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PubMed2001

Luteinizing hormone-dependent activity and luteinizing hormone-independent differentiation of rat fetal Leydig cells.

Addition of 5x10(-2) U/ml recombinant luteinizing hormone (LH) to testes from fetuses at 16.5 day post conception (dpc) cultured for 5 days increased the number of Leydig cells by 34% and the acute LH-stimulated testosterone production by 600%. To determine whether these positive effects of LH in vitro are physiologically relevant in vivo, fetuses were decapitated on days 16.5 pc (before the onset of LH expression in the hypophysis) or 18.5 pc (before the surge of LH in the fetal plasma) and removed at 21.5 dpc. The number of fetal Leydig cells per testis and the acute LH-stimulated testosterone production by the testes ex vivo were unaltered by decapitation. Since, in all groups, the number of Leydig cells doubled between 16.5 and 18.5 dpc and between 18.5 and 21.5 dpc, these results suggest that neither the appearance of new fully differentiated fetal Leydig cells nor the maintenance of differentiated functions in existing fetal Leydig cells depend on LH during late fetal life, although this hormone is present in the plasma. Decapitation reduced the testosterone concentrations in the plasma (-56%) and in the testis in vivo (-67%) and the basal testosterone secretion of the testis ex vivo (-70%). This suggests that LH is required to maintain the physiological activity of the Leydig cell during late fetal life. However, the decrease of the in vivo testosterone production after decapitation was not sufficient to impair the growth of the Wolffian ducts and the lengthening of the anogenital distance. In conclusion, during late fetal life in the rat, Leydig cells are LH-independent for their functional differentiation and LH-dependent for their activity.

Animals↗
PubMedDate not supplied

Epididymal sperm motion as a parameter of male reproductive toxicity: sperm motion, fertility, and histopathology in ethinylestradiol-treated rats.

The present study was designed to characterize the effect of ethinylestradiol (EE) on epididymal sperm motion using a computer-assisted sperm analysis system (CASA), and to elucidate the correlation between sperm motion endpoints and other measures including fertility, histopathologic, and endocrinologic endpoints. EE was orally given to adult male rats at a daily dosage of 10 mg/kg for 3 and 5 d, and at daily dosages of I and 10 mg/kg for 1, 2, 3, and 4 weeks. Changes in sperm motion were first detected after one week of treatment. Of nine sperm motion parameters, the percentage of motile sperm, velocity, and amplitude of the lateral head displacement (ALH) were decreased in the 10 mg/kg dosing group. Accompanying the decreases in those parameters, the male fertility indices in the 10 mg/kg dosing group were reduced after one week of treatment, and no males in this group could impregnate intact females after 2 weeks or more of treatment. The number of sperm heads in the cauda epididymis in the 10 mg/kg dosing group was reduced to about one-half that in the control group after one week of treatment, whereas the total number of homogenization-resistant advanced spermatids in the testis was not altered and only a slight change was detected in the number and morphology of germ cells in the testis. These results suggest that reduction in the number of epididymal sperm and in sperm motion are not secondary to testicular alteration. However, after 3 weeks of treatment, the number of sperm heads in the testis was drastically reduced with severe atrophy of the seminiferous tubules both in the 1 and 10 mg/kg dosing groups. The profiling of epididymal luminal fluid proteins indicated that two major bands that migrated with molecular weights of about 22 and 23 kDa were weakened and their density was reduced to approximately 70% of the control after 5-d and one week treatments in the 10 mg/kg dosing group. Circulating testosterone declined drastically after 3 d of treatment and remained at undetectable levels with a concomitant decline of circulating LH and FSH, suggesting that EE inhibits testosterone secretion immediately via a negative feedback system, and there follow changes in the accessory reproductive organs including the epididymis. These results indicate that EE affects epididymal spermatozoa before testicular germ cells via a testosterone deficiency, when it is administered at extremely high dosages. The reduction in the sperm motion manifested as decreases in the percentage of motile sperm, ALH, and velocity, is considered to be responsible for the onset of infertility. Sperm motion analysis could be particularly useful for detecting the toxic effects of chemicals that act through the endocrinologic system on the epididymis.

Animals↗
PubMed1988

Treatment with bovine follicular fluid suppresses follicular development in gonadotrophin-releasing hormone-treated anoestrous ewes.

The role of FSH in gonadotrophin-releasing hormone (GnRH)-induced follicular development in anoestrous ewes was investigated using injections of bovine follicular fluid (bFF) to reduce plasma FSH levels. Groups of five animals were treated for 12 h with GnRH (250 ng at 2-h intervals) alone, GnRH plus bFF or saline alone, or for 36 h with GnRH alone, GnRH plus bFF or bFF alone. The administration of bFF (1.5 ml s.c. at 8-h intervals) significantly (P less than 0.05) reduced mean plasma FSH levels, but with the exception of animals treated with bFF alone, had no effect on LH levels. Treatment with bFF alone for 36 h resulted in a significant (P less than 0.05) increase in LH concentrations. There was considerable variation in the number of follicles greater than or equal to 2 mm in diameter in the treatment groups. The mean diameter, oestradiol secretion and number of 'oestrogenic' follicles were significantly (P less than 0.01) reduced in ewes treated with GnRH plus bFF or bFF alone for 36 h compared with those treated with GnRH alone. Testosterone secretion by the follicles was not affected by treatment. These results confirm previous findings that treatment with bFF decreases circulating FSH levels in anoestrous ewes and, moreover, that concurrent administration of bFF and GnRH inhibits the follicular maturation that is induced by treatment with GnRH alone, suggesting that FSH as well as LH is required for follicular maturation in the ewe.

Anestrus↗
PubMed1995

[Toxicity of vanadium to Leydig cells in vitro].

The levels of testosterone secreted by rat's Leydig cells in varied concentrations of V2O5 (0.125, 0.,25, 0.5, 2 and 3 mmol/L) were assayed. The result showed there was no obvious relation between the level of testosterone and the concentration of V2O5. This in vitro study in accord with the result of whole animal research indicates that Leydig cell is not the target of V2O5.

Animals↗
PubMedDate not supplied

[The effect of testosterone on the secretion of prolactin].

For 21 days, nine male monkeys received daily doses, 8 mg of testosterone propionate dissolved in almond oil. After an initial period of 6 days, a control period was observed during which only the almond oil was administered. Each injection was preceded by the taking of a 10 ml blood sample. The prolactin and steroids (testosterone and oestradiol) were measured by radioimmunoassay. For both groups of animals the prolactin serum count increase significantly after 10 days of treatment. This modest increase (approximately 50% a base count) is more systematic among the immature subject than among the mature ones. The oestradiol serum count increased among the same animals on day + 2 and remained at a noticeably high level from day + 2 to day + 20. These results suggest a stimulatory effect of testosterone on the secretion of prolactin due to the conversion of androgen to oestradiol. However a mild testosterone action directly on lactotropic cells is not to be discounted.

Animals↗
PubMed1988

The effects of reduced O2 and antioxidants on steroidogenic capacity of cultured rat Leydig cells.

We have examined the effects of reduced O2 tension and the antioxidant dimethylsulfoxide (DMSO) to determine if O2-derived free radicals are the cause of decreased steroidogenic capacity (testosterone and progesterone production) of cultured rat Leydig cells. Rat Leydig cells were initially cultured under standard conditions of 5% CO2, 95% air (19% O2) with or without DMSO. Addition of DMSO resulted in increased basal testosterone production on days 2, 3 and 4 of culture. hCG (10 mIU)-stimulated testosterone secretion was 2-3 times greater on days 2 and 3 in the presence of DMSO. Lowering the O2 concentration to 5% in the presence of DMSO resulted in even greater hCG-stimulated testosterone production on days 1 to 3. However, the effect of DMSO or low O2 and DMSO were not seen after 5 days. The reduced O2 concentration resulted in an increase in hCG (10 mIU)-stimulated progesterone synthesis throughout the culture, particularly on days 4 to 8. Also, when total steroid (progesterone and testosterone) was determined, cells cultured under reduced O2 conditions responded with increased steroid production on days 1 to 8 in comparison to controls (19% O2). These results demonstrate that lowered O2 concentration and DMSO provide a protective effect resulting in the maintenance of testosterone production and an increase in progesterone synthesis. These findings suggest that free radical-mediated damage of enzymes may result in decreased steroidogenic capacity of cultured Leydig cells.

Animals↗
PubMed1989

Corticotropin-releasing factor receptors and actions in rat Leydig cells.

Rat Leydig cells possess functional high affinity receptors for corticotropin-releasing factor (CRF). CRF inhibited human chorionic gonadotropin (hCG)-induced androgen production in cultured fetal and adult Leydig cells in a dose-dependent manner, but it had no effect on basal testosterone secretion. Comparable inhibitory effects of CRF were observed in the presence or absence of 3-isobutyl-1-methylxanthine. CRF treatment caused a marked reduction of steroid precursors of the androgen pathway (from pregnenolone to testosterone) during gonadotropin stimulation, but it did not influence their basal levels. The inhibitory action of CRF on hCG-induced steroidogenesis was fully reversed by 8-bromo-cAMP but was not affected by pertussis toxin. The action of CRF was rapid; and it was blocked by coincubation with anti-CRF antibody. CRF caused no changes in hCG binding to Leydig cells, and in contrast to other target tissues, CRF did not stimulate cAMP production, indicating that CRF receptors are not coupled to Gs in Leydig cells. These studies have demonstrated that CRF-induced inhibition of the acute steroidogenic action of hCG is exerted at sites related to receptor/cyclase coupling or cAMP formation. The inhibitory effects of CRF in the Leydig cell do not occur through the Gi unit of adenylate cyclase, but could involve pertussis toxin-insensitive G protein(s). These observations demonstrate that CRF has a novel and potent antireproductive effect at the testicular level. Since CRF is synthesized in the testis and is present in Leydig cells, it is likely that locally produced CRF could exert negative autocrine modulation on the stimulatory action of luteinizing hormone on Leydig cell function.

1-Methyl-3-isobutylxanthine↗
PubMed1996

Quantitative microscopic changes in the mole rat's accessory sex organs during an annual cycle.

BACKGROUND: The mole rat, Spalax ehrenbergi, is a solitary, aggressive subterranean rodent. The present study summarizes a year-round investigation of morphological changes in the mole rat's accessory sex organs. METHODS: Mole rats maintained in the laboratory were killed after 3 months of acclimation; additional animals trapped in the wild were killed immediately. The accessory sex organs were processed for routine histological examination. Tissues were fixed in Bouin's solution, embedded in paraffin blocks, and stained by hematoxylin-eosin. A systemic sampling approach was used to photomicrograph the tissues for histomorphometric assessment. RESULTS: The volume fraction (Vv, mean +/- SEM) of prostate connective tissue from animals kept in captivity increased significantly in January (0.49 +/- 0.05 mm3/mm3) and April (0.43 +/- 0.04 mm3/mm3) but only 0.26 +/- 0.03 mm3/mm3 in November. In the field group, the Vv of prostate connective tissue was significantly higher in January (0.58 +/- 0.08 mm3/mm3) and April (0.62 +/- 0.08 mm3/mm3) and lower in November (0.44 +/- 0.03 mm3/mm3) and February (0.43 +/- 0.03 mm3/mm3), with a concomitant decrease in prostate tubuli and lumen. The prostate tubuli star volume (v*) in laboratory animals increased in November (0.009 +/- 0.002 mm3) and May (0.09 +/- 0.02 mm3). The same pattern was shown in the field group, with a significant increase in December (0.012 +/- 0.002 mm3) and March (0.007 +/- 0.001 mm3). The Cowper tubuli Vv in the captive animals increased during February (0.24 +/- 0.02 mm3/mm3), with a concomitant reduction in the connective tissue (0.05 +/- 0.02 mm3/mm3). The Cowper tubuli v* in same animals increased in December, April, and July (1.37 +/- 0.18 x 10(-4) mm3, 0.94 +/- 0.10 x 10(-4) mm3, 1.52 +/- 0.20 x 10(-4) mm3, respectively). In field group, a slight decrease in star volume took place from November to May (1.25 +/- 0.16 mm3 to 0.39 +/- 0.05 mm3, respectively). Testosterone levels appeared to be higher in the field group than in the laboratory group. In December the values were 1.62 +/- 0.15 ng/ml in the field group and 0.55 +/- 0.12 ng/ml in the laboratory group, and in May the laboratory group values were 1.66 +/- 0.12 ng/ml. CONCLUSIONS: In captivity and in the field, male mole rats probably undergo an annual cycle of accessory gland tissue structural changes that are correlated with testosterone secretion.

Animals↗
PubMed1976

Effect of sexual maturation and androgens on prostaglandin levels in tissues of the male reproductive system in mice.

Prostaglandins E and F were measured in the testis, epididymis, vas deferens, and seminal vesicles of CD-1 mice from 2 to 8 weeks of age. The concentration of PGF was higher than that of PGE in all organs studied, except for the vas deferens. The concentration of prostaglandins (PGs) was age-dependent, showing a progressive decline from immaturity to adulthood. However, in the testis, there was an apparent transient increase in the concentration of PGs in the seminal vesicle changed very little between the ages of 5 and 8 weeks. The vas deferens had a significantly higher PG concentration than any of the organs studied, and a unique pattern of changes in the levels of PGE and PGF with age. In the vas deferens of two- and three-week-old mice, the concentration of PGF was higher than the concentration of PGE, but after 4 weeks of age PGE became somewhat more abundant than PGF. Treatment of immature mice with testosterone propionate (TP) produced significant changes in PG concentrations, resulting in PG levels resembling those of adult animals. The treatment also changed the ratio of PGE to PGF in the vas deferens (from 1:2 to 1:1). Hereditary dwarf mice had higher levels of PGs in the tissues of the male reproductive system than did their normal littermates. The treatment of dwarf mice with TP generally reduced the concentration of PGs in their reproductive system and resulted in a PG pattern more characteristic of normal adult males of the same strain. The data demonstrate pronounced changes in PG levels in the tissues of the male reporductive system of mice during sexual maturation. From the present study and from previous findings, it can be concluded that these changes can be accounted for by an increase in testicular testosterone secretion.

Age Factors↗
PubMedDate not supplied

Integration of new regulatory strategies into the network of an endocrine control system: limitation of androgen secretion by rat testis is achieved by substrate-dependent modulation of P450XVII enzyme concentration and catalytic efficiency.

In addition to the well-known control circuits involved in the regulation and adaptation of testicular androgen biosynthesis, it is proposed that two new control strategies are involved in the maintenance of steady-state testosterone secretion rates by testicular Leydig cells. Cytochrome P450XVII (steroid-17 alpha-monooxygenase/steroid-17,20-lyase), one key enzyme in steroid hormone biosynthesis, responds to external human choriogonadotropin stimulation with an oxygen-dependent and substrate flux-dependent inactivation and decomposition, and increased substrate availability decreases the efficiency of androgen formation in favour of abortive intermediate leakage. These results are discussed as a paradigm of substrate-dependent modulation of cytochrome P450 activities.

Aldehyde-Lyases↗
PubMed1998

Dispersal status influences hormones and behavior in the male spotted hyena.

Male spotted hyenas (Crocuta crocuta) reach puberty at 24 months of age and then invariably emigrate from their natal clans 1 to 38 months later. Thus there are two classes of reproductively mature males in every Crocuta clan: adult natal males born in the clan and adult immigrant males born elsewhere. In one free-living hyena population in Kenya, these two groups of males were compared with respect to measures of aggression, social dominance, sexual behavior, and circulating hormone levels. Adult natal males engaged in higher hourly rates of aggression than did immigrants, won all fights with immigrants, and were socially dominant to immigrants. In addition, adult natal males engaged in far lower hourly rates of sexual behavior with resident females than did immigrants, and natal males were never observed to copulate with natal females. Mean basal plasma cortisol values did not differ between the two groups of adult males, but cortisol concentrations in immigrants were positively correlated with tenure in the clan and with immigrant male social rank. Adult natal males had plasma testosterone levels significantly lower than those of immigrants. Social rank and plasma testosterone values were positively correlated among immigrant males. Thus two different relationships appear to exist between circulating testosterone and social rank in male Crocuta: one apparent in immigrants and the other in natal adult males. Our results suggest that dispersal might disinhibit testosterone secretion in postpubertal male hyenas.

Aggression↗
PubMed1997

In vitro effects of Celiptium and MR 14504 on mature rat Leydig cell testosterone production.

Percoll-purified mature rat Leydig cells have been used to evaluate the testicular toxicity of two highly potent intercalating agents (Celiptium and MR 14505). Testosterone secretion in the absence and in the presence of human chorionic gonadotropin (hCG) was measured to assess Leydig cell function. Celiptium and MR 14504 induce time- and dose-related inhibitory effects on the production of testosterone by Leydig cells, both in the presence and in the absence of hCG, whatever the concentration of hCG used. We have observed that MR 14504 is about 5 times more potent as an inhibitor of rat Leydig cell steroidogenesis than Celiptium without inducing any cell toxicity. The present study indicates that the Leydig cell is an additional potential site for the primary toxic effects of these drugs in the adult rat testis.

Animals↗
PubMed1979

Hyperprolactinaemia and hypogonadism in men: response to exogenous gonadotrophins.

Three male patients with pituitary tumours and marked hyperprolactinaemia were investigated. Their prolactin (PRL) levels ranged from 210 to 2500 ng/ml. The subjects had clinical and laboratory characteristics of hypogonadotrophic hypogonadism. All were treated with human chorionic gonadotrophin (HCG) and in one subject human menopausal gonadotrophin (HMG) was given in addition. In all three patients, despite the persistence of hyperprolactinaemia, serum testosterone had risen to normal levels within 4--17 days after starting HCG. Despite the normal testosterone level, impotence persisted in two patients and the third had persistently decreased libido. The hypogonadism in these patients may be related to an absolute reduction in gonadotroph number secondary to destruction by tumour mass. Alternatively, hyperprolactinaemia may inhibit the synthesis or release of the gonadotrophins or LHRH. Despite hyperprolactinaemia, pharmacological doses of HCG induced testosterone secretion in all these three subjects.

Adult↗
PubMed1992

Effect of decapitation and chronic in-vivo treatment with a gonadotrophin-releasing hormone agonist on testicular steroidogenesis in the rat fetus.

To study the effect of in-vivo gonadotrophin-releasing hormone (GnRH) treatment on testicular testosterone production during late fetal life in the rat, 18.5-, or 20.5-day-old fetuses were decapitated and injected with either long-acting microcapsules containing the GnRH agonist D-Trp-6-GnRH or vehicle only. Two days later, fetal and maternal plasma was collected and fetal testes were removed and incubated for 6 h in medium with either 100 ng LH/ml or without LH. The GnRH agonist concentrations in the plasma of GnRH-treated decapitated male fetuses were comparable in the two age-related groups (5 nmol/l). After treatment of the fetus with D-Trp-6-GnRH, the agonist was recovered in maternal plasma, showing that this peptide can cross the fetal-maternal barrier. In 22.5-day-old decapitated vehicle-treated male fetuses, the plasma testosterone level dropped to that observed in control female fetuses, and treatment of decapitated male fetuses with the GnRH agonist did not further reduce it. At both days 20.5 and 22.5, basal in-vitro testosterone secretion by testes from decapitated vehicle-treated fetuses was lower than secretion by testes from intact control fetuses from the same litter, but LH-stimulated secretion was similar in both groups. Both basal and LH-stimulated secretion by testes from GnRH-treated decapitated fetuses was lower than secretion by testes from vehicle-treated decapitated fetuses and larger reductions were measured on day 22.5 than on day 20.5 (-48 vs -18% for basal secretion, and -76 vs -40% for LH-stimulated secretion).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Regulation and perturbation of testicular functions by vitamin A.

In addition to playing a fundamental role in very diverse processes such as vision and the growth and differentiation of numerous types of cell, vitamin A (retinol) and its principal biologically active derivative, retinoic acid, are clearly involved in the regulation of testicular functions in rodents. An excess of vitamin A leads to testicular lesions and spermatogenetic disorders, and a deficiency induces early cessation of spermatogenesis and adversely affects testosterone secretion. Furthermore, mice mutant for retinoic acid alpha receptors and retinoid X beta receptors are sterile. Retinoids appear to exert an action on the three main testicular types of cell (Sertoli, germinal and Leydig cells), as they act on the signalling pathways and Sertoli cell metabolism, and modify numerous factors secreted in Sertoli cells. Retinoids also appear to be necessary for the proliferation and differentiation of A spermatogonia, and for spermiogenesis. In addition, vitamin A deficiency leads to atrophy of the accessory sex organs after decreased testosterone production. Recent studies have shown that retinoids already affect these three types of cell in fetuses. Curiously, the effects of retinoids on fetal and adult testis seem opposed.

Animals↗
PubMed1986

[Changes in sexual functioning in the male rat after total or anterior deafferentation of the mediobasal hypothalamus].

After complete deafferentation of the mediobasal hypothalamus in male rats, the luteinizing hormone content increased in the blood which correlated with an increasing of testosterone secretion, weight of seminal glands and additional sexual organs. Half of the operated animals preserve copulating ability. The content of folliculo-stimulating hormone in the blood of animals after the complete deafferentation was decreased, particularly in non-copulating males. After the interior deafferentation of the mediobasal hypothalamus in the rats, the luteinizing hormone and testosterone contents in the blood did not change but the weight of seminal glands and concentration of folliculo-stimulating hormone in the blood decreased. The data obtained suggest different mechanisms of control of the luteinizing and folliculo-stimulating hormones secretion in male rats, the connection of the mediobasal hypothalamus with anterior hypothalamus and preoptic area being necessary for normal secretion of the folliculo-stimulating hormone.

Animals↗
PubMed1984

Characteristics of the inhibitory effect of chronic treatment with an LHRH agonist on testicular steroidogenesis in the dog.

Daily subcutaneous administration for 3 months of the potent LHRH agonist (D-Ser(TBU)6, des-Gly-NH2(10] LHRH ethylamide (25 micrograms) to adult dogs having spontaneous benign prostate hyperplasia (BPH) causes a marked inhibition of testicular androstenedione and testosterone secretion. This inhibition of delta 4-androgen secretion is accompanied by a decrease of testicular progestin precursors and 5 alpha-androgen metabolites, thus suggesting that, in dog, the loss of testicular steroidogenic activity, induced by the administration of an LHRH agonist, is due to a total inhibition of testicular steroidogenesis. In plasma, the concentration of both testosterone and dihydrotestosterone is also markedly depressed while androstane-3 alpha, 17 beta-diol levels remain unchanged. Measurement of prostatic steroid content has shown that administration of the LHRH agonist as well as castration is associated with a marked decrease in androstenedione, testosterone, and dihydrotestosterone levels in prostate while there is a small inhibition of androst-5-ene-3 beta, 17 beta-diol, androstane-3 beta, 17 beta-diol, dehydroepiandrosterone, and estrone concentrations in this tissue. The present data show that treatment with an LHRH agonist in the dog causes a marked inhibition of testicular steroid secretion similar to the one observed in adult men, and suggest that steroids from adrenal origin may also be involved in prostatic function.

17-alpha-Hydroxyprogesterone↗
PubMed2000

Corticosterone inhibits normal and FSH-induced testicular recrudescence in the lizard, Mabuya carinata.

Administration (ip) of 1, 10, or 20 microg corticosterone (alternate days for 30 days) to adult male Mabuya carinata did not affect the seasonal recrudescence of spermatogenesis whereas administration of 40 microg corticosterone did result in inhibition of spermatogenesis. Further, administration of FSH (10 IU/lizard/alternate day for 30 days) during the quiescent phase of the testicular cycle stimulated spermatogenetic and steroidogenic activity of the testis as shown by significant increases in the mean number of spermatogonia, spermatocytes, and spermatids and serum levels of testosterone. In addition there were abundant spermatozoa in the lumen of the tubules in FSH-treated lizards. Administration of 10 IU FSH + 40 microg corticosterone (per lizard on alternate days for 30 days) increased the mean number of primary and secondary spermatocytes whereas the mean number of spermatids did not show significant variation compared with that of controls. Further, the mean numbers of spermatocytes and spermatids and serum levels of testosterone were significantly less when compared to those of FSH alone treated lizards. In addition, FSH-induced development of epididymis was also inhibited by corticosterone treatment. The results indicate that corticosterone inhibits FSH-induced testicular recrudescence, possibly by suppressing testosterone secretion in M. carinata.

Animals↗