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PubMed1996

Changes in circulating hormone concentrations, testes histology and testes ultrasonography during sexual maturation in beef bulls.

Nine groups of bull calves (n = 5 to 6 per group) were castrated every 5 wk from 5 to 45 wk of age, and the stages of spermatogenesis were identified histologically. Prior to castration, the testes of each calf were examined by ultrasonography, and the pixel intensities of the parenchyma were quantitated. Testis ultrasonograms were also recorded every 2 wk from 10 bull calves between 2 and 40 wk of age. Blood samples were collected at weekly intervals until castration. There was an early transient rise in circulating LH concentrations between 4 and 25 wk of age, while circulating FSH concentrations were high initially but decreased between 14 and 30 wk of age. Circulating testosterone concentrations increased gradually from 6 to 35 wk of age and then rapidly to 42 wk of age. There was a progressive increase in the more mature cell types during spermatogenesis as the animals aged, with the most dramatic changes occurring between 15 and 45 wk of age. Outer seminiferous tubule diameter increased between 10 and 45 wk of age, with the most rapid increase occurring from 30 wk of age. Inner tubule diameter increased between 30 and 35 wk of age. The echogenicity of the testes (as determined by ultrasonography) increased between 20 and 40 wk of age. From these data we conclude that testis echogenicity increased during the most active phase of growth of the seminiferous tubules as more mature germ cells were produced. Cessation of the early rise in gonadotrophin secretion immediately preceded this active phase of testicular development. Testosterone secretion rose markedly with the production of mature spermatozoa.

Journal Article↗
PubMed1992

Investigation of familiar and novel chemosensory stimuli by golden hamsters: effects of castration and testosterone replacement.

Estrous hamsters secrete an odorous vaginal discharge that intact male hamsters investigate vigorously during copulatory behavior. Castrated animals are not attracted to this vaginal discharge. In this study we observed that repeated exposure of intact and castrated hamsters to this vaginal discharge reliably produced habituation of investigatory behavior. Presentation of the odor from a novel female to a habituated male caused an increase in investigation (dishabituation). Castration produced a decrease in investigation within 1 week of surgery. However, the surgery did not produce a decrease in dishabituation until 3 months afterward. Testosterone treatment increased chemosensory investigation in castrated animals. It seems likely that the dishabituation observed in this study may represent a sensory component of the Coolidge Effect.

Animals↗
PubMedDate not supplied

Testicular dysfunction in the adjuvant-induced arthritic rat.

Adjuvant-induced arthritis, an autoimmune disease similar to rheumatoid arthritis, was used to investigate possible mechanisms of immune system modulation of the reproductive system. This laboratory previously reported that arthritic male rats have reduced serum testosterone and elevated serum LH concentrations. In the experiments described here, serum prolactin levels were not significantly different in arthritic animals compared with non-injected control animals. Neither reduced food consumption of arthritic rats nor the injection vehicle appear to cause a reduction of serum testosterone. Serum corticosterone was significantly elevated in the arthritic group compared with both the non-injected or the vehicle-injected control animals. Testicular cells from arthritic animals secrete significantly less testosterone in vitro compared with cells from non-injected control animals, both basally and in response to dbcAMP and hCG. In summary, the reduced serum testosterone of arthritic animals appears to be the result of a testicular dysfunction.

Animals↗
PubMed1997

Endocrine correlates of personality traits: a comparison between emotionally stable and emotionally labile healthy young men.

An initial sample of 120 healthy young men was screened by a personality questionnaire and 15 subjects each with highest and lowest scores respectively on emotionality (emotionally labile, EL subjects and emotionally stable, ES subjects) were recruited for a study on the relationship between the degree of emotionality and the basal secretion of stress-sensitive hormones during night-time. The nocturnal urinary excretion of cortisol, testosterone, adrenaline, noradrenaline and melatonin was measured over a period of 5 consecutive nights. The average amounts of each hormone excreted per night were not different between the two extreme groups. The variability of the excretion during the 5 nights of cortisol and testosterone, but not of adrenaline, noradrenaline and melatonin, was significantly higher in EL compared to ES subjects. The larger fluctuations in the nocturnal secretion of these two (and no other) hormones in EL subjects indicate that emotional lability is associated with a more labile regulation of cortisol and testosterone secretion. The observed intraindividual variability of basal stress hormone secretion may contribute to the vast interindividual variability noticed in psychoneuroendocrine stress research, especially in emotionally labile subjects.

Adolescent↗
PubMed1996

The metabolism of testosterone by dermal papilla cells cultured from human pubic and axillary hair follicles concurs with hair growth in 5 alpha-reductase deficiency.

Androgens regulate the growth of many human hair follicles, but only pubic, axillary, and scalp hair growth occur in men with 5 alpha-reductase deficiency. This suggests that 5 alpha-dihydrotestosterone is the active intracellular androgen in androgen-dependent follicles, except in the axilla and pubis. Since the dermal papilla plays a major regulatory role in hair follicles and may be the site of androgen action, we have investigated androgen metabolism in six primary lines of cultured dermal papilla cells from pubic and axillary hair follicles; previous studies have shown that beard cells take up and metabolize testosterone, retaining and secreting 5 alpha-dihydrotestosterone. After 24 h preincubation in serum-free Eagle's medium 199, 100-mm dishes of confluent cells were incubated for 2 h with 5 nM [1,2,6,7-3H]testosterone. Media were collected and the cells washed with phosphate-buffered saline and extracted with chloroform: methanol (2:1). After the addition of unlabeled and 14C-labeled marker steroids, the extracts were analyzed by a two-step thin-layer chromatography system; steroid identity was confirmed by recrystallization to a constant 3H/14C ratio. Beard and pubic dermal papilla cells were also incubated for 24 h, and the medium was analyzed at various times. The results from pubic and axillary primary cell lines were similar. In both cells and media the major steroid identified was testosterone, but significant amounts of androstenedione were present, indicating 17 beta-hydroxysteroid dehydrogenase activity; androstenedione was also identified within the cells, but a small amount of 5 alpha-dihydrotestosterone was only identified in one pubic cell line. Beard dermal papilla cells secreted large amounts of 5 alpha-dihydrotestosterone into the medium over 24 h in contrast to pubic cells, which produced only very small amounts. The pubic and axillary cell results contrasts with the observations of pronounced 5 alpha-dihydrotestosterone in beard cells and confirm that androgen metabolism in cultured dermal papilla cells reflects the parent follicle's ability to respond to androgen in the absence of 5 alpha-reductase type II in vivo. This supports our hypothesis that androgen acts on hair follicles via the dermal papilla and suggests that cultured dermal papilla cells may offer an important model system for studies of androgen action.

Cells, Cultured↗
PubMed1999

Effect of short-term testosterone treatment on leptin concentrations in boys with pubertal delay.

Testosterone administration increases growth hormone (GH) secretion and decreases the plasma leptin concentration in men. We evaluated the effect of increased GH secretion due to short-term testosterone treatment on leptin concentrations. Ten boys aged 14.8 +/- 0.2 (mean +/- SE) years with transient GH deficiency caused by pubertal delay were evaluated before and after (3 months) 4 intramuscular injections of 100 mg testosterone heptylate, given at 15-day intervals. The leptin concentration decreased from 5.4 +/- 1.3 to 3. 6 +/- 1.1 microgram/l (p < 0.001), despite a weight gain of 3.4 +/- 0.5 kg. There were significant increases in body mass index (BMI), from -0.2 +/- 0.5 to 0.2 +/- 0.5 SD, p < 0.005, in GH peak after stimulation test, from 6.3 +/- 0.5 to 21.7 +/- 2.9 microgram/l, p < 0. 0003, in plasma testosterone, from 0.6 +/- 0.1 to 6.5 +/- 1.3 microgram/l, p < 0.001, in insulin-like growth factor-I (IGF-I), from 152 +/- 21 to 330 +/- 30 microgram/l, p < 0.0001, and in IGF-binding protein-3 (IGFBP-3), from 4.2 +/- 0.5 to 5.4 +/- 0.4 mg/l, p < 0.01. But there were no changes in blood glucose (4.7 +/- 0.1 and 4.8 +/- 0.1 mmol/l), or plasma fasting insulin (9.0 +/- 1.2 and 8.1 +/- 1.3 mIU/l). The leptin concentrations were positively correlated with the BMI before (p < 0.03) and after (p < 0.04) testosterone, but not with the GH peak after stimulation, or with plasma testosterone, IGF-I or IGFBP-3. The leptin and insulin concentrations after testosterone treatment were positively correlated (p < 0.04). Thus, short-term testosterone treatment of boys with pubertal delay decreases their leptin concentrations. The lack of correlation with GH secretion or with its changes, despite the dramatic increase in GH secretion, and the lack of change in insulin are additional features suggesting that testosterone increases the leptin concentration mainly by an effect on adipose tissue.

Adolescent↗
PubMed1989

Growth hormone (GH) responsiveness to GHRH in normal adults is not affected by short-term gonadal blockade.

The effects of changes in circulating gonadal steroids on GH secretion elicited by GHRH challenge (1 microgram/kg) in normal adults volunteers (aged 18-24 years), were evaluated in 10 women and 10 men before and after gonadal blockade was achieved by a GnRH agonist (1500 micrograms/day by nasal spray for 40 days). To see if the effect of testosterone on GH secretion was dependent on its aromatization to estradiol (E2), GHRH tests were performed in 7 normal men prior to administration of testosterone enanthate (250 mg im), 8 days after this treatment had began, and again after E2 receptor blockade with tamoxifen (30 mg for 2 days plus 10 mg on the third day 2 h before the GHRH test, po) administered 8 days after testosterone enanthate. The study of the functional status of the somatotropes at the time of GHRH testing was made according to our previous postulate. Short-term gonadal blockade did not affect the parameters of GH response to GHRH in neither women nor men. Thus, the functional blockade of the gonads may be advisable as an adjunct therapy in the treatment of hypothalamic GH-deficiency during the peripubertal stage. In the other group of men, administration of testosterone enanthate significantly increased GHRH-elicited GH release, but this was reverted after E2 receptor blockade. Since the hypothalamic-somatotrope rhythm was altered by both these pharmacological manipulations, it appears that testosterone acts on GH release mainly at the suprapituitary level, and that this action is secondary to its aromatization to E2.

Adolescent↗
PubMed1983

Intraovarian localization of luteinizing hormone/human chorionic gonadotropin stimulation of testosterone and estradiol synthesis in the pregnant rat.

The objective of this investigation was to determine whether LH acts directly on luteal cells to stimulate testosterone and estradiol synthesis or whether it stimulates follicular and/or interstitial production of androgen and thus provides androgen substrate for luteal cell production of estradiol. Pregnant rats were injected with 1.5 IU human CG (hCG) twice daily sc between days 12 and 14. On day 14, blood was obtained from both the jugular and ovarian vein. Corpora lutea (CL), follicles, and interstitium were isolated and incubated at 37 C for 4 h. Estradiol, testosterone, and progesterone levels were measured in the peripheral circulation, ovarian vein plasma, tissues, and medium. After hCG treatment, no ovulation occurred, rats remained pregnant, and progesterone levels in the serum and in the ovarian vein plasma remained unchanged. In contrast, estradiol and testosterone levels in the ovarian vein increased from 0.7 +/- 0.1 and 0.6 +/- 3.4 ng/ml, respectively, in vehicle-treated rats to 12.5 +/- 3.5 and 4.8 +/- 1.4 ng/ml in hCG-treated animals. In vivo treatment with hCG dramatically increased the in vitro capacity of luteal cells to synthesize de novo both testosterone and estradiol but had no stimulatory effect on progesterone synthesis. Testosterone synthesis by CL increased from 21 +/- 4 to 255 +/- 114 pg/CL whereas estradiol synthesis rose from 30 +/- 7 to 4481 +/- 641 pg/CL. hCG also increased follicular synthesis of both estradiol and testosterone. The interstitium responded to the hCG challenge with a 50-fold increase in testosterone synthesis but with no change in estradiol production. To determine whether hCG rapidly stimulates ovarian production of testosterone, both in vivo and in vitro approaches were used. In the in vitro experiments, CL follicles, or interstitium obtained from day 14 pregnant rats were incubated with or without 3 IU hCG. In the in vivo experiments, day 14 pregnant rats were injected with 3 IU hCG iv and were bled from the jugular and ovarian veins 0.5 and 2 h later. No increase in testosterone and estradiol production was observed after a short challenge with hCG. In summary, this study demonstrates that in the pregnant rat a sustained increase in serum hCG activity stimulates ovarian secretion of both testosterone and estradiol. We conclude that LH can act to induce the synthesis and/or activation of enzyme(s) involved in the conversion of progesterone to androgen in luteal tissue. The results also demonstrate that LH stimulates the synthesis of androgens but not of estradiol in interstitial tissue and confirms the finding that LH stimulates follicular production of both testosterone and estradiol.

Animals↗
PubMedDate not supplied

[Sertoli-Leydig cell tumour (arrhenoblastoma) in a patient with polycystic ovary syndrome: clinical, ultrasonographic, hormonal and histopathological evaluation].

UNLABELLED: Nowadays, the polycystic ovary syndrome is considered the most common endocrinopathy in women. A patient referred for oligomenorrhea or amenorrhea, will probably be classified as suffering from this syndrome if at least one of the three characteristics of the syndrome is present: 1. polycystic ovaries (ultrasonographic finding); 2. hirsutism, and 3. hyperandrogenism. However, differential diagnosis of PCOS must also include patients with menstrual disorders and hirsutism, suffering from disorders of the pituitary gland (hyperprolactinaemia or acromegaly), disorders of adrenal glands (congenital classical or non-classical adrenal hyperplasia) or androgen secreting ovarian tumours. CASE REPORT: A PCOS patient with a very high serum testosterone level -8.2 nmol/L (normal concentrations 0.7-3.47 nmol/L), and clinical signs of hyperandrogenism, which had been deteriorating during the monitoring period of approximately two years, is presented. The first ultrasound examination diagnosed polycystic ovaries, having a volume at the upper limit of normal range (7.9 cml). After one year ultrasound showed an asymmetrical enlargement of the right ovary (volume 25.34 cm3). Three months later a tumour of the right ovary was diagnosed (Figure 1). Salpingo-oophorectomy was performed. Microscopic analysis indicated without doubt the presence of a Sertoli-Leydig cell tumour of intermediate differentiation (Figure 2). DISCUSSION: In adolescence, congenital adrenal hyperplasia and adrenal tumours may be a source of elevated androgen concentrations. Adrenal tumours usually also cause excess secretion of dehidroepiandrosteron-sulfate (DHEAS). However, rare cases of adrenal tumours with excess testosterone secretion, but with normal or even low DHEAS levels, have also been reported. Adrenal carcinoma can cause virilization, however, in this case excess cortizole secretion is also frequently present. In young patients, the most common state accompanied by hyperandrogenism is PCOS. Hyperthecosis is also accompanied by high testosterone levels, but an ultrasound finding of cystic ovaries is not typical for this condition. Androgen-secreting ovarian tumours are a more common cause of hyperandrogenism than hyperthecosis. Sertoli-Leydig cell tumours are tumours of sexual cords and ovarian stroma. They present as unilateral, solid tumours (bilateral in < 3% of cases). In all cases when they are histologically well or intermediately differentiated, as in our patient, they are limited to the ovary. The percentage of Sertoli-Leydig cell tumours, manifesting endocrine activity has not been established, but it most probably amounts to about 50%, while virilization develops in about 1/3 of patients. In tumours showing hormonal activity the testosterone level is elevated, while the DHEAS level is within the normal range. Analysis of our patient confirmed the immense importance of detailed anamnesis, physical examination and regular control check-ups. Asymmetrical ovarian volume, especially if accompanied by unusually high testosterone concentrations, very probably points to an ovarian tumour, and when dealing with a patient with progressive hirsutism and/or virilization, even with a negative ultrasound finding, the clinician should remain suspicious and careful and request control examinations.

Adolescent↗
PubMed1985

Effect of the long-term administration of corticotropin-releasing factor on the pituitary-adrenal and pituitary-gonadal axis in the male rat.

The effect of the continuous exposure to ovine corticotropin-releasing factor (oCRF) was measured in adult male rats. The intravenous infusion of 0.75 nmol oCRF/h to intact rats over a 24-h period was accompanied by a peak of ACTH and corticosterone secretion that occurred during the first 90 min of administration of the releasing factor, followed by a decrease to lower, but still above control, values. Additionally, corticotropin-releasing factor (CRF)-treated rats had decreased plasma testosterone levels. The subcutaneous administration of 0.075 or 0.75 nmol oCRF/h to intact rats for 7 d also resulted in elevations of both plasma ACTH and corticosterone levels comparable to those measured after a 24-h exposure to the releasing factor, as well as dose-related hypertrophy of the adrenals and increases in pituitary ACTH content. In these animals, CRF markedly inhibited luteinizing hormone (LH) (but not follicle-stimulating hormone [FSH] ), testosterone, and PRL secretion and decreased seminal vesicle weights. All the effects of CRF were mimicked by exogenously administered ACTH. By contrast, with the exception of FSH secretion, which was slightly elevated by CRF, neither CRF nor ACTH were able to significantly modify reproductive parameters in adrenalectomized animals, which suggests that the elevation of circulating levels of adrenal steroids induced by peripherally administered CRF represents major mediators of CRF-induced inhibition of fertility. These results indicate that in the rat, the continuous stimulation of the pituitary-adrenal axis by peripherally administered CRF causes some degree of desensitization of the pituitary-adrenal axis, but is still accompanied by persistent elevations of the circulating levels of both ACTH and corticosteroids. The increased secretion of adrenal steroids by CRF-treated rats is believed to participate in the disruption of reproductive parameters observed in these rats.

Adrenal Glands↗
PubMed1994

Effects of Trypanosoma congolense infection on the pituitary gland of Baoulé bulls: immunohistochemistry of LH- and FSH-secreting cells and response of plasma LH and testosterone to combined dexamethasone and GnRH treatment.

The effects of Trypanosoma congolense infection were investigated at the pituitary level on trypanosome resistant Baoulé bulls (aged 3-6 years), using immunohistochemistry of LH- and FSH-secreting cells and a combined dexamethasone and GnRH challenge. The pituitaries of two control and five naturally infected Baoulé bulls were removed after slaughter and the LH- and FSH-secreting cells were examined immunohistochemically, using specific polyclonal antibodies against beta LH and beta FSH. No significant impairment of the labelling and distribution of LH- and FSH-secreting cells was seen in infected bulls when compared with control animals. No parasites were found in the pituitary glands. Plasma LH and testosterone concentrations were determined in eight control and eight infected bulls by enzymeimmunoassay and radioimmunoassay techniques, respectively. Blood samples were collected at intervals of 30 min two times before and nine times after dexamethasone treatment (20 mg i.m.). GnRH (Busereline: 20 micrograms, i.m.) was injected 4.5 h later and samples were collected every 15 min for 180 min. After dexamethasone treatment, LH and testosterone concentrations declined dramatically in both groups. Four hours after treatment, the mean testosterone concentration for both groups was 0.44 ng ml-1. After GnRH injection, LH concentrations in the infected group increased rapidly to a mean maximum value of 30 ng ml-1 by 165 min. In contrast, the increase in LH concentration in non-infected bulls was more gradual and the mean maximum value, reached at the same time, was only 20 ng ml-1. Testosterone concentration increased rapidly and in a similar manner in both groups for the first 90 min (0.08 +/- 0.04 ng ml-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Effects of gonadal steroids on somatotroph function in the rat: analysis by the reverse hemolytic plaque assay.

The mechanism by which gonadal steroids modulate GH secretion is not known. We have used the reverse hemolytic plaque assay to examine whether gonadal steroid-induced modulation of GH secretion is effected by changes in the population of somatotrophs and/or alterations in their secretory properties. Two groups of Sprague-Dawley rats were studied: group 1 (n = 6) comprised male (M), castrate (Cx), and testosterone-replaced castrate male (Cx + T) rats and group 2 (n = 5) consisted of male (M), female (F), and 17 beta-estradiol-replaced castrate male (Cx + E) rats. The number of plaque-forming cells (expressed as both absolute number and a percentage of all cells) was determined, and secretory status was assessed by measuring plaque areas in response to 0, 0.01, 0.1, 1, 10, and 100 nM GHRH. While mean basal GH plaque areas were similar among the treatment groups of group 1, the maximal GH plaque area was significantly decreased in Cx [16.8 +/- 2.4 vs. 26.4 +/- 3.9 X 10(6) microns2 (mean +/- SEM); P less than 0.05], but not in Cx + T (27.5 +/- 4.1 microns2) rats. The GHRH EC50 was unaffected by castration or T replacement. The percentage and absolute population of somatotrophs were reduced in Cx, but not in Cx + T, rats, while the numbers of lactotrophs remained unchanged in these treatment groups. For group 2, the mean peak GH plaque area was reduced in Cx + E (16.5 +/- 2.9 microns2; P less than 0.001) compared to that in M rats (36.2 +/- 2.3 microns2), but was not significantly different from that in F (13.0 +/- 1.5 microns2) rats. The EC50 was significantly (P less than 0.025) greater in Cx + E (10.9 +/- 2.3 nM) and F (7.9 +/- 1.6 nM) compared to M rats (2.8 +/- 0.7 nM). The absolute somatotroph and lactotroph populations were increased in Cx + E compared to M and F rats, as were the populations of other pituitary cell types. Testosterone enhances GH secretion by increasing the secretory capacity, but not the sensitivity, of somatotrophs to GHRH and by recruiting the function of a subpopulation of somatotrophs. Estradiol reduces the secretory capacity and sensitivity of somatotrophs to GHRH, but increases the population of somatotrophs, lactotrophs, and non-GH- and non-PRL-secreting cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMedDate not supplied

[Monitoring the treatment of precocious puberty with a GnRH-analog (buserelin): comparison of the GnRH-test with nocturnal pulsatility of LH, testosterone and 17-beta-estradiol].

We studied in 10 children (3 boys and 7 girls), affected by precocious puberty and treated for a period of more than 6 months with the GnRH-analog Buserelin, the efficacy of the GnRH test versus the study of spontaneous nocturnal secretion of LH, testosterone and 17 beta-estradiol as a means of testing the gonadotropin suppression. All the subjects have shown a total suppression of LH during the GnRH test as well as a nocturnal profile of LH, testosterone and 17 beta-estradiol of a prepubertal pattern. Clinically all the patients were treated successfully. Considering the effectiveness of both investigations, we conclude that the GnRH test combined with clinical observation is a single and valid means of testing the pharmacological treatment for precocious puberty.

Buserelin↗
PubMed1979

[Participation of the hypothalamus in the pituitary and testicular responses to administration of the antiandrogen 4-nitro-3-trifluoro-methylisobutyranilide].

The effect of the antiandrogen 4-nitro-3-trifluoro-methylisobutyranilide (flutamide, NFBA) on the content of follitropine, lutropine and testosteron in the blood plasma as well as on the testicular activity of the steroid delta 5-3 beta-Ol-dehydrogenase (SD) has been studied in male rats with intact and destroyed hypothalamic median eminence. In sham-operated rats with intact hypothalamus the levels of lutropin, follitropin, testosteron and the enzymatic activity were 5, 2, 4 and 3-4 times as increased, respectively, under the effect of NFBA. After destroyal of the hypothalamic median eminence NFBA treatment did not change follitropin secretion, while lutropin, testosteron plasma levels and SD activity were only 1 1/2-2 times higher, i.e. significantly less as compared to those in sham-operated animals. The data obtained suggest the most important role of the hypothalamus in pituitary and testicular responses to NFBA administration.

3-Hydroxysteroid Dehydrogenases↗
PubMedDate not supplied

Testosterone in sera of workers exposed to acrylonitrile.

Testosterone was measured through three consecutive years in sera from young and adult male subjects working in a chemical factory exposed to some complex chemical noxae, the major exposure being acrylonitrile (vinylcyanid). In the first yr, (group A), the blood was collected on May 1975 (no 39), the II-nd yr (group B) on March (no 109) and the III-rd yr (group C) on May (no 149). The exposure time varied in each group between 6 mos and 7-10 yrs. For comparison, blood samples were collected from 145 men of comparable age grouped in nonexposed: blood donors (no 37) (group a), new workers (no 23) (group b) and exposed to other chemical noxae in the same factory: Na cyanid (group c, no 23), cyan derivatives (group d, no 22) and pyrolysis (group no 39). The seasonal testosterone variations being considered, the Student's 't' test applied to the hormonal levels in acrylonitrile groups A, B and C showed non significant differences. However, the comparison of the testosterone concentrations in sera of the groups A, B and C vs the control groups investigated during the same month of the year showed much lower levels of the hormone in the first groups (p less than 0.001). These data are suggesting that the exposure to acrylonitrile either by direct participation to the technological chain or by working in the same noxious environment may influence the testosterone synthesis and/or secretion.

Acrylonitrile↗
PubMed1979

Estradiol and testosterone levels in the peripheral and ovarian circulations in patients with endometrial cancer.

Estradiol and testosterone levels in the peripheral and ovarian circulation of patients with endometrial cancer and of postmenopausal women were studied. These levels proved to be the same in the two groups. The ovaries of neither group secreted estradiol. The testosterone level in the ovarian circulation of all examined women was four times higher than that in the peripheral circulation, thus indicating the ovarian origin of testosterone.

Aged↗
PubMedDate not supplied

Involvement of inhibin in the regulation of follicle-stimulating hormone secretion in the young adult male Shiba goat.

The roles of inhibin and testosterone in the regulation of gonadotropin secretion were investigated in young adult male Shiba goats (8-12 months of age). Plasma levels of inhibin but not testosterone abruptly decreased after hemicastration (75% of the initial level), concomitant with a progressive rise in plasma levels of FSH. Removal of the remaining testis at 33 days after the hemicastration quickly decreased plasma levels of both inhibin and testosterone and induced a progressive increase in plasma FSH and LH. Implantation of testosterone sheets immediately after castration suppressed the increase in plasma FSH in part only, whereas the increase in LH secretion was almost completely suppressed. An i.v. injection of antiserum against [Tyr30] porcine inhibin alpha(1-30) resulted in a significant increase in plasma FSH in a dose-dependent manner, without altering plasma concentrations of LH. These findings clearly indicate that both inhibin and testosterone physiologically regulate FSH secretion and that testosterone is the principal gonadal factor regulating LH secretion in the adult male goat.

Animals↗
PubMed1993

GnRH in the male dog: dose-response relationships with LH and testosterone.

Dose-response relationships between GnRH and LH, and between GnRH and testosterone, were investigated in six male dogs by intravenous administration of a GnRH analogue at different doses. Each dose of GnRH analogue induced an immediate rise in the plasma concentration of LH and then a rise in plasma testosterone concentration. Irrespective of the dose used, the rise in testosterone began 10 min after the GnRH injection. Administration of GnRH at doses of 0.01, 0.1, 1, 10 and 100 micrograms kg-1 resulted in maximum LH concentrations in plasma (mean +/- SEM; n = 6) of 22 +/- 7, 27 +/- 6, 40 +/- 7, 57 +/- 13 and 56 +/- 10 micrograms l-1, respectively. These doses induced maximum concentrations of testosterone in plasma (mean +/- SEM; n = 6) of 16 +/- 4, 20 +/- 4, 22 +/- 3, 22 +/- 4 and 24 +/- 7 nmol l-1, respectively. The lag time between peak concentrations of LH and testosterone varied from 35 to 55 min. The calculated maximum response of testosterone to LH, secreted by the anterior pituitary after GnRH injection, was 1.8 times higher than to GnRH. It was concluded that intravenous administration of GnRH induced marked and dose-dependent increases in plasma concentrations of LH and testosterone, and that there does not appear to be a direct effect of GnRH on Leydig cells in male dogs.

Animals↗