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[Effect of luliberin and chorionic gonadotropin on luteinizing hormone and testosterone levels in the blood of monkeys under acute stress].

The effect of immobilization stress on luteinizing hormone (LH) and testosterone (T) secretion following injections of luliberin (LH-RH) and human chorionic gonadotropin (HCG) was investigated in male hamadryas baboons. It was established that in control animals a single injection of HCG (4500 IU) led to a more prolonged and more demonstrable increase of plasma testosterone concentration than injection of a pharmacological dose (100 micrograms) of LH-RH. Preliminary stimulation of the testes with LH-RH did not prevent the stress-induced inhibition of testosterone despite the fact that LH secretion in intact and stress-exposed baboons did not differ significantly over 2.5 h after drug injection. At the same time stress did not inhibit the testicular response in baboons pretreated with HCG (4500 IU), although the level of T concentration in stress-exposed animals was lower than in control. The data obtained suggest that disturbed interaction between hypophyseal tropic hormone and the testes underlie the inhibitory effect of stress.

Acute Disease↗
PubMed1984

Inhibition of prolactin secretion by moderate and high doses of testosterone.

The effects of different doses of testosterone on basal and stimulated secretion of prolactin (PRL) were investigated. Intact female mice of the S/W strain were injected sc with 0, 1, 10, 20, 50, 250, 500, 1000, 2500, or 5000 micrograms of testosterone propionate (TP) once daily for 4 weeks. Serum testosterone concentrations of TP injected mice rose 2- to 5-fold above those of controls at 1- to 50-micrograms doses, and 25- to 600-fold over controls in mice given higher doses of the steroid. Administration of 1 microgram of TP, the lowest dose tested, had no significant effects on basal serum PRL concentrations and only slightly inhibited the release of PRL induced by perphenazine, but the weight and PRL concentration of the pituitary gland were significantly depressed. However, at doses of 10, 20, and 50 micrograms TP, perphenazine-induced PRL release, pituitary PRL concentration, and pituitary gland weight were all reduced in a dose-related manner. The basal serum PRL concentrations decreased by the time the dose of TP reached 50 micrograms. In contrast, higher doses of TP (250 micrograms and above) reversed the suppression of these parameters: pituitary gland weight and basal serum PRL levels were restored to control levels, whereas pituitary PRL concentrations and perphenazine-induced PRL release were partially restored. These results suggest that administration of moderate and large doses of testosterone may suppress natural episodic and acute releases of PRL.

Animals↗
PubMed2005

Inhibition of CYP450scc expression in dioxin-exposed rat Leydig cells.

Polychlorinated dibenzo-p-dioxins, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) have been recognized as highly potent developmental and reproductive toxins. We have previously demonstrated effects of TCDD in modulating the expression of rat Sertoli cell secretory products and markers for cell-cell interaction. In this study, we examined the direct biological effects of TCDD in rat Leydig cell primary cultures. Mature rat Leydig cells were purified by Percoll gradient centrifugation and the cell purity was determined by 3beta-hydroxysteroid dehydrogenase (3beta-HSD) staining and a testosterone induction assay. To examine TCDD-induced biological consequences, we measured the changes in the secretion of progesterone and testosterone, as well as transcript levels of some selected steroidogenic enzymes (i.e. StAR, P450scc, 3beta-HSD and CYP17alpha), in TCDD/human chorionic gonadotropin (hCG) co-treated cells. Our results indicated that TCDD (0.2 or 2 ng/ml) treatment significantly suppressed hCG (5 or 10 ng/ml)-induced testosterone secretion. The suppressive effect aligned with a reduction of progesterone secretion (P<0.05), as well as a decrease of P450scc mRNA and protein expression (P<0.05). The mechanistic action of TCDD was found to be via the reduction of cellular cAMP levels in the hCG-treated cells. This observation was further confirmed, as the TCDD-mediated suppressive effect could be reversed by dibutyryl cAMP co-treatment. The data indicate that TCDD can modulate cAMP signaling in rat Leydig cells to affect the process of steroidogenesis.

3-Hydroxysteroid Dehydrogenases↗
PubMed1991

Differential steroid and gonadotropin response by individual tertiary porcine follicles in vitro. Possible physiologic role of atretic follicles.

Since atretic follicles contain significant amounts of androgen and/or progesterone in their follicular fluid, we examined whether they also contribute to ovarian steroid secretion. Steroid secretion by atretic porcine follicles and their responsiveness to FSH was assessed by a perifusion system that allows for separate dynamic incubation of whole follicles in vitro. Identically treated nonatretic follicles of comparable size served as a reference group. The extent of granulosal pyknosis, on which the staging of atresia was based, was inversely related to follicular estradiol (E2) secretion and its responsiveness to FSH. Both basal and FSH-stimulated secretion of testosterone (T), androstenedione (A), and progesterone (P) were maintained by follicles in all stages of atresia. Secretion of A by late atretic follicles was greater than that in earlier stages or by nonatretic follicles. Atretic follicles may therefore release comparable or larger amounts of androgen and P into their intraovarian environment than do nonatretic follicles. We examined whether steroids secreted by atretic follicles in vitro could be utilized by nonatretic follicles. A static incubation system was used that allows for simultaneous incubation of a number of individual follicles. When nonatretic follicles were exposed to A, T, or P in physiologic concentrations (10(-7)-10(-5) M), their secretion of E2 increased 2-8-fold. Doses of FSH or LH that stimulated follicular steroid in vitro had no additional stimulatory effect when combined with A or P treatment, respectively. In conclusion, atretic follicles may contribute significantly to intraovarian levels of androgen and P.(ABSTRACT TRUNCATED AT 250 WORDS)

Androgens↗
PubMed1975

Testosterone and 5alpha-reduced androgen secretion by rabbit testes-epididymides perfused in vitro.

Mass spectrometric determinations confirmed that testosterone, 5alpha-androstan-17betaol-3-one, 5alpha-androstan-3alpha, 17beta-diol and 5alpha-androstan-3beta, 17beta-diol were present in venous effluent of in vitro perfused rabbit testes-epididymides. Testosterone, dihydrotestosterone, 3alpha-androstanediol and 3beta-androstanediol were secreted at 3.1 plus or minus 0.9, 0.7 plus or minus 0.2, 0.4 plus or minus 0.1 and 0.6 plus or minus 0.1 mug/h when testes-epididymides were perfused with an artificial medium containing 2.5 ng/ml NIH-LH-S17, ovine. Surprisingly, testosterone constituted only 64% of the total mass of the four androgens secreted. These results probably reflect in vivo androgen secretion since hourly collections of spermatic vein blood from anesthetized rabbits contained 2.7 plus or minus 0.9, 0.8 plus or minus 0.3, 0.15 plus or minus .04 and 0.5 plus or minus 0.2 mug of testosterone, dihydrotestosterone, 3alpha-androstanediol and 3beta-androstanediol, respectively. Once again testosterone constituted only 64% of the total mass of the four androgens.

Androstanes↗
PubMed1979

Fine structural studies of rat seminal vesicle in castrated and intact animals following estrogen treatment.

The effect of estradiol and/or testosterone upon secretion by seminal vesicle in castrated and intact rats was assessed in young adult Sprague-Dawley rats, using light microscopy (LM), transmission (TEM) and scanning (SEM)electron microscopy. Hormones were injected daily for ten days beginning ten days after castrations were performed. The normal rat seminal vesicle, as revealed by SEM, was characterized by a large saccular lumen with highly folded walls. Cell surfaces were covered with microvilli, or occasionally displayed a protruding, ruffled surface, sparsely covered with short microvilli. Cytology was normal in testosterone-treated animals. Estradiol treatment of castrated animals stimulated secretion by seminal vesicle epithelial cells as evidenced by the presence of normal secretory bodies, the presence of RER, and moderately hypertrophied Golgi complexes. These glands were not heavier than were glands from castrated, untreated animals, although the epithelial cells were significantly taller. Secretion was maintained in intact animals treated with estradiol, although glands were smaller and epithelial height was reduced. Estradiol and testosterone treatment in combination did not appear to have an additive effect on secretion, weight of the gland, or epithelial height. The following results support the hypothesis that estrogen-induced prolactin synthesis and release may be involved in the mechanism by which estradiol effected stimulation of seminal vesicle epithelium. Prolactin-treated, castrated animals exhibited focal areas of stimulated epithelium. In hypophysectomized animals (untreated controls), the seminal vesicle epithelium retained some secretory bodies and secretory fluid in the glandular lumen; epithelial height was taller than that in castrated controls. Estrogen treatment reduced the epithelial height to that of castrated controls; there was no evidence of secretion. This suggests that in the absence of anterior pituitary hormones, including prolactin, the stimulatory effect of estradiol on seminal vesicle epithelium was nullified. In adrenalectomized/castrated animals, estradiol treatment stimulated secretion in seminal vesicle epithelium just as in non-adrenalectomized/castrated animals. This indicates that the adrenal gland plays a non-essential role in the action of estrogen on seminal vesicle epithelium.

Adrenal Cortex Hormones↗
PubMed1978

Decreased Leydig cell responsiveness in the testicular feminized male rat.

The Stanley-Gumbreck pseudohermaphrodite or testicular feminized male (tfm) rat exhibits a decreased Leydig cell sensitivity to human CG (hCG) measured by androgen and cyclic-3',5',-adenosine monophosphate production in vitro. These changes were associated with an 80% reduction in the number of LH receptors in the tfm testis, when compared on the basis of equivalent amounts of testis particle protein or per 10(6) isolated Leydig cells. Androstenedione and not testosterone is the major androgen secreted by the tfm Leydig cell and androstenedione secretion is, therefore, a more appropriate end point than testosterone secretion for Leydig cell function in tfm animals. A dose of hCG (3 ng/2 ml) which elicited a near maximal response in androgen production from the decapsulated testes and Leydig cell suspensions of normals rats, did not significantly stimulate androgen production from Leydig cells of the tfm animals. A much higher dose of hCG (200 ng/2 ml) gave a response from the tfm Leydig cells which was comparable to that obtained with 3 ng from Leydig cells of normal littermates. This indicates that the small number of LH receptors on the tfm Leydig cell membrane are functional and that the reduction in receptor number results in a decrease in the sensitivity of response to LH rather than a reduction in the maximum steroid response.

Androgen-Insensitivity Syndrome↗
PubMed1987

Action of GnRH on steroid secretion by luteal cells of cyclic and early pregnant sows in vitro.

The effect of GnRH was studied on progesterone (P4), oestradiol-17 beta (E2) and testosterone (T) secretion by porcine luteal cells from the 13th day of the oestrous cycle and the 18th day of pregnancy. Trypsin-dispersed luteal cells (5 X 10(4) cells/ml) were incubated in medium 199 with 10% calf serum with or without GnRH in doses of 0.1, 1, 10 and 100 mg/ml and with 1 microgram LH and 50 U/ml hCG. The concentration of P4, E2 and T in the medium was estimated by radioimmunological method after 6 hours of incubation. The results showed that GnRH had no effect on the secretion of the investigated steroid hormones by luteal cells from cyclic sows. GnRH at a dose of 10 g inhibited E2 secretion and at a dose of 1 ng T secretion by cells from pregnant sows. LH and hCG stimulated release of P4 by luteal cells in both physiological stages. The conclusion drawn was that GnRH does not act directly on luteal cells of cyclic sows but may inhibit E2 and T secretion by cells of pregnant sows.

Animals↗
PubMed1978

[Dynamic study of the hypothalomo-hypophyseal-gonadal axis in patients with Klinefelter's syndrome].

Detailed clinical and hormonal studies were performed in 30 male patients with Klinefelter syndrome, proved by karyotyping. Diagnostic tests with LH-RH were carried out with application of 100 microgram of LH-RH as single stimulation and as long-term application for 7 days. Plasma levels of LH, FSH and testosterone were measured by specific radioimmunoassay. Th single LH-RG application stimulated both LH and FST secretion, while testosterone level remained unchanged in patients with Klinefelter syndrome. Long-term stimulation decreased basal LH and FSH levels and pituitary response to LH-RH . became close to normal. The testosterone level increased significantly in most patients with Klinefelter syndrome. This suggests that the Leydig cells in Klinefelter syndrome improved their activity, showing some functional reserve.

Adolescent↗
PubMed1976

A case of male pseudohermaphroditism associated with elevated LH, normal FSH and low testosterone possibly due to the secretion of an abnormal LH molecule.

A 27 year old female is described who had 46,XY chromosome complement, ambiguous external genitalia with elevated LH, slightly above normal FSH and low testosterone. Her plasma testosterone level increased 15-20 fold after HCG stimulation (5000 IU X 3). then returned to prestimulation level 3 months later. This was possibly due to the secretion of an abnormal LH molecule which is immunoreactive but biologically inactive in the human.

Adult↗
PubMed1994

Role of aromatization in testosterone-induced inhibition of luteinizing hormone secretion in female turtles, Trachemys scripta.

Both 17 beta-estradiol (E2) and testosterone (T) were shown to inhibit in vitro pituitary LH secretion in the turtle Trachemys scripta. Since T was approximately 500 times less potent than E2, and 5 alpha-dihydrotestosterone was even less active than T, the inhibitory action of T may result from its aromatization to estrogen. We utilized both in vivo and in vitro approaches to elucidate the roles of T and estrogen in the negative feedback of pituitary LH secretion. Gonadectomy of adult (vitellogenic) females significantly elevated plasma LH. Adult females treated with fadrozole (an aromatase inhibitor) with or without daily injections of keoxifene (an antiestrogen) also showed an increase in plasma LH to a level comparable to that observed in gonadectomized females, whereas plasma LH levels of juvenile females treated with fadrozole remained undetectable. In vitro LH secretion in response to GnRH in juvenile females was significantly inhibited by 48-h exposure to 50 ng/ml T or 100 pg/ml E2. Both fadrozole (200 microM) and keoxifene (200 nM) significantly blocked this T-induced inhibition of LH secretion, demonstrating that T lacks intrinsic inhibitory activity. Confirmation of the inhibition of aromatase activity by fadrozole comes from metabolic studies of 1 beta-[3H]androstenedione using turtle brain, ovary, and pituitary. In vitro, fadrozole altered the metabolism of 1 beta-[3H]androstenedione and inhibited aromatase activities in these tissues. These results indicate that the inhibitory effect of T is largely mediated through its aromatization to estrogen, and that estrogen is primarily responsible for the suppressed LH secretion in vitellogenic adult turtles.

Androstenedione↗
PubMed1996

Diurnal rhythm of 17 beta-estradiol secretion throughout pubertal development in healthy girls: evaluation by a sensitive radioimmunoassay.

Puberty is initiated by a nocturnal rise in gonadotropin secretion, which, in boys, results in an increased nocturnal secretion of testosterone. To characterize any similar diurnal rhythm of 17 beta-estradiol in healthy girls, we determined the secretion of 17 beta-estradiol before and during puberty. The study group consisted of 45 healthy girls whose height SD scores ranged from -3.7 to +4.9 compared with Swedish growth reference values. One to 6 profiles of 17 beta-estradiol (7 samples/24 h) were obtained from each girl during puberty and from 21 of the girls before clinical signs of puberty (a total of 76 serum profiles). Serum 17 beta-estradiol concentrations were determined using a modified RIA. The detection limit for the RIA was 1.8 fmol/tube, which corresponded to a serum level of 7.8 pmol/L in extracted serum. It was considered that levels above 50 pmol/L could be determined accurately without extraction. The serum levels of 17 beta-estradiol in prepubertal girls were, in most cases, below the detection limit, except in the morning, when in 17 of the 21 prepubertal girls, serum 17 beta-estradiol levels were just above the detection limit. All girls in early puberty (Tanner breast stage 2) had measurable serum levels of 17 beta-estradiol in the morning, whereas 10 of these 15 girls had levels below the detection limit around midnight. Later in puberty (Tanner breast stages 3 and 4), but before menarche, the diurnal rhythm was more obvious, with high levels of 17 beta-estradiol during the latter part of the night and in the morning. This diurnal rhythm was lost by 1 yr after menarche. There was a high degree of correlation between serum concentrations of 17 beta-estradiol and bone age, whereas there was much less, if any, correlation between 17 beta-estradiol and levels of sex hormone-binding globulin or dehydroepiandrosterone sulfate during puberty. We conclude that the nocturnal rise in gonadotropin secretion during puberty in girls is accompanied by an increased secretion of 17 beta-estradiol in the morning. This diurnal rhythm is lost 1 yr after menarche. Determination of 17 beta-estradiol levels in the morning could be useful in determining the initiation of puberty, whereas determinations in the late evening could provide information on the tempo of puberty.

Adolescent↗
PubMed1994

Influence of aging on acetohexamide reductase activities in liver microsomes and cytosol of male rats.

The influence of aging on the reductase activity of acetohexamide, an oral antidiabetic drug with a ketone group, was examined in liver microsomes and cytosol of male rats. Acetohexamide reductase activities in liver microsomes of male rats at 26 and 31 months of age were much lower than that in liver microsomes of male rats at 9 weeks of age. Testectomy markedly decreased acetohexamide reductase activity in liver microsomes of the 9-week old rats and the decreased enzyme activity was significantly increased by testosterone administration. These results indicate, at least in part, that aging decreases the enzyme activity by decreasing the secretion of testosterone from the testes. On the other hand, aging (26 months of age) did not affect acetohexamide reductase activity in liver cytosol of male rats, although the enzyme activity at 31 months of age was slightly but significantly lower than that in liver cytosol of male rats at 9 weeks of age. Testectomy or testosterone administration had no effect on the enzyme activity in liver cytosol of 9-week old male rats.

Aging↗
PubMed2005

Plasma leptin levels of elite endurance runners after heavy endurance training.

A decrease in testosterone levels and an increase in cortisol levels are observed in male athletes with the overtraining syndrome (OTS). Cortisol causes blood leptin levels to rise and testosterone has an inverse relationship with blood leptin levels. Therefore, we hypothesized that the hormonal changes as a result of OTS induce an increase in leptin. To test this hypothesis, we examined the relationship among changes in leptin, testosterone and cortisol in thirteen male collegiate distance runners (aged 20.3+/-1.1 years) before and after an 8-day strenuous training camp. Runners ran 284.1+/-48.2 km during the training camp. Body fat percentages and plasma glucose concentrations decreased significantly after the training. Non-ester fatty acids and total cholesterol concentrations in blood were unchanged. Serum cortisol concentrations showed a significant increase after the training camp (from 11.82+/-2.00 microg/dl to 16.78+/-3.99 microg/dl), and serum testosterone decreased significantly (from 408.0+/-127.6 ng/dl to 265.2+/-97.6 ng/dl). The ratio of testosterone to cortisol (TCR) dropped by 50% after training (from 35.62+/-13.69 to 16.94+/-8.47). These results suggest that the subjects reached a state of the OTS. Contrary to our hypothesis, plasma leptin was not significantly changed (from 1.34+/-0.29 ng/ml to 1.49+/-0.18 ng/ml). Delta Plasma leptin was not significantly correlated with delta serum cortisol, delta TCR or delta fat percentage. However, delta serum testosterone was positively correlated with delta plasma leptin (r=596, p<0.05). Plasma leptin concentrations might modulate the secretion of testosterone in overtraining conditions. In conclusion, the change in blood leptin level is independent of the changes in cortisol, TCR and fat percentage in highly trained male athletes in the state of the OTS.

Adult↗
PubMed1979

Mechanism of glucocorticoid-induced inhibition of prostaglandin synthesis.

In order to study the mechanism of steroid-induced inhibition of prostaglandin (PG) secretion, we have used rat renomedullary interstitial cells grown in tissue culture as an in vitro model. These cells have been shown by radio-immunoassay to produce high amounts of prostaglandins, mainly PGE2 and PGF2 alpha. Using (3H) dexamethasone, we have demonstrated in our cultures the existence of glucocorticoid binding sites which exhibit all the characteristics of physiological glucocorticoid receptors. Comparison between the biological activity (i.e. the ability to inhibit PG secretion) of the various steroids tested (dexamethasone, corticosterone, aldosterone, progesterone and estradiol) and their affinities for the glucocorticoid binding sites reveals a striking correlation between these two parameters. Steroids which bind to the receptors also inhibit prostaglandin secretion whereas testosterone and estradiol, which have a very weak affinity for the glucocorticoid binding sites do not inhibit PG secretion. In addition, actinomycin D (0.1 microgram/ml) and cycloheximide (0.1 microgram/ml) are able to abolish the inhibitory effect of dexamethasone on PG secretion. Our results indicate that the action of corticosteroids on prostaglandin secretion, which is believed to be the basis of their anti-inflammatory properties, is mediated through receptor occupancy and requires RNA and protein synthesis.

Animals↗
PubMed1977

Sex steroid production by the human fetus: its role in morphogenesis and control by gonadotropins.

Normal male genital differentiation requires fetal testicular secretion of both testosterone and the nonsteroidal müllerian-inhibitory factor. It appears that secretion of testosterone, at least during the critical period of differentiation, occurs in response to stimulation by CG, although pituitary LG may influence Leydig cell function in later fetal life. To date, there is no evidence to support a similar endocrine function for the fetal ovary in female genital differentiation. In both sexes normal fetal pituitary gonadotropin secretion appears to be required for maturation of the germ cells and related elements. The pattern of FSH and LH secretion in the fetus reflects gradual maturation of a functional hypothalamo-pituitary unit responsive to feedback inhibition by sex steroids. The higher levels of gonadotropins in female fetuses from from 12--20 weeks suggest either that this maturation occurs earlier in males than in females, or, more probably, that feedback recognition of androgens is established before gestation reflects development of an estrogen-mediated feedback mechanism, and in addition the possible influence that hormones, such as prolactin or placental estradiol, may have on testicular steroidogenesis.

Androgens↗
PubMed1994

Prolactin- and testosterone-induced inhibition of LH secretion after orchidectomy: role of preoptic and tuberoinfundibular gamma-aminobutyric acidergic neurones.

The inhibitory amino acid neurotransmitter gamma-aminobutyric acid (GABA) may play an important role in the regulation of LH-releasing hormone secretion. The present study examined the effect of prolactin on GABAergic neuronal activity in microdissected brain regions of the orchidectomized rat, to determine whether inhibition of LH secretion after castration by acute hyperprolactinaemia was associated with prolactin-induced changes in GABAergic neuronal activity. The effects of prolactin were contrasted with the effects of testosterone on hypothalamic GABAergic neurones after orchidectomy. GABA concentrations were measured by high pressure liquid chromatography in eight microdissected brain regions in untreated rats and 60 min after inhibition of the GABA catabolic enzyme GABA transaminase by injection of amino-oxyacetic acid (AOAA). The rate of GABA accumulation in microdissected brain regions following injection of AOAA was taken as an index of GABAergic neuronal activity. Rats were divided into seven experimental groups: intact controls, 2 days after castration, 2 days after castration with prolactin treatment (2.5 mg ovine prolactin injected s.c. every 12 h, starting at the time of castration), 2 days after castration with testosterone replacement (30 mm silicone elastomer implant containing crystalline testosterone), 6 days after castration, 6 days after castration with prolactin treatment, and 6 days after castration with testosterone replacement. Both 2 and 6 days after castration, plasma LH was markedly elevated above levels in intact rats, and AOAA-induced GABA accumulation was significantly decreased in the diagonal band of Broca at the level of the organum vasculosum of the lamina terminalis, in the medial preoptic nucleus and in the median eminence. Hyperprolactinaemia significantly reduced LH levels 2 days but not 6 days after castration. GABAergic neuronal activity, however, was not significantly affected by prolactin at either time. Testosterone replacement blocked the postcastration elevation in plasma LH and prevented the castration-induced suppression of GABAergic neuronal activity both 2 and 6 days after castration. There were no castration- or hormone-induced changes in GABAergic neurones observed in the medial or lateral septum, caudate nucleus, cingulate cortex or arcuate nucleus. These results demonstrate that the activity of GABAergic neurones terminating in the rostral hypothalamus and the median eminence is positively regulated by testosterone, and that these steroid-sensitive GABAergic neurones may be important in the negative-feedback control of LH secretion. Inhibition of LH secretion by hyperprolactinaemia, however, may not be mediated by changes in GABAergic neuronal activity.

Animals↗