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PubMed1989

Effect of a traditional Chinese herbal medicine (san zhuang wan) on the hypothalamus-pituitary-testis axis of the immature rat.

San Zhuang Wan (SZW) is a traditional Chinese herbal medicine used to treat male impotence. The mechanism of its therapeutic effect is not known nor have any of its potential physiologic actions been investigated. We examined the effect of SZW administered by gavage, on the reproductive system of the prepubertal male rat. After 10 days treatment of 21-day-old rats the concentration of testosterone in serum and testicular weight had decreased whereas the serum concentration of luteinizing hormone (LH) had significantly increased. When administered to gonadectomized rats SZW partially restored the weight of the accessory sex organs and concentration of LH toward normal, but serum androgen concentration was not changed. In vitro assessment of fragments of testicular tissue or purified Leydig cells for responsiveness to maximal doses of LH or cyclic AMP showed that SZW significantly reduced testosterone secretion in response to either stimulant. The data demonstrate that SZW has potent effects on the reproductive axis of the pubertal male rat. At least one locus for such action is on the Leydig cell at a point distal to the formation of cyclic AMP. Further study is necessary to determine whether these effects could be involved with or independent of the mechanism of the therapeutic action of SZW.

Animals↗
PubMed1991

Stress induced changes in testis function.

The mechanism through which chronic stress inhibits the hypothalamic-pituitary-testicular axis has been investigated. Chronic restraint stress decreases testosterone secretion, an effect that is associated with a decrease in plasma gonadotropin levels. In chronically stressed rats there was a decrease in hypothalamic luteinizing hormone-releasing hormone (LHRH) content and the response on plasma gonadotropins to LHRH administration was enhanced. Thus the inhibitory effect of chronic stress on plasma LH and FSH levels seems not to be due to a reduction in pituitary responsiveness to LHRH, but rather to a modification in LHRH secretion. It has been suggested that beta-endorphin might interfere with hypothalamic LHRH secretion during stress. Chronic immobilization did not modify hypothalamic beta-endorphin, while an increase in pituitary beta-endorphin secretion was observed. Since we cannot exclude that changes in beta-endorphin secreted by the pituitary or other opioids may play some role in the stress-induced decrease in LHRH secretion, the effect of naltrexone administration on plasma gonadotropin was studied in chronically stressed rats. Naltrexone treatment did not modify the decrease in plasma concentrations of LH or FSH. These findings suggest that the inhibitory effect of restraint on the testicular axis is exerted at hypothalamic level by some mechanism other than opioids.

Adrenal Glands↗
PubMed1989

Seasonal changes in plasma testosterone concentrations in response to administration of hCG in a desert rodent, the sand rat (Psammomys obesus).

In adult male sand rats inhabiting the Béni-Abbès area (Algeria), testicular endocrine activity increased in early summer (June-July), was highest in autumn-winter and decreased throughout spring. Testosterone secretion by the testis of the sand rat was stimulated (by 10-60-fold) throughout the year by exogenously administered hCG (25 i.u.). However, the response exhibited annual changes mainly characterized by a marked increase in early summer (June-July); the response to hCG was depressed in autumn and became minimal in winter and in early spring. The results strongly suggest that the summer onset of testicular endocrine activity is, at least in part, due to an increase in the testis sensitivity to LH.

Animals↗
PubMed1991

The form and function of the Leydig cells in hypophysectomized rams treated with pituitary extract when spermatogenesis is disrupted by heating the testes.

The morphology and in-vivo function of the Leydig cells were studied in rams when spermatogenesis had been disrupted by a single exposure of the testes 20 days earlier to a temperature of about 42 degrees C for 45 min. To avoid complications due to changed negative feedback from the testes to the pituitary with consequent changes in the degree of gonadotrophic stimulation, ten of the animals (five heated and five unheated) were surgically hypophysectomized when the testes were heated and then treated twice daily with pituitary extract. Six intact rams (three heated and three unheated) were also studied. The heat-affected testes were about half the size of the unheated testes, and blood plasma flow was closely related to testis weight. There were no differences in the testosterone concentrations in spermatic venous blood, testicular lymph or rete testis fluid, or in oestradiol in spermatic venous plasma from heated or unheated testes. Consequently, testosterone secretion by the heat-affected testes was markedly reduced, and the concentrations in jugular blood were also lower in the heat-affected rams than in controls. The volume of the interstitial tissue was less in absolute terms in the heat-affected rams, but it made up a greater fraction of the testes. The absolute volume of the blood plus lymph vessels, and their fraction of the interstitial tissue were lower in the heat-affected testes, although there was no effect on their volume as a fraction of the whole testis. The heat-affected testes of the hormone-treated rams had fewer Leydig cells, but each cell was larger; no equivalent difference was found in the intact rams. However, the dose of pituitary extract chosen was somewhat excessive, as there were higher than normal concentrations of FSH, LH and testosterone in jugular blood plasma, of testosterone and oestradiol in testicular venous blood plasma and of testosterone in rete testis fluid in the hormone-treated hypophysectomized rams. The testes of the unheated hypophysectomized rams increased in size by about 20% during treatment with pituitary extract, although testicular blood plasma flow was lower per unit weight of testis. The absolute volume of each Leydig cell and the total volume in absolute terms and as a fraction of the interstitial tissue was greater in the hormone-treated than in the untreated rams, but not the volume as a fraction of the whole testis. The total number of Leydig cells was higher in the hormone-treated unheated rams than in all the other rams taken together.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1998

Time-course effects of human recombinant luteinizing hormone on porcine Leydig cell specific differentiated functions.

Since recombinant hormones are considered as safer and more reliable in their bioactivity than extractive hormones, the recently available human recombinant luteinizing hormone (r-hLH), will probably replace hCG in the near future, for clinical purposes. This prompted us to investigate whether or not, and by which mechanisms, r-hLH can induce a desensitization of signal transduction and/or an up-regulation of steroidogenic capacity in Leydig cells. The effects of a 30 min to 24 h exposure to r-hLH (10(-9) M) on the differentiated functions of cultured immature porcine Leydig cells were studied by measuring the following parameters: LH/hCG receptor number and mRNA, hCG-, cholera toxin- and forskolin-induced cAMP production, G protein alphas subunit content of the membrane, hCG-, cholera toxin-, forskolin-, 8Br-cAMP-, 22R-OH-cholesterol-, progesterone-, 170H-progesterone-, DHEA-, delta4-androstenedione-induced testosterone secretion and StAR, 3beta-HSD, cytochrome P-450scc and P-450c17 mRNAs. hCG binding sites and LH/hCG receptor mRNA were slowly down regulated by r-hLH, reaching 47+/-1 and 18+/-7% of control at 24 h, respectively. Down-regulation of both hCG- and cholera toxin-induced cAMP production occurred earlier and was more marked, and at 24 h represented only 2.7+/-0.5 and 12.5+/-3.6% of control. Due to the synergistic effect of r-hLH and forskolin on cAMP production, the forskolin-induced cAMP was higher in r-hLH treated than in control cells, but this response also declines with time and was, at 24 h, only 32% of that observed at 30 min. This decreased cAMP production was associated with a less marked decline in the amount of membrane content of Galphas protein. The testosterone production in response to hCG, cholera toxin, forskolin and 8Br-cAMP declined to reach a nadir at 6 h but increased thereafter and at 24 h was significantly higher than in control cells. In contrast, the conversion of several precursors into testosterone remained stable or increased slightly during the first hours of r-hLH treatment and significantly increased at 24 h and this was associated with an increase of StAR, 3beta-HSD, P-450scc and P-450c17 mRNAs. Taken together, the present results indicate that, despite the marked down-regulation of transmembrane signaling, r-hLH increased the steroidogenic capacity of Leydig cells by increasing the expression of several genes encoding the proteins involved in testosterone synthesis.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1991

Antide (Nal-Lys GnRH antagonist) suppression of pituitary-testicular function and sexual behavior in group-living rhesus monkeys.

The ability of a Nal-Lys gonadotropin releasing-hormone antagonist (Antide) to suppress pituitary-testicular function and male sexual behavior was studied in seven group-living adult male rhesus monkeys. Each male received a single 15 mg/kg b.wt. subcutaneous injection of Antide dissolved in equal volumes of propylene glycol and sterile water. Prior to Antide treatment, and at two, four, and eight weeks after Antide, males received an IV bolus of GnRH (50 ng/kg) to assess pituitary and testicular function. For four weeks before and eight weeks after Antide treatment, blood samples and behavioral observations were collected three times weekly in a 74-member heterosexual group. Antide levels increased to more than 150 ng/ml 24 h postinjection and remained above 15 ng/ml for 30 days postinjection. Circulating LH and T were significantly reduced within 24 h following Antide, and remained significantly lower than pretreatment levels in all males for 5 weeks after Antide. T levels rose above 1 ng/ml while Antide levels were still significantly elevated in four males. Both LH and T returned to pretreatment levels by seven weeks post-Antide and then showed a second significant decrease during the eighth study week. Pituitary responsiveness to exogenous GnRH was reduced by Antide and remained below pretreatment levels eight weeks after Antide treatment. Testosterone secretion in response to exogenous GnRH was significantly reduced at two and four weeks post-Antide, but was at pretreatment levels by eight weeks after Antide. Male sexual behavior declined significantly within one week after Antide treatment, almost ceased completely by four weeks after Antide, and returned to pretreatment levels by seven weeks post-Antide.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1977

An investigation into gonadal dysfunction in patients with idiopathic haemochromatosis.

Endocrine studies were performed on twelve patients with proven idiopathic haemochromatosis. Basal gonadotrophin levels and/or their responses to LH releasing hormone (LHRH) were low in nine patients, all of whom showed low plasma testosterone levels and clinical evidence of hypogonadism. Those patients with normal gonadotrophin responses had higher testosterone values, suggesting that the poor testosterone secretion was primarily due to inadequate trophic stimulation. No patient showed hypothyroidism of hypothalamic-pituitary origin, while the cortisol response to hypoglycaemia was normal in all six patients studied. GH responses were more variable and difficult to interpret, since the number of the patients studied was small and the degree of hypoglycaemia after insulin was unpredictable.

Adult↗
PubMed1989

Long-term reproductive cycles in rams after pinealectomy or superior cervical ganglionectomy.

Long-term cycles in diameter of the testes, colouration of the sexual skin and plasma concentrations of testosterone, FSH and prolactin were monitored in groups of pinealectomized (PINX), superior cervical ganglionectomized (SCGX), and control Soay rams living near Edinburgh (56 degrees N). In Exp. 1, PINX, SCGX and control rams were kept outside for 4 years, and well defined seasonal cycles in each of the reproductive parameters were evident in all 3 groups (e.g. testosterone cycle length assessed by sine-wave analysis: 12.08 +/- 0.17, 12.39 +/- 0.14 and 12.15 +/- 0.10 months for PINX, SCGX and control rams respectively). Qualitative differences, however, were apparent between the groups in the timing and amplitude of the reproductive cycle. The seasonal peak in reproductive function occurred from July to September in the PINX and SCGX rams, some 2 months earlier in the year than in controls, while the amplitude of the cycle was less marked in the PINX and SCGX rams. There were no significant differences between the experimental groups in the seasonal cycle in the plasma concentrations of prolactin. In Exp. 2, SCGX and control rams were kept indoors under an artificial environment with a 32-week light cycle and constant nutrition for 4 years. Compared to the controls, in which the reproductive changes were synchronized to the driving light cycle, the SCGX rams showed poorly defined reproductive cycles of lower amplitude and longer period (e.g. testosterone cycle length: 57.8 +/- 6.1 and 32.1 +/- 0.2 weeks for SCGX and control rams, respectively). There was evidence of a cycle in some of the reproductive parameters in the SCGX rams with a period close to 32 weeks during the second half of the study (e.g. testosterone cycle 32.4 +/- 0.8 weeks), which was taken to indicate social induction from the neighbouring control rams. In two further short-term experiments, SCGX rams showed a decline in testicular activity in response to receiving a restricted diet (60% of controls) and an increase in testosterone secretion in response to exposure to oestrous ewes. The overall results illustrate that PINX and SCGX rams can generate long-term synchronized cycles in pituitary and testicular activity. The animals are apparently unable to respond to changes in daylength due to the loss of the functional pineal gland but they remain competent to respond to other environmental cues such as changes in nutrition, temperature and social factors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

Ghrelin: novel regulator of gonadal function.

Ghrelin, the endogenous ligand of the GH secretagogue receptor (GHS-R), has been recently involved in the regulation of a large array of endocrine and non-endocrine functions, including the control of GH secretion, food intake and energy balance. However, despite the proven link between energy homeostasis and fertility, and the clear-cut reproductive effects of other regulators of energy homeostasis and growth, the potential role of ghrelin in the control of gonadal function has so far received little attention. We review herein our recent work on the characterization of the expression and biological actions of ghrelin in rat and human gonads. Expression of ghrelin was demonstrated in mature Leydig cells of rat and human testis, as well as in steroidogenically active luteal and interstitial hilus cells of the ovary. Gonadal expression of the functional ghrelin receptor, the GHS-R type 1a, was also shown in Sertoli and Leydig cells of the testis and in follicular, luteal, surface epithelial and interstitial hilus cells of the ovary. In terms of function, ghrelin inhibited in a dose-dependent manner, stimulated testicular testosterone secretion in vitro and modulated Leydig cell proliferation in vivo as well as the expression of relevant testicular genes, such as that encoding stem cell factor. Additional reproductive effects of ghrelin have been recently substantiated, as ghrelin was able to both suppress LH secretion in vivo and decrease LH responsiveness to GnRH in vitro. Overall, it is proposed that, through systemic and local actions, ghrelin may cooperate with other key regulatory signals, such as leptin, in the integrated control of energy balance and gonadal function.

Animals↗
PubMed1982

Luteinizing hormone in cervical mucus.

The presence of material like luteinizing hormone (LH) in cervical mucus has not been previously reported. In this study, we show that in human cervical mucus there is LH-like material detectable by radioimmunoassay (RIA) and by bioassay. The content of LH in the cervical mucus of five donors was measured by RIA in samples of mucus obtained daily throughout the menstrual cycle. The concentration of LH in mucus obtained during ovulation was lower than in mucus obtained during the early follicular phase or mucus obtained during the luteal phase. This material exhibits LH-like biologic activity because increasing volumes of cervical mucus added to isolated mice Leydig cells stimulates testosterone secretion by these cells, in a parallel dose-related fashion, to increasing quantities of human chorionic gonadotropin (hCG). No immunologic cross-reactivity of the cervical mucus was observed with an antiserum specific for the beta-subunit of hCG. Taken together, the results of the present study suggest the presence of an LH-like substance within the cervical mucus that exhibits both the immunologic and biologic properties of LH.

Animals↗
PubMedDate not supplied

Virilizing adrenal ganglioneuroma containing Leydig cells.

An adrenal medullary ganglioneuroma containing Leydig cells and revealed by a virilizing syndrome in a 56-year old woman is presented. The syndrome, associating with masculinization an elevated serum testosterone level and a normal urinary 17 ketosteroids, is uncommon in adrenal tumours. The tumour was located by computed tomographic (CT) scan and treated by right adrenalectomy. Microscopic examination showed typical features of an adrenal medullary ganglioneuroma containing Leydig cells with Reinke crystalloids. Positive immunohistochemical study confirmed the testosterone secreting nature of the cells. The presence of Leydig cells in the adrenal gland is discussed according embryogenic studies: 1. the common origin of the gonad and the adrenal cortex from the coelomic epithelium, 2. the vicinity of adrenocortical gland and gonad during embryogenesis, 3. the thecal metaplasia of mesenchymal cells, 4. the development of Leydig cells from Schwann cells. Fourth case published in the world literature.

Adrenal Cortex Hormones↗
PubMed1990

Pharmacokinetics and endocrine effects of slow release formulations of LHRH analogues.

The LHRH agonists are antigonadotropic agents for reversible ovarian suppression in gynaecology and in oncology. In oncology, pituitary inhibition is maintained with high release rates preferably by implant or microcapsule injection. The pharmacokinetics of buserelin after injection, infusion, and during implant treatment (controlled release) are described. The release rate is monitored by urinary buserelin excretion (fractional excretion of 30% of the daily dose). During therapy, LHRH agonists in serum are measured by specific radioimmunoassays, with or without extraction. A more convenient non-invasive procedure is to measure the amount of buserelin in 24-h urine samples (during injections or nasal spray), or the urinary buserelin/creatinine ratio in morning urine samples (during infusions or implants). After high dose injection, buserelin has a half-life of 80 min, therapeutic plasma concentrations are maintained for 8-12 h. In long-term maintenance with buserelin implants (polylactide-glycolide, 75:25), serum concentrations and urinary excretion showed an extended plateau phase indicating a suitable dose interval of 2-3 months. In endometriosis and leiomyoma, the minimum release rate (urinary buserelin) required for maintenance of steroid suppression was established (buserelin excretion of about 0.5 microgram/g creatinine). Buserelin implants in prostate carcinoma are effective for 2 or 3 months, after a single dose of 6.6 or 10 mg buserelin, respectively. A consistent suppression of serum testosterone secretion was confirmed for more than 2 yr. Buserelin microparticles are effective in rhesus monkeys to completely suppress follicular maturation and oestrogen secretion during 4-6 weeks after a single dose of 3.6 mg buserelin. Recent results on the controlled release of an LHRH antagonist (Hoe 013) from biodegradable microparticles in rats with DMBA-induced mammary tumours indicate that tumour suppression by LHRH antagonists is well tolerated and highly effective. The local tolerance at the injection site of antagonist microparticles is excellent as in the case of LHRH agonists like buserelin.

Animals↗
PubMed1985

Hyperprolactinemia inhibits development of Leydig cell tumors in aging Fischer rats.

In inbred CDF (Fischer 344) male rats autopsied at the age of 18-24 months, testicular tumors were present in 24 of 36 control animals but in none of 28 males rendered hyperprolactinemic by transplantation of anterior pituitaries from adult females under the renal capsules. In another experiment, microscopically detectable Leydig cell adenomas were present in each of 11 control animals at the age of 14.5 months but in none of 11 males in which hyperprolactinemia was induced by treatment with diethylstilbestrol. Development of testicular tumors had initially little effect on basal and hCG-stimulated plasma testosterone and androstenedione levels but eventually led to atrophy of the seminal vesicles. Incubated tumor tissue produced large quantities of progesterone and responded to hCG in vitro by an increase in progesterone but not testosterone secretion. Daily sperm production and epididymal sperm reserves were significantly reduced already during early stages of Leydig cell tumor development. We propose that hyperprolactin prevents development of Leydig cell tumors by suppression of plasma LH levels and suggest that age-related reductions in gametogenic and steroidogenic functions of the testes in Fischer rats are due to development of Leydig cell tumors rather than to aging per se.

Age Factors↗
PubMed1991

Regulation of testicular P-450 cholesterol side-chain cleavage and P-450 C17-20 lyase/C17 hydroxylase enzymes in the neonatal and adult rat.

Adult Leydig cells respond to LH or hCG with an initial stimulation of testosterone secretion followed by LH receptor down-regulation and blockade of androgen biosynthesis. In contrast, fetal Leydig cells respond with increased LH receptor number and enhanced steroidogenesis. In this study, the molecular mechanisms of high-dose hCG treatment on steroidogenesis in adult and neonatal testes (containing predominantly the fetal generation of Leydig cells) were examined using two recombinant DNA clones specific for enzymes of the rat steroidogenic pathway (P-450 cholesterol side-chain cleavage enzyme, P-450scc and P-450 17 alpha-hydroxylase/C17-20 lyase, P-450c17). We treated adult (60 days of age) and neonatal (2 days of age) rats with a single high dose of hCG (600 IU/kg), sc. The high dose of hCG caused neonatal testicular P450scc and P450c17 mRNA levels to increase, and stimulated adult testicular P450scc mRNA levels, but caused a decrease in adult P450c17 mRNA levels. These studies suggest that high doses of hCG regulate testosterone production differently in adult and fetal Leydig cells at a pretranslational level of the P450c17 enzyme, while mRNA for P450scc is stimulated in both the adult and fetal Leydig cell.

Aging↗
PubMed1995

Erythropoietin and testicular steroidogenesis: the role of second messengers.

It has been demonstrated that erythropoietin (EPO) influences rat and human Leydig cell steroidogenesis, stimulating testosterone production through a direct and specific receptor-mediated mechanism. The aim of this study was to investigate the mechanism by which recombinant human erythropoietin (rHuEPO) exerts its stimulatory effect on rat Leydig cells. Recombinant human EPO did not induce, at any dose tested (10(-10) to 10(-13) mol/l), an increase in either cAMP or cGMP, suggesting that in Leydig cells the effect of rHuEPO does not involve the adenylate or guanylate-cyclase systems. The role of transmembrane calcium flux in rHuEPO-stimulated steroidogenesis was studied by evaluating the effect of calcium channel blocker, verapamil, and by the 45Ca2+ uptake method. Verapamil did not influence rHuEPO-induced testosterone secretion and rHuEPO did not modify calcium recycling, indicating that calcium transmembrane flux is not involved in the rHuEPO effect. The protein kinase C inhibitor staurosporine (10, 30, 100 and 300 nmol/l) inhibited rHuEPO-stimulated testicular steroidogenesis in a dose-dependent manner. This indirect evidence suggests that the stimulatory effect of rHuEPO on rat Leydig cells may involve protein kinase C activation.

Alkaloids↗
PubMed1998

Treatment of men with paraphilia with a long-acting analogue of gonadotropin-releasing hormone.

BACKGROUND: Men with deviant sexual behavior, or paraphilia, are usually treated with psychotherapy, antidepressant drugs, progestins, and antiandrogens, but these treatments are often ineffective. Selective inhibition of pituitary-gonadal function with a long-acting agonist analogue of gonadotropin-releasing hormone may abolish the deviant sexual behavior by reducing testosterone secretion. METHODS: In an uncontrolled observational study, we treated 30 men (mean age, 32 years) with severe long-standing paraphilia (25 with pedophilia and 5 with other types of abnormal behavior) with monthly injections of 3.75 mg of triptorelin and supportive psychotherapy for 8 to 42 months. The efficacy of therapy was evaluated monthly by the Intensity of Sexual Desire and Symptoms Scale and yearly by the Three Main Complaints questionnaire. RESULTS: All the men had a decrease in the number of deviant sexual fantasies and desires, from a mean (+/-SD) of 48+/-10 per week before therapy to zero during therapy (P<0.001), and a decrease in the number of incidents of abnormal sexual behavior (from 5+/-2 per month to zero, P<0.001) while receiving triptorelin. These effects were evident after 3 to 10 months of therapy (P<0.001) and persisted in all 24 men who continued therapy for at least 1 year. The men's mean serum testosterone concentration fell from 545+/-196 ng per deciliter (18.9+/-6.8 nmol per liter) before therapy to 23+/-14 ng per deciliter (0.8+/-0.5 nmol per liter, P<0.001) after 42 months of triptorelin. The main side effects were erectile failure, hot flashes, and decrease in bone mineral density in some men. CONCLUSIONS: Continuous administration of triptorelin, a long-acting agonist analogue of gonadotropin-releasing hormone, together with supportive psychotherapy, may be an effective treatment for men with severe paraphilia.

Adult↗
PubMed1988

Hypothalamic-pituitary gonadal axis in boys with primary hypothyroidism and macroorchidism.

Nine of 15 boys with severe long-standing primary hypothyroidism were found to have macroorchidism. All 15 patients had elevated thyroid-stimulating hormone levels. However, only those patients with testicular enlargement had striking elevations of serum prolactin and gonadotropin values. The response to gonadotropin-releasing hormone in our patients was blunted, in contradistinction to that of children with true precocious puberty. In spite of the elevated levels of luteinizing hormone, the serum testosterone levels were in the prepubertal range, explaining the lack of peripheral manifestations of androgenic effect. Improvement of testosterone secretion followed decreasing prolactin levels with bromocriptine administration, suggesting an inhibitory effect of prolactin on luteinizing hormone action at the Leydig cell. We conclude that testicular enlargement is the result of continuous follicle-stimulating hormone stimulation and that the term "true precocious puberty" is not appropriate in children with hypothyroidism and macroorchidism unless the hypothalamic-pituitary gonadal axis is shown to be at the pubertal stage.

Adolescent↗
PubMed1987

Annual cycle of liveweight and reproductive changes of farmed male fallow deer (Dama dama) and the effect of daily oral administration of melatonin in summer on the attainment of seasonal fertility.

Entire bucks (N = 7) exhibited pronounced liveweight gains over spring and summer months (October-February), to reach a peak mean weight of 59.8 kg, and rapid liveweight losses over the rutting period (April-May) with a minimum mean liveweight of 54.2 kg. Mean neck girth and serum testosterone levels increased during late summer (January-March) and peaked at 387 mm and 12 ng/ml respectively immediately before the onset of the rut (April). Thereafter both measures declined during winter and spring months (June-December). Bucks castrated prepubertally (N = 11) exhibited similar but less pronounced changes in mean liveweight and neck girth, in the absence of any change in testosterone secretion. Peak mean testicular diameter of entire bucks (39 mm) occurred immediately before the rut and was followed by testicular regression over winter and spring months (June-November), such that the testes attained their minimum mean size of 18 mm diameter in early summer (November). Motile spermatozoa were absent from ejaculates collected in summer (November 1983, 1984; January 1984). However, ejaculates collected pre-rut (late March), immediately post-rut (June) and in early spring (September) contained successively increasing numbers of motile spermatozoa. A further 14 polled, entire bucks were given orally 5 mg (N = 7; Group A) or 20 mg (N = 7; Group B) melatonin at 15:30 h daily from 1 December 1983 to 14 January 1984 (45 days). Seven control bucks (Group C) received vehicle ration only. The measurements taken for bucks in Groups A and B were not significantly different (P greater than 0.1) on any sampling date and the data for these 2 groups were pooled. Mean serum testosterone concentrations and mean ejaculate volume were not significantly different between melatonin-treated and control bucks on any sampling date, although other measures exhibited significant differences (P less than 0.05) at various treatment or post-treatment dates: melatonin-treated bucks showed a transiently greater increase in neck muscle development during and immediately after treatment, a slight retardation of liveweight gain between 45 and 75 days after treatment, an earlier peak in maximum mean testicular diameter and an earlier onset of sperm presence in ejaculates.

Animals↗