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PubMed1996

Testosterone regulates gonadotropin-releasing hormone-induced calcium signals in male rat gonadotrophs.

As the GnRH-induced secretion of gonadotropins is critically dependent upon an increase in the intracellular calcium ion concentration ([Ca2+]i) and modulated by gonadal factors, the effects of gonadal steroids on the pattern of calcium mobilization in single gonadotrophs of the male rat were examined using the fluorescent Ca2+ indicator fura-2/AM. In cells from intact rats, low concentrations of GnRH induce repetitive oscillations in [Ca2+]i, whereas spike-plateau responses are observed at higher concentrations in single gonadotrophs. After castration, there was a significant change in the relationship between the GnRH concentration and the changes in [Ca2+]i. Increasing concentrations of GnRH (to 1 micron) generate fewer spike-plateau responses in gonadotrophs from castrate rats, with oscillatory responses predominating. This change develops with time after castration, with the proportion of cells oscillating in response to 100 nM GnRH peaking by 7 days. This effect of castration on GnRH-induced [Ca2+]i signals was reversed by treatment with testosterone propionate (100 microgram/100 g BW-day). Castration-induced decreases in serum testosterone, seminal vesicle, and prostate weights and increases in serum LH concentration were also corrected by testosterone propionate treatment. These findings demonstrate that testosterone regulates GnRH-stimulated Ca2+ signals in gonadotrophs and suggest that gonadal steroids exert a regulatory role in the secretion of gonadotropins at the level of Ca2+ mobilization.

Animals↗
PubMed1990

Testosterone increases TSH-beta mRNA, and modulates alpha-subunit mRNA differentially in mouse thyrotropic tumor and castrate rat pituitary.

TSH, LH and FSH, the three pituitary glycoprotein hormones, are each composed of a common alpha-subunit and a hormone specific beta-subunit. Testosterone is known to regulate all three intact hormones differently in the rodent. However, there is only one gene encoding the common alpha-subunit. In order to elucidate the effects of testosterone on TSH subunit synthesis and its regulation of the common alpha-subunit, two in vivo models were studied: castrate rat pituitary was used as a gonadotropin-enriched tissue; and mouse thyrotropic tumor was used as a thyrotropin-enriched tissue. Male castrate rats were treated with testosterone propionate, 500 micrograms/100 g BW, sc, for 11 days. Testosterone increased plasma TSH to 131% of control values (P less than 0.02), while plasma LH fell to undetectable levels, and plasma alpha-subunit fell to 14% of control values (P less than 0.001). Testosterone increased TSH-beta mRNA to 237% of control values (P less than 0.02), while alpha-subunit mRNA fell to 20% of control values (P less than 0.001). Hypothyroid mice bearing thyrotropic tumors were treated with testosterone propionate, 150 micrograms/100 g BW, sc, for 11 days. In this model plasma TSH-beta and alpha-subunit concentrations are 1000-fold higher than in non-tumor bearing animals, and the contribution of pituitary gonadotropes to plasma subunit concentrations is negligible. "Total" TSH-beta and alpha-subunit concentrations were estimated as one-half of intact TSH plus the respective free subunit concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Induction of reversible antifertility with a crude ethanol extract of Citrullus colocynthis Schrad fruit in male rats.

A crude 50% ethanol extract of Citrullus Colocynthis Schrad was administered orally to male albino rats for evaluation of antifertility effects. The animals were divided into five groups: group A was a vehicle-treated control group; treatment groups B, C, and D received 100 mg/kg/day C. Colocynthis extract for periods of 20, 40, and 60 days, respectively, and group E animals received the extract at 100 mg/kg/day for 60 days followed by 60 days of recovery. For androgenicity evaluation of the extract, the animals were divided into four groups: group F animals were castrated 30 days before the experiment to serve as controls, and group G, H, and I were subjected to castration 30 days before the experiments, followed by administration of fruit extract (100 mg/kg/day p.o.), testosterone propionate (0.01 mg/rat/alternate day s.c.), and fruit extract along with testosterone propionate, respectively, for 30 days. Significantly reduced cauda epididymis sperm motility and density, number of pups, fertility, and circulatory levels of testosterone were observed in all treatment groups. The weights of testes, epididymis, seminal vesicle, and prostate were significantly decreased in groups B, C, and D. The weights of all organs in the different groups of the androgenicity study were markedly decreased in group F when compared with group A, in group G when compared with group F, and in group I when compared with group H, and increased in group H when compared with group F. The serum testosterone levels also showed a similar pattern. The concentration of testicular cholesterol was significantly elevated, while protein, sialic acid, acid and alkaline phosphatase concentrations were decreased. The histoarchitecture of the testes showed degenerative changes in the seminiferous epithelium, arrest of spermatogenesis at the secondary spermatocyte stage, cytolysis, and the lumen filled with eosinophilic material. Histometric parameters except Sertoli cell nuclear area and number of round spermatids showed marked alterations. All altered parameters restored to normal in group E. No changes were observed in body weight, litter size, hematology, and serum biochemistry. In conclusion, a 50% ethanol extract of C. Colocynthis showed an antiandrogenic nature, thereby reduced reversible infertility in male albino rats.

Animals↗
PubMed2003

Effect of testosterone and season on proenkephalin messenger RNA expression in the preoptic area of the hypothalamus in the ram.

Enkephalin appears to exert an inhibitory action on LH secretion, but whether testosterone regulates enkephalin gene expression is unknown. This study tested the hypothesis that testosterone and/or season modulate preproenkephalin mRNA expression in specific areas of the hypothalamus. Romney Marsh rams were castrated (wethers) either during the breeding season or nonbreeding season and received intramuscular injections of either oil or testosterone propionate (five/group). Blood samples were taken for the assay of plasma LH and testosterone. Preproenkephalin mRNA expression was quantified in hypothalamic sections by in situ hybridization. Mean plasma LH concentrations were reduced and the interpulse interval for LH pulses was greater in testosterone propionate-treated wethers compared with oil-treated wethers, with no change in LH pulse amplitude. Testosterone propionate treatment reduced proenkephalin expression in the diagonal band of Broca, the caudal preoptic area, and the bed nucleus of the stria terminalis. Seasonal differences in proenkephalin expression were observed in the bed nucleus of the stria terminalis, lateral septum, periventricular nucleus, and paraventricular nucleus. No differences were observed between treatments in seven other regions examined. We conclude that testosterone and season regulate proenkephalin mRNA levels in the preoptic area/hypothalamus in the ram in a region-specific manner.

Animals↗
PubMed1975

The proliferative response of the coagulating gland of the castrated mouse under continuous androgen stimulation: an experimental and computer simulation model.

The proliferative response of the coagulating gland of the castrated male mouse has been examined during continuous treatment with testosterone propionate. Fourteen days after castration, s.c. daily injections of testosterone propionate were begun. Mitotic (Im) and labelling (IL) index values were obtained at 3 h intervals for up to 100 h after the initial injection. These showed a biphasic response, in which IL reached a maximum at 30 and 70 h, and Im at approximately 45 and 75 h. Fraction-labelled mitoses (FLM) curves were begun 24, 48, and 72 h after the first androgen injection. In each curve the first wave of labelled mitoses rose to 100% and showed a square form indicating little spread in the durations of the G2 and S phases. Values of 7.5, 1.3 and 0.7 h were obtained for the durations of DNA synthesis (ts), the post-synthetic period (tG2) and of mitosis (tm) respectively. In none of the FLM curves was it possible to demonstrate a second wave of labelled mitoses and direct measurement of the cell cycle time (Tc) was not obtained. Continuous tritiated thymidine labelling indices revealed that after a latent period of 25 h, DNA synthesis began and labelling rose rapidly to 80% by 45 h and then more slowly to 95% by 97 h. Cell population changes during androgen stimulation estimated from measurements of total glandular DNA indicated that the number of cells present in the glands remained constant during the first 30 h after stimulation and thereafter increased to approximately 2-3 times the original value. The data are compared with a mathematical model which assumes that the cell population of castrated mice when stimulated passes from a GO compartment through successive waves of DNA synthesis and mitosis. After each cell division the cells may leave or remain in the proliferative cycle. This model has been subjected to computer simulation using the cell cycle parameters obtained in the kinetic experiments. There was good agreement between the stimulation and experimental results in the Im and IL curves, continuous labelling, and total cell number experiments. The simulation of FLM curves was less successful. Although the first wave of labelled mitoses was clearly seen the model predicts a distinct second wave of labelled mitoses. It is concluded that this does not appear because of variation in the duration of G1.

Animals↗
PubMed2005

Evaluation of estrogenic and androgenic activity of butylated hydroxyanisole in immature female and castrated rats.

We evaluated the estrogenic and androgenic activity of butylated hydroxyanisole (BHA) using immature rat uterotrophic assay and Hershberger assay. To investigate (anti-) estrogenicity, BHA alone or with 17beta-estradiol was administered to 20-days-old immature female rats for three consecutive days. Absolute and relative uterine weights were significantly decreased by BHA (50, 100, 250, 500 mg/kg) alone and 17beta-estradiol-stimulated weights of uterine and vagina were also decreased by BHA (500 mg/kg), while uterine epithelial cell height was not affected. In Hershberger assay, BHA alone or with testosterone propionate (TP) was administered daily to 51-days-old castrated male rats for 10 days. BHA alone or with testosterone propionate (TP) caused no significant effect on androgen-dependent accessory sex organ weights; seminal vesicle/coagulative glands, glans penis, Cowper's gland, ventral prostate gland and levator ani plus bulbocarvernosus muscle. Although, the relative weight of ventral prostate gland was increased by the co-treatment of BHA 250 mg/kg with TP 0.4 mg/kg compared to that of TP alone, the relative and absolute weights of other androgen-dependent organs and absolute and formalin-fixed ventral prostate gland weight showed no changes. Our studies suggest that BHA have anti-estrogenic activity for the decrease of uterine weight in immature female rat but have negligible effect on the androgenic activity in castrated male rats.

Animals↗
PubMed1985

A quantitative assessment of the gametogenic and androgenic properties of testicular steroids in hypophysectomized rats.

The ability of testicular steroids to maintain the quantitative aspects of spermatogenesis was compared with reference to their androgenic properties. Hypophysectomized rats were injected daily with 0.2 mg progesterone, 20 alpha-dihydroprogesterone, 3 beta-hydroxy-5 alpha-pregnan-20-one, testosterone or testosterone propionate for 30 days beginning 2 days after the operation. Testosterone propionate was the most potent steroid tested both in terms of its peripheral androgenic effects and its ability to prevent the post-operative decline in the weight of the testis and seminiferous tubules and the numbers of germ cells throughout their differentiation. The natural androgen, testosterone, exhibited weak gametogenic properties and only partly maintained the normal measures of spermatogenesis. Progesterone exhibited low intrinsic androgenic potency yet was significantly more effective than testosterone in maintaining spermatogenesis; it prevented the degeneration of spermatocytes during the later stages of meiotic prophase and the reduction divisions resulting in an increased yield of step 7 spermatids. Low androgenic and gametogenic properties were exhibited by 20 alpha-dihydroprogesterone and 3 beta-hydroxy-5 alpha-pregnan-20-one. These results may indicate that testosterone produced locally in the seminiferous tubules from progesterone is more effective in maintaining spermatogenesis than androgens entering from the circulation. Alternatively, progesterone may act more directly on the germ cells than previously envisaged.

20-alpha-Dihydroprogesterone↗
PubMed1990

Gonadal steroid regulation of substance P (SP) and SP-encoding messenger ribonucleic acids in the rat anterior pituitary and hypothalamus.

Substance P-like immunoreactivity (SP-LI) is present in the rat anterior pituitary (AP) and in hypothalamic neurons that may be involved in the control of AP secretion and/or reproductive function. The presence of multiple SP-encoding mRNAs and tachykinin peptides and their regulation by steroid hormones were examined in APs and hypothalami from normal, gonadectomized, and steroid-treated male and female rats. SP-encoding mRNAs were identified by nuclease protection assays of RNA, and tachykinin peptides were identified by combined HPLC-RIA of tissue extracts, beta- and gamma-preprotachykinin (PPT) mRNAs and SP, neurokinin A, and neuropeptide gamma peptides were identified in the AP. The alpha-, beta-, and gamma-PPT mRNAs and SP, neurokinin A, neuropeptide gamma, neuropeptide K, and neurokinin B peptides were present in hypothalamic tissue. Previous studies have established that in the AP, SP is differentially regulated by gonadal steroids; estrogen decreases and androgen increases AP SP. Steroid effects were further analyzed in experiments using RIAs to measure SP levels in the AP and median eminence (ME) of steroid- and oil-treated gonadectomized rats. To assess whether steroids alter steady state PPT mRNA levels and presumably SP synthesis in these tissues, potential effects on AP and hypothalamic SP-encoding mRNAs were determined. Ovariectomized rats treated for 10 days with estradiol benzoate showed a 50% decrease in AP SP and a 90% decrease in AP beta- and gamma-PPT mRNAs compared to ovariectomized oil-treated controls. Estradiol benzoate replacement had no effect on SP levels in the isolated ME, but did cause a 50% increase in alpha-, beta-, and gamma PPT mRNAs in the hypothalamus. Although there was no significant effect of testosterone propionate on AP SP levels in castrated males, 10 days of testosterone propionate replacement did cause a significant increase in beta- and gamma PPT mRNAs in the AP. No androgen effects were seen on either ME SP or hypothalamic SP-encoding mRNAs. These data demonstrate that estrogen up-regulates SP-encoding mRNAs in the hypothalamus, whereas it down-regulates SP-encoding mRNAs in the pituitary. These results implicate SP and other tachykinins derived from the SP gene as steroid-regulated modulators of AP secretion and possibly reproductive function.

Animals↗
PubMed1976

[Effect of neonatal injections of estradiol, testosterone and cryproterone acetate on plasma and testicular testosterone and on the genital system in adult male mice].

On day old male mice received a single injection of oestradiol benzoate, testosterone propionate or cyproterone acetate in order to study their action on testicular development, particularly testosterone secretion. Oestrogenization of newborn males leads, when the animals mature, to a high proportion or cryptorchidism, to atrophy of testes and seminal vesicles, and inhibition of spermatogenesis. Testosterone levels were reduced in the plasma. Testosterone propionate produced moderate reduction of testicular weight but spermatogenesis was not impaired. Plasma testosterone level was reduced. Cyproterone acetate increased significantly testicular testosterone level.

Animals↗
PubMed1996

Effect of aging on erythropoietin secretion in male rats.

The secretion of erythropoietin (EPO) and testosterone in response to hypoxia in old (22-25 months), middle (mid)-aged (15-17 months), adult (6-7 months), and young (3 months) male rats was studied. Rats of different ages were bled by cardiac puncture before and subsequent to 8 h exposure to 12% O2. The metabolic clearance rate of EPO was determined by a single-injection method. The effects of orchidectomy and replacement of testosterone propionate on plasma EPO concentrations were also investigated. Analysis of the direct effects of testosterone on EPO release from kidney tissue was carried out in an in vitro study. Both basal and hypoxia-induced EPO levels were lower in old rats than in mid-aged, adult, and young rats (p < .01). Plasma testosterone levels decreased in response to hypoxia in all rats (p < .01 for young, adult, and mid-aged rats, and p < .05 for old rats). The old rats also had lower plasma testosterone levels following hypoxia when compared with other rats (p < .05). The metabolic clearance rate of EPO was not affected by age. Orchidectomy decreased rat plasma EPO concentration (p < .05). This decrease could be restored to intact levels after testosterone propionate replacement. Both 10(-10) M (p < .05) and 10(-9) M (p < .01) testosterone stimulate EPO release from kidney tissue in vitro. Our findings indicate that the basal levels of plasma EPO and testosterone are decreased, and the hypoxia-induced EPO is also diminished with aging in male rats. These data suggest that the mechanism of tolerance to hypoxia and the endocrine function of the kidneys in male rats during the aging process are testosterone-dependent.

Aging↗
PubMed1989

Vulvar dystrophies: an evaluation.

Of 86 patients diagnosed as having vulvar dystrophy in a 10-year period 56 (65.1%) had hyperplastic dystrophy, 23 (26.7%) had lichen sclerosus and 7 (26.7%) had mixed vulvar dystrophy. The diagnoses were made by colposcopic or toluidine blue directed biopsies. Fluorinated corticosteroids were given to patients with hyperplastic dystrophy with a response rate of 90.1%. Patients with lichen sclerosus received topical testosterone propionate and the response rate was 87.7%. Topical fluorinated corticosteroids followed by testosterone propionate was given to patients with mixed dystrophy and 85.8% of the patients responded. Surgical therapy was reserved for patients with failed medical treatment.

Adult↗
PubMed2000

Timing of prenatal androgen excess determines differential impairment in insulin secretion and action in adult female rhesus monkeys.

This study determined whether timing of prenatal androgen excess resulted in differential impairment of insulin-glucose homeostasis in adult female rhesus monkeys. Ten female rhesus monkeys exposed to testosterone propionate starting on gestational day 40 (early treated), 9 females exposed to testosterone propionate starting between gestational days 100-115 (late treated), and 15 control females were studied. The modified minimal model was used to examine various measures derived from an i.v. glucose tolerance test, with regression analysis performed between these variables and body mass index. In addition, the disposition index (DI) and the hyperbolic relationship between insulin sensitivity (S(I)) and acute insulin response to glucose were examined. Early treated females demonstrated impaired pancreatic beta-cell function, as shown by diminished DI and decreased percentile ranking for the hyperbolic relationship between S(I) and acute insulin response to glucose. In contrast, late treated females exhibited both an increase in DI and a negative relationship between body mass index and S(I). These results suggest that prenatal androgen excess in female rhesus monkeys, regardless of gestational timing, perturbs insulin-glucose homeodynamics, with androgen excess in early and late gestation impairing pancreatic beta-cell function and altering insulin sensitivity, respectively.

Animals↗
PubMed2004

L-prostaglandin D synthase expression and regulation in mouse testis and epididymis during sexual maturation and testosterone treatment after castration.

Lipocalin-type prostaglandin D synthase (L-PGDS) is highly expressed in the adult testis and epididymis of many mammals. The present study was to investigate L-PGDS expression in mouse testis and epididymis during sexual maturation, and the effects of testosterone replacement on L-PGDS expression in epididymis by in situ hybridization and immunohistochemistry. Both L-PGDS mRNA and protein were highly expressed in the interstitial tissue of adult testis. L-PGDS mRNA was first detected on d 30 after birth and exhibited an abundant signal in adult caput and cauda epididymis. L-PGDS immunostaining was first observed on d 30 after birth. There was a strong level of L-PGDS immunostaining in adult epididymis. Castrated male mice were treated with either vehicle or testosterone propionate following 3 d postcastration. L-PGDS expression steadily declined in a time-dependent fashion in control groups. No L-PGDS mRNA expression or immunostaining was detected in the controls for 12 d. When the castrated mice were treated with testosterone propionate for 5 or 12 d, L-PGDS expression was significantly increased in the whole epididymis. These data suggest that L-PGDS expression in mouse epididymis gradually declined in parallel to the declining concentration of endogenous androgen after castration and increased with the treatment of exogenous testosterone, indicating that L-PGDS expression in mouse epididymis was modulated by androgen levels. However, differential expression in different areas of the epididymis may also be influenced by factors derived from the testis.

Animals↗
PubMed1999

Effect of androgens on the cranial suspensory ligament and ovarian position.

Androgens have been postulated to have a major role in testicular descent via regression of the cranial suspensory ligament, which in normal rodents anchors the ovary to the retroperitoneum near the lower pole of the kidney. This study aimed to quantitate the degree of descent of the foetal ovary in androgen-treated female mice to determine the role of androgens in regression of the cranial suspensory ligament and descent of the testis. Time-pregnant mice were injected with testosterone propionate or methyl testosterone (2.5-3.0 mg) in vehicle on day 13 or 14. Control animals received vehicle only. Newborn mice were anaesthetised and dissected for macroscopic anatomy of the ovary, which was quantified by measuring the vertical distance from the lower pole of the kidney to the lower pole of the ovary. Histological analysis was also performed. The external genitalia were masculinised in all females exposed to prenatal androgens. The ovaries of treated animals were mobile, with no cranial suspensory ligament, and located slightly caudal to the kidney. Wolffian duct structures were identifiable, but the gubernaculum was qualitatively unchanged compared with control females. The ovary was displaced caudally (P< 0.001), but only 15-25% of the distance to the lower abdomen. Exogenous androgens induce regression of the cranial suspensory ligament, causing the ovary to be more mobile and lower in the abdominal cavity. However, since the testicular position at birth is at or below the bladder neck, androgen-mediated regression of the cranial suspensory ligament is only an adjunct to the control of transabdominal testicular descent.

Animals↗
PubMed1982

Plasma testosterone levels and sexual performance of young obese male Zucker rats.

The sexual behavior of obese male Zucker rats was studied at the age of 7, 8, 9, 10, 11, 14, and 16 weeks. Between 12-14 weeks of age, obese rats were treated with 400 micrograms testosterone propionate daily. Plasma testosterone levels were determined at the age of 10, 14, 16, and 20 weeks. Compared to lean rats, the sexual performance of the obese rats was abnormal at all ages. Plasma testosterone levels of obese rats were significantly lower at the age of 20 weeks but not at the age of 10 and 16 weeks, compared to those of their lean littermates. At the age of 14 weeks, after 2 weeks of testosterone treatment, plasma testosterone concentration rose to levels significantly higher than those of their lean littermates. However, there was no improvement in their sexual behavior following this period of hormone treatment. This study strongly suggests that obese male Zucker rats have abnormal reproductive function at all ages and that testosterone deficiency is not a primary cause of this abnormality.

Age Factors↗
PubMed2005

Could neonatal testosterone replacement prevent alterations induced by prenatal stress in male rats?

The present study was designed to examine whether testosterone replacement is able to prevent some effects of maternal restraint stress--during the period of brain sexual differentiation--on endocrine system and sexual behavior in male rat descendants. Pregnant rats were exposed to restraint stress for 1 h/day from gestational days 18 to 22. At birth, some male pups from these stressed rats received testosterone propionate. The neonatal testosterone replacement was able to prevent the reduction in anogenital distance at 22 days of age observed in pups from stressed pregnant rats as well as prevents the decrease in testosterone levels during the adulthood of these animals. Testosterone replacement in these males also presented an improvement in sexual performance. In this way, testosterone replacement probably through increasing neonatal level of this hormone was able to prevent the later alterations caused by the prenatal stress during the period of brain sexual differentiation.

Animals↗
PubMed1990

Effects of trenbolone acetate and testosterone on growth and on plasma concentrations of corticosterone and ACTH in rats.

The effects of trenbolone acetate (TBA) on growth and on plasma concentrations of corticosterone were examined in male and female rats. At 5 weeks of age, rats were injected with TBA (0.8 mg/kg) dissolved in peanut oil, or with oil alone, daily for 10 days. In female rats, TBA caused an increase in weight gain (20-38%), a reduction in adrenal weight (19%) and a reduction in plasma concentrations of corticosterone (55%). In contrast, TBA-treated male rats showed no significant increase in weight gain, no significant change in adrenal weight and no reduction in plasma concentrations of corticosterone. The mechanism by which adrenal activity was suppressed in TBA-treated female rats was examined and the response compared with that to testosterone. Female rats (8 weeks old) were injected daily either with oil vehicle, TBA (0.8 mg/kg) or testosterone propionate (0.8 mg/kg). Testosterone increased weight gain (24%), but the growth response to TBA treatment was significantly greater (97%). A reduction in plasma concentrations of corticosterone (45%) was again observed in response to TBA. However, testosterone increased plasma concentrations of corticosterone (52%) above those of control values. Neither androgen affected plasma concentrations of ACTH. Finally, the effects of TBA were examined in 6-week-old female rats, to characterize further the apparent age-related increase in responsiveness. The growth response of 6-week-old rats (60-74%) was intermediate between that seen in 5- and 8-week-old animals. It is concluded that part of the anabolic activity of TBA may be related to a reduction in circulating concentrations of corticosterone.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗