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PubMed1982

Pituitary and plasma levels of luteinizing hormone and follicle-stimulating hormone in male and female rabbit fetuses.

To study the ontogenesis of fetal pituitary gonadotrophin synthesis and release, LH and FSH were measured by radioimmunoassay in fetal rabbit pituitary glands and blood of both sexes from day 18 of gestation until birth. Results on levels of testicular and plasma testosterone were also included. Immunoreactive LH was first detected on day 19 in the pituitary gland and on day 20 in the plasma of fetuses of both sexes. Pituitary FSH was first measurable in both male and female fetuses at 24 days of gestation. Levels of FSH could not be detected in the blood of male fetuses at any time during gestation. In females, FSH could be measured in the circulation from day 27 of gestation until birth. These results show that (1) the ontogeny of pituitary LH and the onset of testosterone secretion are closely correlated and take place between 18 and 20 days of gestation just before the beginning of differentiation of the male genital tract, and (2) the highest concentrations of pituitary LH and FSH are observed, in both sexes, in late gestation after days 24-25.

Animals↗
PubMed1984

Activity of LH receptor, LH-stimulated cyclic AMP and testosterone production in the Leydig cell of heat-acclimatized rats.

Key reactions associated with the capacity of the isolated Leydig cell to synthesize testosterone were studied in male rats acclimatized to a hot environment (33-35 degrees C, 25-40% relative humidity) and controls (20-22 degrees C, 30-50% relative humidity). The results demonstrate that acclimatization to heat coincides with: (1) a lower number of human chorionic gonadotrophin (hCG) receptors (P less than 0.01) in the Leydig cell, (2) higher affinity of the Leydig cell for hCG (P less than 0.05), (3) lower hCG-stimulated cyclic AMP production (P less than 0.05) by the Leydig cell and (4) lower capacity of the Leydig cell to synthesize testosterone (P less than 0.01) after hCG challenge. It is suggested that the major cellular alteration responsible for the decreased testosterone secretion by the Leydig cell lies distal to the step involving the binding of the trophic hormone to its receptor and that heat-acclimatization induces changes in the integrity of the various cellular membranes leading to the impeded function of adenylate cyclase and 17 beta-hydroxysteroid oxidoreductase.

Acclimatization↗
PubMed1998

Differentiation of adult Leydig cells in the neonatal rat testis is arrested by hypothyroidism.

The effects of propyl thiouracil (PTU)-induced hypothyroidism on testicular interstitial cells and androgen secretion in vitro in the neonatal rat were investigated using Sprague Dawley rats of 1, 7, 14, and 21 days. The results revealed that the fetal Leydig cell (FLC) number per testis was unchanged between and within treatment groups at all ages tested. FLC size was 50% smaller in 21-day controls than in all other groups. Adult Leydig cells (ALCs) were present at Days 14 and 21 in controls but were absent in PTU rats. ALCs approximated FLCs of 21-day controls in size. ALC number per testis showed a sharp increase at Day 21. 11ss-HSD1-positive cells were absent in 21-day PTU testes, but a few were present in 21-day control testes. Testosterone secretion per testis was unchanged in 1- to 21-day controls and 7- to 21-day PTU rats. However, at Day 21, a significantly lower value was seen in controls compared to PTU rats. Testicular androstenedione secretion was not significantly different between control and PTU rats up to 14 days, but a sharp rise was observed in controls at Day 21. At this age, androstenedione levels in PTU rats were similar to those at younger ages. In summary, histological studies showed that hypothyroidism prevented the hypotrophy of FLC and the emergence of ALC in the neonatal rat testis, and agreed favorably with results concerning testicular androgen secretion in vitro. These findings suggest that thyroid hormones have a regulatory role in precursor cell differentiation into Leydig cells in the neonatal rat testis to establish the ALC population.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1987

The dynamics of the testosterone response of perifused mouse Leydig cells to hCG and arginine vasopressin.

The effect of hCG and Arginine-Vasopressin (AVP) on testosterone production by purified mouse Leydig cells was examined under dynamic conditions in a perifusion system. A rapid and dose-dependent increase in testosterone release was induced by a 5 min exposure of the cells to increasing concentrations of hCG (0.01 to 1 ng/ml). The testosterone response to hCG was Gaussian in distribution with a peak value by 100 min. A 12 h pretreatment of Leydig cells with 10(-5) M AVP enhanced testosterone accumulation in the perfusate under basal conditions, but markedly reduced the hCG-stimulated testosterone production. The basal and hCG-stimulated testosterone secretion profiles by freshly isolated Leydig cells were, however, unaffected by the continuous presence of the same dose of AVP. These results support the finding that AVP acts directly on Leydig cells. They support the hypothesis of a possible role of neurohypophysial peptides on reproductive functions in the mouse by modulating steroidogenesis at the testicular level.

Animals↗
PubMedDate not supplied

Involvement of arachidonic acid and the lipoxygenase pathway in mediating luteinizing hormone-induced testosterone synthesis in rat Leydig cells.

Evidence has been introduced linking the lipoxygenase products and steroidogenesis in Leydig cells, thereby supporting that this pathway may be a common event in the hormonal control of steroid synthesis. On the other hand, it has also been reported that lipoxygenase products of arachidonic acid (AA) may not be involved in Leydig cells steroidogenesis. In this paper, we investigated the effects of PLA2 and lipoxygenase pathway inhibitors on steroidogenesis in rat testis Leydig cells. The effects of two structurally unrelated PLA2 inhibitors (4-bromophenacyl bromide (BPB) and quinacrine) were determined. BPB blocked the LH- and Bt2cAMP-stimulated testosterone production but had no effect on 22(4)-OH-cholesterol conversion to testosterone. Quinacrine caused a dose-dependent inhibition of LH- and Bt2cAMP-induced steroidogenesis. The effects of different lipoxygenase pathway inhibitors (nordihydroguaiaretic acid (NDGA), 5,8,11,14-eicosatetraynoic acid (ETYA), caffeic acid and esculetin) have also been determined. Both NDGA and ETYA inhibited LH- and Bt2cAMP-stimulated steroid synthesis in a dose-related manner. Furthermore caffeic acid and esculetin also blocked the LH-stimulated testosterone production. Moreover, exogenous AA induced a dose-dependent increase of testosterone secretion which was inhibited by NDGA. Our results strongly support the previous concept that the lipoxygenase pathway is involved in the mechanism of action of LH on testis Leydig cells.

Acetophenones↗
PubMed1996

The combined effect of alcohol and physical exercise on serum testosterone, luteinizing hormone, and cortisol in males.

The combined effect of alcohol and physical exercise on the serum levels of testosterone, luteinizing hormone, and cortisol was studied in healthy male volunteers by performing an exhaustive ergometer exercise (1) followed by alcohol intoxication (induced by 1.5 g of alcohol/kg body weight), (2) during alcohol intoxication (induced by 0.8 g of alcohol/kg body weight), and (3) during hangover (13 hr after a dose of 1.5 g of alcohol/kg body weight). Physical stress immediately before alcohol administration prolonged the depressant effect of alcohol on testosterone secretion. This seemed to be mainly a consequence of direct inhibition at the testicular level, even though the role of luteinizing hormone as a contributory regulatory factor cannot be totally ruled out. Cortisol response to exercise was not modified by alcohol under any of the experimental conditions.

Adult↗
PubMed1997

Long-term outcome of male-limited gonadotropin-independent precocious puberty.

Long-term outcome of five new cases of male-limited precocious puberty (MPP) is reported. Three patients had positive family history. One patient was untreated; 2 boys received cyproterone acetate (2.0-3.6 mg/kg/daily) without clinical effects. Two patients were treated with ketoconazole (600 mg/daily); in 1, GnRH analogue therapy (Buserelin, 1,600 microg/day) was added after 6 months of effective ketoconazole treatment for development of central precocious puberty. The other patient did not develop central puberty under ketoconazole treatment and improved his predicted adult height from 172.4 to 181.1 cm. Four patients reached final height [B.A. (therapy cyproterone acetate): age 22.0 years, -2.0 SDS; B.G. (untreated): age 15.5 years, -1.7 SDS; M.M. (therapy cyproterone acetate): age 19.5 years, -1.6 SDS; M.F. (therapy ketoconazole plus GnRH analogue): age 21.3 years, -2.2 SDS]; three had reduced testicular volume (B.A.: -1.6/-1.6 SDS; B.G.: -2.1/-2.1 SDS; M.F.: -2.4/-1.9 SDS); one (M.F.) showed oligospermia. We concluded that in MPP cyproterone acetate treatment did not improve final height; ketoconazole was effective in reducing testosterone secretion, but its real effect on final height cannot be determined; the timing of central puberty may be precocious, suggesting that an adjunctive GnRH analogue treatment may be needed. In some patients, testicular impairment may be present in young adulthood.

Androgen Antagonists↗
PubMed1991

[Penoscrotal hypospadias with XXYY chromosome pattern].

This is the report of a boy, 2 years and 4 months of age who presented with an penoscrotal hypospadia with normal appearing testes. Physical examination and routine laboratory tests revealed--besides a broad base of the nose and clinodactyly--no abnormality. The boy exhibits a normal speech development with retarded global intellectual development. Investigation of the hormon status revealed a disturbance of testosteron secretion and a hypergonadotropic hypogonadism. Chromosomal analysis in lymphocyte cultures revealed a XXYY karyotyp. This chromosomal pattern is seen in 3% of patients with Klinefelter syndrom; the estimated frequency is 1 in 25,000 population. A combination of an XXYY chromosomal pattern with a penoscrotal hypospadia has not been reported in the literature so far.

Child, Preschool↗
PubMedDate not supplied

[Radioimmunological and biochemical study of the reaction of the adenohypophysis, testes and adrenals in rats and guinea pigs to the administration of the antiandrogen, 4-nitro-3-trifluoromethylisobutyranilide].

A study was made of the influence of antiandrogen 4'-nitro-3'-trifluorome-thylisobutyranilide (niftolide) on the content of the luteinizing hormone, testosterone and corticosterone in the rat blood plasma, the content of testosterone in the blood plasma and on the 17-OCS and 17-KS urinary excretion in guinea pigs. The data obtained pointed to a marked intensification of lutropin and testosterone secretion. The observed changes are explained by the capacity of niftolide to block the inhibitory influence of the androgens of the feed-back mechanism of the gonadotropin secretion control. It is suggested that niftolide can be used for the investigation of the functional condition of the hypothalamo-hypophysio-testicular system. Niftolide had no effect on the indices of the glucocorticoid activity of the adrenal glands in rats and guinea pigs.

17-Hydroxycorticosteroids↗
PubMed1999

Effect of FSH infusion on follicle development in GnRH agonist-treated gilts.

The aim was to investigate the effect of infusion of purified FSH alone on follicle development in hypogonadotrophic GnRH agonist-treated gilts. Large-White hybrid gilts (n = 12) were treated during the mid-luteal phase and again after 28 days (day 0) with a potent slow releasing GnRH agonist. On day 3, seven gilts were infused for 168 h with 1.5 S1 units oFSH h-1 (equivalent to 1.5 units of bioactivity of NIH-FSH-S1 standard) and blood samples were collected. Ovaries were then recovered and all follicles > or = 1 mm in diameter were dissected and incubated for 2 h in 1 ml Eagle's minimum essential medium. The ovaries were recovered from the remaining five GnRH agonist-treated gilts on day 10 and also from five cyclic gilts during the late follicular phase (controls). Plasma FSH concentrations in GnRH agonist-treated gilts were lower (P < 0.01) than in follicular phase controls, increased (P < 0.001) after 1 h of FSH infusion and reached a plateau similar (P > 0.1) to that of controls after 8 h. Basal LH concentrations were similar (P > 0.1) between GnRH agonist-treated and control gilts and remained unchanged (P > 0.1) throughout the infusion period. GnRH agonist treatment reduced (P < 0.01) basal oestradiol concentrations compared with control gilts. Infusion with FSH alone increased (P < 0.001) plasma oestradiol concentrations after 96 h compared with those before infusion; when the animals were killed oestradiol concentrations were higher (P < 0.01) in GnRH agonist-treated gilts infused with FSH than in controls. This was also apparent by vulval swelling and behavioural oestrus. There were more follicles > or 1 mm in diameter in the GnRH agonist-treated groups than in the controls (184, 153 and 86 per animal; P < 0.01). Infusion with FSH increased the maximum follicle diameter (GnRH agonist: < 4 mm; FSH infused: < 12 mm; controls: < 10 mm) and tended to increase (P < 0.07) the mean number of follicles > or = 6 mm diameter per animal (FSH infused: 53; controls: 21). Total oestradiol production in vitro by follicles > or = 1 mm was higher (P < 0.01) in GnRH agonist-treated gilts infused with FSH and in follicular phase controls than in animals treated with GnRH agonist alone. However, oestradiol and testosterone secretion in vitro per follicle > or = 6 mm in diameter was lower (P < 0.05) in FSH-infused animals than in controls. In summary, although infusion of FSH alone stimulated the growth of multiple follicles of preovulatory size in GnRH agonist-treated gilts, steroidogenic output by individual follicles was impaired.

Analysis of Variance↗
PubMed1997

Improved survival in patients with locally advanced prostate cancer treated with radiotherapy and goserelin.

BACKGROUND: We conducted a randomized, prospective trial comparing external irradiation with external irradiation plus goserelin (an agonist analogue of gonadotropin-releasing hormone that reduces testosterone secretion) in patients with locally advanced prostate cancer. METHODS: From 1987 to 1995, 415 patients with locally advanced prostate cancer were randomly assigned to receive radiotherapy alone or radiotherapy plus immediate treatment with goserelin. The patients had a median age of 71 years (range, 51 to 80). Patients in both groups received 50 Gy of radiation to the pelvis over a period of five weeks and an additional 20 Gy over an additional two weeks as a prostatic boost. Patients in the combined-treatment group received 3.6 mg of goserelin (Zoladex) subcutaneously every four weeks starting on the first day of irradiation and continuing for three years; those patients also received cyproterone acetate (150 mg orally per day) during the first month of treatment to inhibit the transient rise in testosterone associated with the administration of goserelin. RESULTS: Data were available for analysis on 401 patients. The median follow-up was 45 months. Kaplan-Meier estimates of overall survival at five years were 79 percent (95 percent confidence interval, 72 to 86 percent) in the combined-treatment group and 62 percent (95 percent confidence interval, 52 to 72 percent) in the radiotherapy group (P=0.001). The proportion of surviving patients who were free of disease at five years was 85 percent (95 percent confidence interval, 78 to 92 percent) in the combined-treatment group and 48 percent (95 percent confidence interval, 38 to 58 percent) in the radiotherapy group (P<0.001). CONCLUSIONS: Adjuvant treatment with goserelin, when started simultaneously with external irradiation, improves local control and survival in patients with locally advanced prostate cancer.

Adenocarcinoma↗
PubMed2006

Ethanol prevents development of destructive arthritis.

Environmental factors are thought to play a major role in the development of rheumatoid arthritis. Because the use of ethanol is widespread, we assessed the role of ethanol intake on the propensity to develop chronic arthritis. Collagen type II-immunized mice were given water or water containing 10% (vol/vol) ethanol or its metabolite acetaldehyde. Their development of arthritis was assessed, as well as the impact of ethanol on leukocyte migration and activation of intracellular transcription factors. Mice exposed daily to this dose of ethanol did not display any liver toxicity, and the development of erosive arthritis was almost totally abrogated. In contrast, the antibody-mediated effector phase of collagen-induced arthritis was not influenced by ethanol exposure. Also, the major ethanol metabolite, acetaldehyde, prevented the development of arthritis. This antiinflammatory and antidestructive property of ethanol was mediated by (i) down-regulation of leukocyte migration and (ii) up-regulation of testosterone secretion, with the latter leading to decreased NF-kappaB activation. We conclude that low but persistent ethanol consumption delays the onset and halts the progression of collagen-induced arthritis by interaction with innate immune responsiveness.

Animals↗
PubMed1978

Improvement in the fertility of streptozotocin-diabetic male rats following treatment with insulin and human chrionic gonadotropin.

Diabetes was produced in male rats with streptozotocin. Some of them were subsequently treated with exogenous insulin, human chorionic gonadotropin (hCG) or both. The rats were tested six weeks later for fertility, testosterone secretion and spermatogenesis. Diabetes was found to inhibit all three parameters of fertility. Accessory gland atrophy was restodred following the treatment with insulin and much improved with insulin plus hCG. In a diabetic control group on restricted food intake, insulin alone did not significantly improve fertility, whereas hCG enhanced steroidegenesis and spermatogenesis but not fertility. Treatment with both hCG and sinulsin gave the best results.

Animals↗
PubMed1977

Beckwitt-Wiedemann's syndrome with medullary sponge kidneys, agonadism and persistent testosterone production.

A patient with Beckwitt-Wiedemann's syndrome is described in which associated malformations were hemihypertrophy of the body, medullary sponge kidneys and absence of testes and internal ducts. On the other hand, we demonstrated biochemically the existence of testosterone secretion, with active response to a 3-day HCG stimulation as well as prepuberty levels LH and FSH. This demonstrated the existence of functioning Leydig's cells. The diagnosis of agonadism and anorchia could not be entirely true since they lead to an erroneous conclusion that there always are some disseminated Leydig's cells.

Abnormalities, Multiple↗
PubMed1987

Mouse hybrid sterility and testicular function.

Crosses of BALB/c female mice and inbred wild male mice (PWD, PWK) produce fertile female progeny, but the male offspring are sterile. The hybrid male sterility is a direct action of the hybrid sterility genes Hst-1s and Hstws. Previous reports concluded that spermatogenic arrest effected the sterility. However, the testicular steroidogenesis of hybrid sterile male mice has not been elucidated. In the present report, the steroidogenic capacity of hybrid sterile and parental strain males was directly assessed by quantifying testosterone secretion by maximally stimulated testes perfused in vitro. Additionally, Leydig cell mass and germ cell volumes were morphometrically determined. The experimental results confirm the deleterious impact of the Hst-1s/Hstws genotype on spermatogenesis and demonstrate for the first time that the steroidogenic capacity of hybrid sterile testes is reduced. The biochemical defects that cause the impairment of testicular function are unknown.

Animals↗
PubMed1982

Chronic pulsatile low dose GnRH therapy for induction of testosterone production and spermatogenesis in a man with secondary hypogonadotropic hypogonadism.

Prolonged intermittent treatment with low doses of GnRH was given to a 23-yr-old man with secondary hypogonadotropic hypogonadism. The patient had experienced sudden onset of diabetes insipidus followed by progressive decrease of gonadotropins and gonadal function. Modern radiological techniques did not reveal any organic genesis. A small portable computerized infusion pump connected to a sc catheter was used for the 220-day GnRH therapy. One microgram gnRH was administered every 90 min during the first 90 days and 5 micrograms GnRH every 90 min during the following 130 days. During the prolonged GnRH treatment testosterone secretion normalized, libido and potency improved, and ejaculation returned. Spermatogenesis became close to normal and the subject's wife became pregnant after 181 days of treatment. The prolonged treatment with the small infusion pump was well accepted and did not interfere with the patient's daily life activations. Thus, chronic pulsatile low dose GnRH treatment can restore normal pituitary-gonadal function in idiopathic male hypogonadotropic hypogonadism.

Adult↗
PubMed1996

Continued desensitization of the pituitary gland in young bulls after treatment with the luteinizing hormone-releasing hormone agonist deslorelin.

The objective in this study was to evaluate pituitary and testicular function in young bulls during and after treatment with the LHRH agonist deslorelin. The primary focus was to ascertain the period required for a return to typical LH and testosterone secretion after cessation of treatment with deslorelin, in order to establish whether desensitization was a phenomenon restricted to the pituitary or also occurred at the testes. Brahman bulls, 13.0 +/- 0.6 mo of age and 224 +/- 5 kg, were allocated to four groups and received treatment as follows: group C (n = 5), control, received no treatment; group C + LHRH (n = 5), control, received LHRH tests (50 micrograms LHRH i.m.) at the same times as group D + LHRH below; group D (n = 5), received deslorelin (approximately 200 micrograms/day) for 28 days; group D + LHRH (n = 5), received deslorelin for 28 days and were given LHRH test (50 micrograms LHRH i.m.) on Day 28 of treatment and on Days 2, 4, 8, 12, 16, and 20 after treatment. Deslorelin induced acute increases (p < 0.01) in plasma concentrations of LH and testosterone within 2 h, after which concentrations of both hormones declined by 24 h. From Day 6 to Day 28 of the treatment period, plasma LH concentrations were similar for treated and control bulls. During the same period, concentrations of plasma testosterone were greater (p < 0.01) in treated than in control bulls. Mean concentrations of both LH and testosterone were lower in treated than in control bulls for approximately one week after cessation of deslorelin treatment. Bulls treated with deslorelin did not exhibit a release of LH in response to exogenous LHRH on Day 28 of treatment. A relatively small but significant (p < 0.05) release of LH occurred on Day 4 after cessation of treatment with deslorelin (group D + LHRH, 0.49 +/- 0.11 ng/ml; group C + LHRH, 7.17 +/- 0.90 ng/ml). LH release in response to LHRH in bulls previously treated with deslorelin increased to Day 12 and then remained constant to Day 20 after cessation of treatment. However, LH release in these bulls remained significantly lower compared with that of control bulls during the 20 days after cessation of treatment with deslorelin. Bulls treated with deslorelin had a typical release of testosterone after administration of LHRH on Days 2-20 after discontinuation of treatment, even though there were relatively small releases of LH. Therefore, the pituitary in bulls remained desensitized to LHRH for at least 20 days after cessation of treatment with an LHRH agonist. In contrast, desensitization did not occur at the testes, which retained the capacity for a typical testosterone response to the LH that was released after administration of LHRH.

Amino Acid Sequence↗
PubMed1983

[Modulation of Leydig cell activity by Sertoli cell: an in vitro study].

In vivo studies indicate that FSH can modulate Leydig cells steroidogenic activity. However, in the testis only Sertoli cells contain specific FSH receptors. In order to clarify the mechanism by which FSH exerts this effect on testicular steroidogenesis, purified Pig Leydig and Sertoli cells were cultured alone or in co-culture. Leydig cell activity has been evaluated by two parameters: 1. hCG-stimulated testosterone secretion. 2. LH/hCG binding sites. FSH does not stimulate these two parameters of purified Leydig cells when cultured alone. On the other hand, when Leydig cells are co-cultured with Sertoli cells, FSH significantly increases these two parameters of Leydig cell function. These results suggest that the effect of FSH on Leydig cells is not direct but mediated by Sertoli cells.

Animals↗