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PubMed1987

Specific binding and steroidogenetic effects of atrial natriuretic factor (ANF) in Leydig cells of rats.

Atrial natriuretic factors (ANF) may influence testicular steroidogenesis. This study was conducted to evaluate the presence of specific ANF-binding on isolated adult rat Leydig cells and the effects of ANF on testosterone production. Indirect immunofluorescence technique demonstrates that adult rat Leydig cells possess specific ANF-binding and that rAP-II strongly stimulates the testosterone production. rAP-II exerts its maximal stimulatory effect on the testosterone secretion at low doses (10(-11) M), corresponding at the physiological plasmatic concentration in the adult normal rat. High doses (10(-9)-10(-7) M) of rAP-II show a decline in the stimulatory effect on testosterone secretion. Our data suggest that rAP-II influences the testicular steroidogenesis by a receptorial mechanism; the biphasic effect of rAP-II on the testosterone production may be related to an acute receptorial desensitization phenomena.

Animals↗
PubMed1982

The mode of action of LHRH agonists on the rat Leydig cell.

The relationship between LHRH agonist-receptor interaction and subsequent stimulation of steroidogenesis has been investigated using dispersed adult rat Leydig cells. Binding of 125I-labelled LHRH agonist to these cells was rapid and was readily and completely reversible, which contrasted with the binding of 125I-labelled hCG which was never completely reversible and which became progressively less reversible with increase in time. Following 125I-LHRH agonist-receptor interaction for 5 min at 21 degrees C, over 80% of the bound hormone dissociated at a fast rate (t 1/2 1.5 min) and the remainder at a slower rate (t 1/2 20 min). Following LHRH agonist-receptor interaction for a longer period (45 min) at 21 degrees C, only the slower of these 2 components of dissociation was evident, although binding was still completely reversible. Evidence was also obtained that following preincubation of Leydig cells for 2 hr at 34 degrees C with a near-saturating concentration (2000 pg/ml) of unlabelled LHRH agonist, all or most of the bound hormone dissociated during subsequent incubation at 21 degrees C. Incubation of Leydig cells at 34 degrees C in the continuous presence of either a low dose (1 pM) of hCG or a high dose (2000 pg/ml) of LHRH agonist resulted in similar percentage stimulation of testosterone secretion with a similar time lag (2 h) before this increase was evident. Preincubation with this dose of hCG for as little as 15 or 30 min still led to increased testosterone secretion following removal of the free hormone. In contrast, preincubation with LHRH agonist for up to 2 h was without subsequent stimulatory effect, presumably due to dissociation of the bound hormone from its receptors. Therefore, for LHRH agonist to stimulate Leydig cell steroidogenesis in vitro, it must be present continuously in the incubation medium, and the implications of this with respect to the secretion and mode of action of 'testicular LHRH' in vivo are discussed.

Animals↗
PubMed1998

Expression and effect of insulin-like growth factor I on rat fetal Leydig cell function and differentiation.

Insulin like growth factor I (IGF-I) is believed to be a potent para/autocrine stimulator of Leydig cell function in adult testis. We investigated whether IGF-I is also an intratesticular regulator of fetal Leydig cell function by measuring its production in the fetal testis and its ability to affect testicular steroidogenesis during fetal development. Northern blot analysis revealed one major IGF-I transcript of 7-7.5 kb and two minor transcripts of 3.8 and 1.8 kb in 20.5 day fetal testis. IGF-I was detected by RIA in 16.5 fetal day testes, and the amounts of IGF-I secreted by 16.5 and 20.5 fetal day testes in vitro were much greater than the amounts contained in the testes, indicating active synthesis in culture. The secretion of IGF-I by the fetal testis in vitro was increased with testicular age and time in culture. It was not modified by gonadotropins or (Bu)2cAMP. Testosterone secretion by fetal testes explanted 13.5, 16.5, 18.5, and 20.5 days after conception and cultured in the presence or absence of 100 ng/ml LH for 3 days was not affected by the addition of 50 ng/ml IGF-I to the medium. In contrast, the addition of IGF-I to dispersed fetal testicular cells cultured for 3 days in the presence or absence of LH increased the number of Leydig cells identified by a positive cytochemical reaction for 3beta-hydroxysteroid dehydrogenase (3betaHSD). This was more pronounced with cells from 16.5- day-old fetuses (stage when the fetal Leydig cells are differentiating in vivo) than with 20.5-day-old fetuses cells (stage when the number and the function of fetal Leydig cells are stable or decreasing). It results from both an increased differentiation of mesenchymal cells in fetal Leydig cells and an increase in the mitotic index of the fetal Leydig cells, as inferred from the small increase in the percentage of bromodeoxyuridine/3betaHSD-positive cells. Both LH and IGF-I increased significantly testosterone production by day 16.5 cells. In the presence of LH, a high amount of testosterone was produced per 3betaHSD-positive cell; IGF-I further increased this production. This effect was not observed with day 20.5 cells. The amounts of testosterone produced per 3betaHSD-positive cell cultured in the presence of both LH and IGF-I were more than additive. Like IGF-I, insulin (50 ng/ml) increased testosterone secretion per 3betaHSD-positive cells in cultures of day 16.5 cells, but not in those of day 20.5, cells. Lastly, IGF-I also increased the steroidogenic activity of each Leydig cell in cultures containing (Bu)2cAMP, but its effects were weaker than those observed in the presence of LH. This suggests that IGF-I has sites of action both upstream and downstream cAMP generation. These results suggest that IGF-I acts as paracrine/autocrine factor in the differentiation and activity of fetal Leydig cells.

Animals↗
PubMed1999

Secretion of testosterone and its delta4 precursor steroids into spermatic vein blood in men with varicocele-associated infertility.

Insight into the mechanisms by which steroid hormones are released from the testes was sought by examining the concentrations of progesterone, 17alpha-hydroxyprogesterone, and androstenedione as well as testosterone in spermatic vein blood every 15 min for 4 h in men with varicocele-associated infertility. Coincident discrete secretory episodes of all four steroids were found, and spermatic vein concentrations of testosterone were highly positively correlated to the concentrations of progesterone (r = 0.79), 17alpha-hydroxyprogesterone (r = 0.81), and androstenedione (r = 0.82), respectively. The sum of the four measured steroids per mL plasma was calculated, and testosterone was found to account for 70%, 17alpha-hydroxyprogesterone for 24%, androstenedione for 5%, and progesterone for 1% of the total. In a previous study of the intratesticular steroids in a separate population of men with varicocele-associated infertility, the sum of these four steroids per g tissue was similarly calculated. Testosterone accounted for 70% of the four measured steroids, 17alpha-hydroxyprogesterone for 22%, androstenedione for 4%, and progesterone for 3% of the total. Thus, the relative concentrations of these four steroids are nearly identical in testicular tissue and spermatic vein plasma. From these data we hypothesize that steroids in the testicular interstitium are cosecreted into peripheral plasma in response to stimulation by LH and propose that the mechanism initiating this pulsatile mode of secretion oftestosterone and its precursor steroids may not be coupled to testosterone biosynthesis.

17-alpha-Hydroxyprogesterone↗
PubMed1985

A factor from bursa of Fabricius inhibits in vitro the chorionic gonadotropin response of the chick testis.

The effect of bursa of Fabricius on the endocrine function of the chick testis was studied using an isolated testis cell preparation. Testosterone secretion, both basal and under hCG stimulation, was measured in the incubation medium. The bursal extract inhibited the response of the testis cells to hCG detected as a reduced testosterone secretion. The normal basal secretion of the testis cells was not modified by the bursal extract. To analyze some characteristics of the bursal factor, fractions of approximately known molecular weight were obtained by filtering through Amicon membranes. The active factor was found in the fraction corresponding to 1000-10000 Da. Its activity disappeared after heating of trypsin incubation, suggesting the peptidic nature of the bursal factor. Tissue extracts from gut and spleen did not modify the hCG response of the testis cells. There was inhibition of the hCG response by thymus extracts of the newly hatched chicken. These results add new evidence of a modulatory effect of the immunogenic organs on the endocrine function of the testis in the newly hatched chicken.

Animals↗
PubMed1991

Epidermal growth factor directly stimulates steroidogenesis in primary cultures of porcine Leydig cells: actions and sites of action.

The actions and the mechanisms of action of epidermal growth factor (EGF) in testicular steroidogenesis were investigated using a model of primary culture of purified porcine Leydig cells from immature intact animals. EGF decreased (1.7-fold) human CG (hCG)-induced dehydroepiandrosterone (DHEA) accumulation in the medium whereas it enhanced (2.5-fold) that of testosterone. The maximal and half-maximal effects on both DHEA and testosterone secretions were observed at similar concentrations which were, respectively, 3 (5 x 10(-10) M) and 0.7 (11 x 10(-11) M) ng/ml EGF, after 72-h treatment. EGF effect on DHEA and testosterone secretion was similarly observed whether the cells were acutely (3 h) stimulated with hCG (1 ng/ml) or with 8-bromo-cAMP (10(-3) M). To further localize the steroidogenic biochemical steps affected by EGF, the growth factor action on steroidogenic enzyme activities was investigated. EGF increased delta 5 steroid intermediate (i.e. pregnenolone and DHEA) formation [evaluated in the presence of 10(-5) M of WIN 24540, an inhibitor of 3 beta-hydroxysteroid dehydrogenase/iosomerase (3 beta-HSDI) activity]. However, this stimulation was observed in cells when acutely (3 h) stimulated with hCG (0.01-1 ng/ml) but not when incubated with 22R-hydroxycholesterol (0.01-10 micrograms/ml). Such findings indicate that EGF did not affect cholesterol side chain cleavage cytochrome P450 activity but probably increased cholesterol substrate availability for this enzyme in the inner mitochondria. Moreover, EGF significantly (P less than 0.001) increased delta 5 steroid intermediate (i.e. pregnenolone and DHEA) but not delta 4 steroid intermediate (i.e. progesterone and androstenedione) conversion into testosterone, indicating that EGF enhances 3 beta-HSDI activity. Such effects of EGF are directly exerted on Leydig cells since EGF receptors (Kd = 16 x 10(-11) M) are present in primary cultures of purified porcine Leydig cells. Together, the present findings show that in Leydig cells from intact animals, EGF enhances the gonadotropin action on testosterone formation through an increase in the availability of cholesterol substrate in the mitochondria as well as an increase in the activity of 3 beta-HSDI.

3-Hydroxysteroid Dehydrogenases↗
PubMed1998

[Immuno-endocrine interactions in the testis: possible involvement of Ca2+ in signal transduction pathway in Leydig cells].

The testis is divided, both functionally and anatomically, into two specialised compartments, i.e. the vascular interstitial tissue and avascular seminiferous tubules. Leydig cell steroidogenesis is mainly controlled by luteinizing hormone (LH) secreted from the anterior pituitary. It is well known that LH is able to generate second messengers by adenylate cyclase and the cycle of inositolphospholipids. Also Ca2+ ions are taken into account as an important modulators of Leydig cell steroidogenesis. The aim of this study was to show the effect of macrophage-conditioned medium on the basal and LH stimulated testosterone secretion by mouse Leydig cells in vitro. A source of Leydig cells was the testis of mature, Swiss strain mice. Leydig cells were isolated and cultured for 48 hrs. Testosterone levels were measured radioimmunologically. Intracellular free Ca2+ ions were analysed by computer automatic system 'MAGICAL'. Results indicated that not only LH but also macrophage-conditioned medium were able to modulate testosterone secretion by Leydig cells and increase intracellular calcium concentration. Therefore, it seems possible that the action of proteins secreted from macrophages is mediated through Ca2+ ions which are involved in another signal transduction pathway leading to stimulation of testosterone biosynthesis by Leydig cells in vitro.

Animals↗
PubMed1978

[Effect of ACTH administration on liberation of testosterone by the Leydig cell (author's transl)].

The possible rôle of the Leydig cells ithe changes of testosterone levels induced by ACTH administration is studied. 14 male Wistar rats weighing about 300 g were separated in two groups. One was treated with I mU.I./100 g/day of ACTH i.m. for 6 days and the other with saline solution as control Rats, testes and adrenal glands were weighed and plasma testosterone levels were measured. The Leydig cells dispersed collagenase was inbubated for 120 min at 37 degrees C in the presence and in the absence of 10 mU.I. of HCG. The weight of adrenal glands in the treated rats was greater than in the control group. Treated rats had lower plasma values than the controls. Testosterone secretion by the Leydig cells, in basal situation and after stimulation with HCG, was lower in the treated group. Leydig cells of untreated rats were incubated with 12.5, 6.2, 3.1, 1.5 mU.I. of ACTH and supplemented with 2.5 pU.I. of HCG. No difference in testosterone secretion in either groups was observed.

Adrenal Glands↗
PubMed1995

Direct effects of the pineal hormone melatonin on testosterone synthesis of Leydig cells in Djungarian hamsters (Phodopus sungorus) in vitro.

Leydig cells of adult Djungarian hamsters, stimulated with luteinizing hormone (LH), were co-incubated with melatonin at various concentrations in a primary culture system. Testosterone secretion was only affected by melatonin when cells were stimulated with LH. Maximal suppression was observed at low doses of LH (0.5 ng/ml). These effects are at least partially mediated through the adenylate cyclase system, since melatonin was able to reduce forskolin-stimulated testosterone secretion. These results indicate that the time between pulses of LH can be considered to be most highly effective for tonic melatonin actions.

Animals↗
PubMed1985

Response of interstitial cells of the testes in the house musk shrew, Suncus murinus L., to various gonadotropins.

Testicular interstitial cells of the house musk shrew culture in vitro released testosterone in response to ovine LH with a quite similar dose response relationship to that found in the cells of rats. The dose response curves suggested that a single testicular cell of the shrew has the same potency to secrete testosterone as that of the rat. In the shrew as well as in the rat, neither ovine PRL added alone nor together with oLH could stimulate the testosterone release from testicular cells, although a very limited enhancement of testosterone secretion was observed in the cell cultured with a large dose of oFSH in both species.

Journal Article↗
PubMed1988

The antiandrogen anandron potentiates the castrating effect of the LH-RH agonist buserelin in the rat.

When buserelin (0.04-25 micrograms/kg/day), a potent LH-RH agonist, was administered s.c. daily for 15 days to male rats, prostate weight decreased after a transient increase in the first days of treatment but never as much as after orchidectomy, since testosterone secretion was never totally suppressed. The combination of the pure nonsteroid antiandrogen Anandron (20 mg/kg/day) with even low doses of buserelin led to an immediate decrease in prostate weight that was complete at 15 days. This could be explained (a) by an additivity of effects: inhibition by Anandron of the action of residual testosterone unsuppressed by buserelin on the prostate and prevention by buserelin of the rebound testosterone increase induced by Anandron: (b) by a potentiation by Anadron of the direct castrating effect of buserelin on the testis since testis weight and testosterone secretion were lowered to a greater extent by the combination than by buserelin alone. Anandron might increase the sensitivity of LH-RH receptors to LH-RH agonist in the testes, as has been shown in the pituitary. In contrast, the combination of the antiandrogenic steroid progestin, cyproterone acetate, with buserelin never potentiated the castrating effect of buserelin on testis weight and testosterone and only partially potentiated prostate atrophy. If such actions also exist in the human, the addition of Anandron to LH-RH agonist treatment would not only counter flare-up and adrenal androgen effects on the prostate but would also lower the doses of peptide or the time required for chemical castration.

Administration, Oral↗
PubMed1989

The effects of pulsatile GnRH infusion upon the diurnal variations in serum LH and testosterone in pre-pubertal and pubertal boys.

The aim of the present study was to determine the effects of exogenous GnRH pulsatile infusions on the diurnal variations of LH and testosterone secretion which occur in late pre-puberty and early puberty. GnRH infusions were administered to 12 short stature males in pre-puberty or early puberty, over 6-day periods. In 6 patients, GnRH doses of 2.5, 7.5 and 15 micrograms/pulse were used and 24-h profiles of serum LH and testosterone were measured before and at the end of the infusions. In the remaining 6 patients GnRH was administered at a dose of 7.5 micrograms/pulse and profiles between 21.00 and 06.00 h the following day were determined. Pre-infusion profiles demonstrated nocturnal LH and testosterone rises in all patients. Median pre-infusion serum LH prior to midnight was 2.2 U/l (range 1.0-5.4) rising to 3.7 U/l (range 1.9-10.7) during GnRH administration (p less than 0.005). After midnight, median pre-treatment serum LH concentration was 4.3 U/l (range 2.7-7.5) which remained unaltered by GnRH administration (median 4.8 U/l, range 2.9-7.9, p greater than 0.05). Median pre-therapy serum testosterone before midnight was 0.8 nmol/l (range 0.1-7.1) rising significantly (p less than 0.05) to 4.1 nmol/l (range 0.2-8.0). Following therapy, post-midnight median serum testosterone rose from 4.8 (range 0.4-9.4) to 7.0 nmol/l (range 0.5-13.9, p greater than 0.05). Diurnal variation in LH and testosterone secretion, therefore, is maintained during exogenous GnRH administration to pre-pubertal and pubertal boys. Response to exogenous GnRH pulses may be significantly influenced by endogenous GnRH.

Adolescent↗
PubMed1997

Stimulating effect of both human recombinant inhibin A and activin A on immature porcine Leydig cell functions in vitro.

In addition to the regulation of FSH secretion, it has been clearly shown that inhibin and activin have paracrine/autocrine effects in the gonads. We have studied the effect of human recombinant inhibin A and human recombinant activin A on immature porcine Leydig cells in vitro. Leydig cells were prepared by collagenase digestion of testes from 3-week-old piglets, purified on Percoll gradient, then cultured in a chemically defined medium. The cells were treated with increasing amounts of inhibin A or activin A (0.5-200 ng/ml). Direct application of either inhibin A or activin A on Leydig cells for 4 or 48 h did not stimulate basal testosterone secretion. Conversely, treatment of the cells for 48 h with either factor resulted in a dose-dependent increase in hCG-stimulated testosterone secretion (10[-9] M hCG, 2 h) with a maximal effect of 2.40 +/- 0.37- and 2.43 +/- 0.37-fold increases for inhibin A and activin A, respectively, and these changes were associated with a slight increase in LH/hCG-binding sites (1.37 +/- 0.19- and 1.24 +/- 0.11-fold increases). In addition, both inhibin A and activin A enhanced messenger RNA (mRNA) levels of LH/hCG receptor (2.75 +/- 0.40- and 2.53 +/- 0.60-fold increases) and cytochrome P450 17alpha-hydroxylase (6 +/- 1- and 3.5 +/- 0.6-fold increases), but had no effect on side-chain cleavage cytochrome P450 or cytochrome P450 aromatase mRNAs. 3beta-Hydroxysteroid dehydrogenase mRNA levels were increased (3.1 +/- 1.3-fold increase) by activin A, but not by inhibin A. However, inhibin A blocked the stimulatory action of activin A. In keeping with these changes in the steroidogenic enzyme mRNAs, both peptides enhanced the conversion of exogenous 22R-hydroxycholesterol and progesterone, but only activin A increased the conversion of dehydroepiandrosterone into testosterone. In conclusion, our findings demonstrate that both inhibin A and activin A have a stimulatory effect on immature porcine Leydig cell differentiated function in vitro. As inhibin has a stimulatory and activin has an inhibitory effect on rat Leydig cell function in vitro, the effects of these factors on Leydig cells seem to be species dependent.

Activins↗
PubMed2006

Toxic effects of zearalenone and alpha-zearalenol on the regulation of steroidogenesis and testosterone production in mouse Leydig cells.

Zearalenone (ZEA) and its derivative alpha-zearalenol (alpha-ZOL) are produced by fungi of the genus Fusarium and, after ingestion via contaminated cereals, may lead to animal fertility disturbances and other reproductive pathologies. The previous study demonstrated the toxic effects of ZEA and alpha-ZOL through disturbances in male fertility and other reproductive pathologies in mice. In this study, we further examined the direct biological effects of ZEA and alpha-ZOL on steroidogenesis production, primarily in Leydig cells of mice. Mature mouse Leydig cells were purified by Percoll gradient centrifugation and the cell purity was determined by 3beta-hydroxysteroid dehydrogenase (3beta-HSD) staining. To examine ZEA and alpha-ZOL-induced biological consequences, we measured testosterone secretion and transcription level of 3 key steroidogenic enzymes including 3beta-HSD-1, P450scc and StAR, in ZEA and alpha-ZOL/human chorionicgonadotropin (hCG) co-treated cells. Our results showed that ZEA and alpha-ZOL (10(-4) M, 10(-6) M and 10(-8) M) significantly suppressed hCG (10 ng/ml)-induced testosterone secretion. The suppressive effect is correlated with a decrease in the level of transcription of 3beta-HSD-1, P450scc, and StAR (P<0.05).

3-Hydroxysteroid Dehydrogenases↗
PubMed1992

Seasonal pattern of luteinizing hormone and testosterone pulsatile secretion in young adult red deer stags (Cervus elaphus) and its association with the antler cycle.

Blood from stages aged 15 months (n = 6) was sampled at monthly intervals every 30 min for 24 h for 12 months, at 45 degrees S in New Zealand. Three extra samplings each for 24 h were carried out at about the anticipated time of antler casting. All samples were analysed for luteinizing hormone (LH) and testosterone and the resulting data further analysed by the Pulsar pulse detection routine. The animals were kept indoors under natural daylength and were fed ad libitum. All animals were weighed, antler status and size recorded and testes diameter was measured on each sampling day. Mean LH and testosterone pulsatily and plasma concentration varied seasonally. LH pulse frequency was low during autumn (2.5 pulses in 24 h), winter (1.0-1.5 pulses in 24 h) and early spring (1 pulse in 24 h) and lowest in late spring (0.2 pulse in 24 h) before rising in summer (1.0-4.0 pulses in 24 h). LH pulse amplitude and mean plasma concentration were low (< 1 ng ml-1) from March to November (autumn-spring); both rose to a peak in January (summer) of 3.4 and 1.6 ng ml-1, respectively. Testosterone pulse frequency was generally similar to LH except that slightly more pulses of testosterone than of LH were detected from March to November and more pulses of LH from November to February (summer). Testosterone pulse amplitude fell from March to November (5.3 ng ml-1 to undetectable) although there was a conspicuous peak in July (midwinter) of almost 5 ng ml-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Studies of nocturnal penile tumescence and sleep electroencephalogram in patients with major depression and in normal controls.

Nocturnal penile tumescence (NPT), sleep electroencephalogram and testosterone secretion were investigated in 25 nonmedicated male patients with an acute episode of major depression. Twelve patients were reassessed after a stable remission and withdrawal of antidepressants. Four of the 25 patients had no NPT activity during acute depression, but this was reversed after recovery. The area under the NPT curve increased after remission, whereas all other NPT variables remained unchanged. Nocturnal testosterone secretion was enhanced after recovery, whereas the sleep structure remained unchanged. The NPT findings for the depressed patients did not differ from those for a control group, even though the latter group was younger. Hence, there are no general NPT changes that could be used to separate depressed patients and normal controls. However, a lack of NPT seems to be a possible, reversible symptom of depression in men.

Adult↗
PubMed1987

Intratesticular steroids and gonadotrophin receptor concentrations in the testes of immature unilaterally cryptorchid rats.

Testicular descent was prevented unilaterally in newborn rats. In this experimental model of cryptorchidism the first morphological changes are noted in the abdominal testis at 16 days of age. Testicular weight was increased in the abdominal testis at 16 days of age, was unaffected at 20 days but was decreased at 30 days of age. The concentrations of LH and FSH receptors, and the hCG-stimulated progesterone and testosterone secretion in vivo were analysed in scrotal and abdominal testes at different ages. LH- and FSH-receptor content per testis were unaffected by cryptorchidism at 12, 16 and 20 days of age but were depressed markedly at 30 days of age. At 20 days of age (but not earlier) hCG-stimulated progesterone was reduced while testosterone secretion remained unchanged. It is concluded that the early functional changes in abdominal testes are not related to changes in gonadotrophin receptor content.

Animals↗