, independent of testosterone status, the profile of IGF-I and the IGFBPs in the GnRH- and testosterone-treated groups were parallel to that reported for the control group with the transition from prepubertal to adult values at about 120 days of age. In conclusion, concentrations of testosterone, IGF-I and IGFBP-3 increase together, but probably independently, during the onset of puberty in male calves.
Animals↗
The role of hypothalamic adrenergic receptors in preventing testosterone-induced androgenization in the female rat brain.
Androgenization of the female neonatal rat brain by testosterone and the subsequent development of persistent estrus in the adult can be blocked by drugs which interfere with normal hypothalamic neuronal function. The mechanism of action of these drugs was studied. A 25-micrograms dose of testosterone propionate at 5 days of age produced a 69% incidence of persistent estrus at 90 days of age. alpha-Methyl-p-tyrosine given with testosterone propionate resulted in an 81% incidence of persistent estrus. Therefore, hypothalamic norepinephrine depletion did not prevent androgenization. Tyramine (100 micrograms) inhibited androgenization to an incidence of 27% by 90 days. Phenoxybenzamine (50 micrograms) and phentolamine (50 micrograms) each reduced the incidence to 0%. Combining the beta-antagonist propranolol with phenoxybenzamine or phentolamine reversed the block in androgenization, resulting in 37% and 50% incidences of persistent estrus, respectively. Tyramine causes the release of neuronal stores of norepinephrine which is turn stimulates alpha- and beta-adrenergic receptors. The action of tyramine implicates adrenergic stimulation as a mechanism for the inhibition of androgenization, but does not define which receptor type is involved. In addition to postsynaptic alpha-blockade, phenoxybenzamine and phentolamine can cause presynaptic alpha-blockade, resulting in increased neuronal norepinephrine release and beta-stimulation. When the beta-antagonist propranolol was added to the alpha-antagonists, the block in androgenization was reversed. Therefore, we conclude that beta-adrenergic receptor stimulation prevents androgenization of the neonatal rat brain.
Animals↗
Pituitary receptor sites for gonadotropin-releasing hormone: effect of castration and substitutive therapy with sex steroids in the male rat.
To examine the role of pituitary gonadotropin-releasing hormone (GnRH) receptors (pit GnRH-R) in the regulation of gonadotropin secretion, male rats were orchidectomized and then selectively received substitutive therapy with sex steroids. Pituitary content of GnRH-R was determined by saturation analysis, using radioiodinated [D-Trp6,(N-Et)Pro5,des-Gly10]GnRH as tracer. Castration produced a rapid and sustained increase of the number of GnRH-R, which doubled after 2 days, and after 10 days the pituitary content of GnRH-R was 258 +/- 23 fmol/pituitary compared to 103 +/- 12 fmol/pituitary for sham-operated control animals. No change of the affinity constant (Ka) was observed (Ka = 1.13 +/- 0.08 X 10(10) M-1; n = 14). Plasma LH increased 5- to 10-fold and FSH-2- to 3-fold after castration, and hypothalamic GnRH content was depleted by 30-60%. Immediate substitution of castrated rats with testosterone propionate (250 micrograms daily) prevented the increases of both plasma gonadotropins and of GnRH-R. Treatment of acutely castrated rats for 7 days with testosterone propionate (50-200 micrograms), 5 alpha-dihydrotestosterone propionate (25-400 micrograms), or estradiol benzoate (2 micrograms) prevented the rise in pit GnRH-R in a dose-related manner and normalized the other parameters studied except that plasma FSH remained slightly elevated. In contrast, when substitutive therapy was started 8 days after castration or later, the 7-day treatment with sex steroids reduced plasma gonadotropins, but pit GnRH-R remained elevated, and hypothalamic GnRH content remained depleted. These results indicate that the marked increase of gonadotropin secretion after castration is mediated at least in part, by an increase in the number of pit GnRH-R. Sex steroids were able to reverse all castration-induced endocrine changes in acutely castrated rats, but in long term castrated animals their action at higher centers to normalize hypothalamic GnRH content, and indirectly, to reduce pit GnRH-R content, was either delayed or ineffective. Thus, the rapid feedback action of sex steroids in long term castrated rats may be predominantly exerted at the pituitary level.
Animals↗
Plasma vasopressin and oxytocin levels in intact goats and in castrated goats given testosterone.
Oxytocin, vasopressin, cortisol and testosterone levels in the plasma were measured by radioimmunoassay in intact male goats as well as in prepubertally castrated goats injected daily, for 2 weeks, with oil vehicle and then, for 4 weeks, with testosterone propionate in oil to study the influence of gonadal steroids on posterior pituitary hormones. Packed cell volume, plasma osmolality and sodium concentration were also measured in all blood samples. Plasma levels of oxytocin, vasopressin and cortisol were similar in the intact and oil-injected castrated goats. Testosterone treatment significantly increased plasma levels of oxytocin (P less than 0.01) in castrated goats but the increased levels were similar to those seen in the intact goats at the same time of year. Plasma levels of cortisol and vasopressin were unaffected by testosterone propionate treatment, whereas packed cell volume was significantly decreased (P less than 0.01). Testosterone treatment of castrated male goats appears not to have any action on pituitary hormones and oxytocin increases in the spring in both intact and castrated male goats.
Animals↗
Androgen receptor antagonism by the organophosphate insecticide fenitrothion.
Organophosphate insecticides represent one of the most widely used classes of pesticides with high potential for human exposure in both rural and residential environments. We investigated the interaction of the organophosphothioate pesticide fenitrothion (O,O-dimethyl O-(4-nitro-m-tolyl) phosphorothioate) with the human androgen receptor (AR). Fenitrothion blocked dihydrotestosterone-dependent AR activity in a concentration-dependent and competitive manner in HepG2 human hepatoma liver cells transiently transfected with human AR and an AR-dependent luciferase reporter gene. Schild regression analysis yielded an equilibrium dissociation constant value of 2.18 x 10(-8) M. To determine the antiandrogenic potential of fenitrothion in vivo, 7-week-old castrated Sprague-Dawley rats were dosed once a day for 7 days with testosterone propionate (50 microg/day, sc) plus gavage doses of either corn oil vehicle or fenitrothion (15 or 30 mg/kg/day). An additional group of rats was given testosterone propionate and flutamide (50 mg/kg/day). Motor activity and acetylcholinesterase activity in whole blood and brain were also assessed. Both fenitrothion and the reference antiandrogen flutamide caused significant decreases in the ventral prostate, seminal vesicle, and levator ani plus bulbocavernosus muscles tissue weights. In contrast, blood acetylcholinesterase activity, a standard biomarker of organophosphate poisoning, was only inhibited at the higher dose of fenitrothion (30 mg/kg). Our results demonstrate that fenitrothion is a competitive AR antagonist, comparable in potency to the pharmaceutical antiandrogen flutamide and more potent, based on in vitro assays, than the known environmental antiandrogens linuron and p,p'-, 2,2-bis(p-hydroxyphenyl)-1,1-dichloroethylene ( p,p'-DDE).
Acetylcholinesterase↗
Dual role of testosterone in fenvalerate-treated mice with respect to thyroid function and lipid peroxidation.
Effects of testosterone propionate (TP, 2.5 mg kg(-1) body weight) in fenvalerate-induced (120 mg kg(-1) body weight) thyroid dysfunction and lipid peroxidation were investigated in male mice. Testosterone propionate aggravated in the inhibition of hepatic type I iodothyronine 5'-monodeiodinase (5'D-I) activity, coupled with a decrease in serum triiodothyronine (T3) concentration in pesticide-treated mice. However, it could ameliorate the toxicity as indicated by decreased hepatic lipid peroxidation (LPO) with a marginal but significant increase in superoxide dismutase and catalase activities following fenvalerate treatment. While protective effects of testosterone on LPO indicated its antiperoxidative property, the decrease in 5'D-I activity could be because of the increased accumulation of fenvalerate in the tissues following TP administration.
Animals↗
Regulation of testicular and Sertoli cell gamma-glutamyl transpeptidase by follicle-stimulating hormone.
Hormonal deprivation achieved by hypophysectomy or gonadotropin-releasing hormone (GnRH)-antagonist treatment of immature rats resulted in markedly lower testicular gamma-glutamyl transpeptidase (GGT) activity than in the testes of age-matched controls. When begun 15 days after hypophysectomy, follicle-stimulating hormone (FSH) treatment significantly increased testicular GGT above that in testes from hypophysectomized controls in a time- and dose-dependent manner. In contrast, testosterone propionate had only a small effect. Testicular GGT was higher in adult hypophysectomized rats treated with FSH from the time of surgery than in untreated hypophysectomized rats; testosterone propionate treatment had no effect. GGT activity in Sertoli cells isolated from GnRH antagonist-treated or hypophysectomized immature rats was also lower than in cells from control rats. FSH treatment from the day of hypophysectomy resulted in Sertoli cell GGT values equivalent to those from intact controls. These data indicate that FSH regulates GGT activity in rat testis and Sertoli cells.
Animals↗
Effects on hamster vaginal development of a single dose of testosterone or estradiol given neonatally.
Postnatal injections of a single dose of testosterone propionate or estradiol benzoate to newborn female hamsters produce a precocious vaginal opening at 5 days of age. Vaginal postnatal development, histologically, has shown that in testosterone-propionate-injected animals sinusal vagina is absent. The Müllerian vagina presented a stimulated epithelium at early ages. After 40 days, the Müllerian epithelium was stratified keratinized, with zones of stratified cuboidal epithelium. In estradiol-benzoate-treated animals, the Müllerian epithelium rapidly changes to stratified keratinized epithelium (10 days), with zones of stratified cuboidal after 20 days of life. The sinusal epithelium was stratified squamous at 10 days, and after 40 days changes to stratified keratinized epithelium were seen. Probably, early changes are due to a direct effect of steroid action. Later effects are due to ovarian secretion. Histologically, no significant changes were observed in the preputial and urethral glands. The clitoris showed malformations.
Age Factors↗
Influence of age and of testosterone on the response of male rats to parachlorophenylalanine.
1. Castrated male rats and male rats that had been castrated as well as adrenalectomized, showed hypersexual behaviour 24 h after treatment with parachlorophenylalanine (PCPA), as did intact rats.2. A dose of PCPA 100 mg/kg was sufficient to induce mounting behaviour; this dose lowered the cerebral 5-hydroxytryptamine (5-HT) to about 50% in 24 h and further to 40% in 72 hours.3. Groups of juvenile male rats treated chronically with PCPA 100 mg/kg or 50 mg/kg, or with testosterone propionate 1.25 mg, showed hair loss after three weeks of treatment (6 injections), because of increased social interaction.4. Groups of intact male rats 9-11 weeks old given testosterone propionate 1.25 mg subcutaneously, showed mounting behaviour 3-5 h after the injection which was indistinguishable from the behaviour seen 24 h after treatment with PCPA 100 mg/kg. The 5-HT content of the brain was not altered by testosterone.5. The number of rats which showed mounting after PCPA treatment did not change with age, but the younger rats made more mounts in the observation time than rats more than three months old.6. The age of castration (3 weeks or 4 months) did not influence the results.
Adrenalectomy↗