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PubMed1987

Effect of photoperiod on the size of the Leydig cell population and the rate of recruitment of Leydig cells in adult Syrian hamsters.

The number of Leydig cells was determined by stereologic procedures in adult Syrian hamsters housed in long days (14L:10D) to maintain testicular activity (active), in short days (5L:19D) for 12-13 wk to induce testicular regression (photoperiod-induced regressed), or in short days for a period of 21 wk or more to allow spontaneous gonadal recrudescence (spontaneously recrudesced). Testes were removed, sliced, fixed, embedded in Epon 812, and observed by bright-field microscopy. Testicular and seminal vesicle weights, plasma testosterone concentration, total Leydig cell volume per testis, and volume of single Leydig cell were greater (p less than 0.01) in active and recrudesced animals than in regressed animals. The density of Leydig cells was greater in the regressed testes, but the total number per testis was not influenced by photoperiod. In Experiment 2, the rate of recruitment of Leydig cells was determined in 5 adult hamsters exposed to long days (active) or 5 hamsters whose testes were regressed by exposure of animals to short days for 13 wk followed by long-day exposure to initiate testicular growth (photoperiod-induced recrudescing). Hamsters were injected for 3 days/wk for 3 wk with tritiated thymidine, 0.5 or 1 microCi/g body weight. Testes were fixed and tissues prepared, as above, and processed for autoradiography. Again, the photoperiod did not influence the number of Leydig cells per testis. Labeling of Leydig cell nuclei revealed that recruitment of new Leydig cells occurred at approximately 1.3% per day in recrudescing testes but also occurred at approximately 0.6% per day in active testes. Without change in the total number of Leydig cells, new Leydig cells were added continually to the existing population in adult hamsters with either recrudescing or active testes.

Animals↗

PubMed1982

The effects of short-term culture and perifusion on LH-dependent steroidogenesis in isolated rat Leydig cells.

Tumour Leydig cells and normal mature Leydig cells lost their steroidogenic response (pregnenolone and testosterone secretion) to LH after 24 h of culture. Immature cells showed a 2-fold increase in the basal pregnenolone secretion and no change in the LH-dependent pregnenolone secretion after 24 h of culture, whereas the LH-dependent steroidogenesis decreased after 48 h. None of the 3 cell preparations showed morphological signs of degeneration during a culture period of more than 7 days. Histochemical 3 beta-hydroxysteroid dehydrogenase activity in isolated immature Leydig cells disappeared during the first 2 days of the culture period and re-appeared after 5--7 days. Testosterone production by mature Leydig cells decreased during the first hours after exposure to LH, whereas pregnenolone secretion remained constant. From these results it was concluded that Leydig cells attached to plastic can be used for investigation of acute actions of LH on steroidogenesis. A perifusion technique for cells attached to plastic was developed and was applied to the kinetics of LH action on steroidogenesis in tumour and immature Leydig cells. The first stimulation of pregnenolone secretion occurred within 5 min, but a full stimulation was only obtained after 20--30 min. This was followed by a gradual decrease in the stimulated steroid secretion to approximately 50% after 60 min.

Animals↗

PubMed1984

Fetal ovarian hilar cells and testicular Leydig cells in various complications of pregnancy.

The presence of ovarian hilar cells in fetuses and neonates whose mothers suffered from complications of pregnancy such as toxaemia of pregnancy, diabetes mellitus, accidental haemorrhage, hydrops foetalis and multiple pregnancy, has been investigated and compared with the presence of testicular Leydig cells in similar conditions. The examination of ovaries from 62 cases with complications of pregnancy and of 113 controls showed that such conditions did not have an influence on the presence of hilar cells in the fetal and neonatal ovary. These findings are in marked contrast to our previous observations in the fetal and neonatal testis where the mean number of Leydig cells was found to be significantly raised in cases associated with complications of pregnancy as compared with controls. This further confirms our view, already expressed in a previous publication on the ovaries and testes of anencephalic monsters, that fetal and neonatal ovarian hilar cells and testicular Leydig cells are not strictly comparable, at least in their response to hormonal stimuli.

Cell Count↗

PubMed1994

Germ cell failure and Leydig cell insufficiency in post-pubertal males after autologous bone marrow transplantation with BEAM for lymphoma.

Thirteen post-pubertal male patients aged 17-25 years were assessed for pituitary-gonadal function 0-3 months prior to and 2-3 months post-bone marrow transplantation for haematological malignancy. All patients had multiagent cytotoxic treatment prior to transplantation and 30% were found to have germ cell dysfunction with abnormal semen parameters before high-dose therapy indicating damage to the germinal epithelium. They also had evidence of reduced Leydig cell reserve even before transplantation. During transplantation all patients sustained sustained gonadal injury, the effect on their germ cells being more pronounced than on the Leydig cells. Fifty per cent had reduction in testicular volume and all had azoospermia 2-3 months post-transplantation. Our results indicate that short-term chemoradiotherapy causes profound damage to the germ cell compartment of the testis, with less severe damage to the Leydig cells, but no overt injury to the anterior pituitary gland. The changes appeared to be identical in patients conditioned with total body irradiation-based protocols and those who received only high-dose chemotherapy prior to bone marrow transplantation.

Adolescent↗

PubMed1990

Development of a new Leydig cell population after the destruction of existing Leydig cells by ethane dimethane sulphonate in rats: an autoradiographic study.

The formation of new Leydig cells in adult male rats was studied after the complete destruction of the original population by ethane dimethane sulphonate (EDS). Following administration of EDS, proliferating interstitial cells were labelled in a pulse-chase experiment by way of three [3H]thymidine injections on days 2, 3 and 4 after EDS administration. Some of the newly formed Leydig cells found 14 days after EDS administration were labelled with [3H]thymidine, indicating that these Leydig cells were derived from precursor cells, most likely mesenchymal cells, that had incorporated [3H]thymidine at days 2, 3 or 4 after EDS administration. At 21 days after EDS administration, the total number of Leydig cells (labelled plus unlabelled) had increased 7- to 16-fold compared with the number of cells that were present 14 days after EDS had been administered. In a second series of experiments, [3H]thymidine was given 2 h before the rats were killed (short-term labelling experiment). In this experiment it was shown that the proliferative activity of the mesenchymal cells, which are presumed to be the precursors of the Leydig cells, after a considerable increase at day 2 after EDS administration, had returned to the control level at day 7. However, the total number of mesenchymal cells (labelled plus unlabelled) remained increased from 2 to 49 days after EDS administration. This indicated that the majority of the new Leydig cells which were formed from day 14 onwards probably did not derive from differentiating mesenchymal cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1984

Granulosa cell, Sertoli-Leydig cell, and unclassified sex cord-stromal tumors associated with pregnancy: a clinicopathological analysis of thirty-six cases.

Seventeen granulosa cell, thirteen Sertoli-Leydig cell and six unclassified sex cord-stromal tumors diagnosed during pregnancy or the puerperium were reviewed. Eleven patients presented with abdominal pain or swelling, five in shock, two with virilization, and one with vaginal bleeding. Three asymptomatic patients were explored because of a palpable mass and one because of an adnexal mass found on ultrasound examination. In thirteen patients the tumor was discovered during a cesarean section; five of them had had dystocia and in eight of them the tumor was an incidental finding. All the tumors were Stage I but 13 of them had ruptured; all but one were unilateral. Hemoperitoneum was present in seven cases. On microscopical examination many of the tumors differed from tumors in the same diagnostic categories occurring in the absence of pregnancy by having a disorderly arrangement of their cells, lacking recognizable differentiation in many areas, showing prominent edema, and containing unusually large numbers of lutein or Leydig cells. The last two features were most obtrusive in tumors removed at term. With one exception the patients were initially treated by conservative surgical procedures. Two of them received chemotherapy and two radiation therapy postoperatively. A hysterectomy and salpingo-oophorectomy was performed at a second operation in eight cases; no residual tumor was found in any of the specimens. Only one patient had a recurrence, which was treated surgically. Follow-up for an average of 4.7 years is available for 30 of the 36 patients; all of them were alive and free of disease at the time of the last examination.

Adolescent↗

PubMed1983

Recurrence of a gonadal stromal cell tumor (Sertoli Leydig cell with heterologous elements) in a teenager.

An unusual case of a moderately well-differentiated, encapsulated, Sertoli Leydig cell tumor with heterologous elements recurring 3 years after a conservative unilateral oophorectomy in a 15-year-old female is reported. This is the first case report of a metastatic Sertoli Leydig cell tumor with mucinous heterologous elements. A relative lack of uniformly accepted histological criteria of these tumors makes prognosis difficult to access. The optimal therapy for recurrent Sertoli Leydig cell tumor is unknown. Initial plans of management of this rare neoplasm, follow-up, and current concepts of treatment of recurrences will be discussed.

Adolescent↗

PubMed1983

Ovarian hilar cells and testicular Leydig cells in anencephaly.

The presence of ovarian hilar cells in anencephaly has been investigated and compared with the presence of testicular Leydig cells in the same condition. The examination of 29 anencephalic ovaries and 49 controls showed that up to 36 weeks of gestation there was a preponderance of ovarian hilar cells in anencephalic monsters as compared with controls. Similar observations were made with regard to ovarian follicles which showed more pronounced maturational changes than controls. However, during the last month of gestation both these processes were more marked in the controls. These findings are in marked contrast to our previous observations on the testes in anencephalic monsters which showed significantly less Leydig cells than controls throughout the third trimester of pregnancy. It is assumed that these appearances are due to the fact that testes and ovaries are not strictly comparable structures and may, therefore, react in a different way to hormonal stimulation. This is of particular interest as the placental chorionic gonadotrophin levels which stimulate the development of testicular Leydig cells and, supposedly, the development of ovarian hilar cells are normal in anencephaly.

Adult↗

PubMed1994

Effects of ethane dimethanesulfonate (EDS) on adult and immature rabbit Leydig cells: comparison with EDS-treated rat Leydig cells.

Ethane-dimethanesulfonate (EDS) has been shown to selectively kill Leydig cells and depress testosterone production in adult rats. A recent study has shown that immature rat Leydig cells are less sensitive to EDS exposure. There is evidence that the rabbit metabolizes EDS to methane sulfonic acid more rapidly than does the rat, reducing exposure to the parent compound. In the study reported here, we examined the effects of EDS on the Leydig cells in both adult and immature rabbits and compared the effects found with those previously reported in the rat. In vivo, EDS exposure demonstrated that Leydig cells from adult rabbits were affected, with both serum and interstitial testosterone production depressed. EDS effects in adult rabbits and rats were compared by exposing explants of testicular parenchyma to EDS in vitro and evaluating testosterone production. With this procedure, the rabbit testis was less sensitive to EDS treatment than the rat, with a 50% reduction rate (EC50) achieved with 2026 microM EDS for the rabbit and with 336 microM EDS for the rat. Perfusion of adult and immature rabbit testis with 430 microM EDS demonstrated the insensitivity of the immature testis to EDS exposure: adult testosterone production was reduced 50% in 3.5 h, whereas no diminution was found in the immature rabbit. EDS exposure of interstitial cell preparations further demonstrated the insensitivity of immature rabbit Leydig cells, with an EC50 of 4397 microM compared to an EC50 of 1137 microM EDS in adult preparations.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

PubMed2006

Anti-apoptotic factor humanin is expressed in the testis and prevents cell-death in leydig cells during the first wave of spermatogenesis.

Humanin (HN) is a 24 amino acids peptide with potent neuro-survival properties that protects against damage associated with Alzheimer's disease. In the present report, we have demonstrated by immunohistochemical analysis and Western blotting the pattern of expression of rat humanin (HNr) in the testis of 10- to 60-day-old rats. The Leydig cells of 10- and 40- day-old rats expressed this peptide at high levels; and in the testis of 60-day-old rats the expression of HNr expanded to include Leydig, endothelial, peritubular and germ cells. As monitored by Western blotting, HNr was released into the medium of cultures of Leydig cells isolated from 10-, 40-, and 60-days-old rats. HNr stimulated the incorporation of [(3)H]TdR into DNA of Leydig cells from 10-days-old rats, in a manner that indicated promotion of cell survival rather than an increase in the rate of cell multiplication. This peptide also enhanced steroidogenesis by cultured Leydig cells from 10- to 40-day-old rats both alone and synergistically with IGF-I. The expression of HNr in cultured Leydig cells increased in response to GH and IGF-I. In summary, we demonstrated here that HNr was expressed at all stages of maturation in the rat testis. This peptide promoted the survival of Leydig cells in culture and interacted with IGF-I to stimulate DNA synthesis and steroidogenesis. We propose that HNr is a novel testicular anti-apoptotic factor.

Animals↗

PubMed1984

Acute responses of Leydig cells to hCG: evidence for early hypertrophy of Leydig cells.

The cross-sectional area of Leydig cells has been studied in rats following a single injection of 100 IU hCG. Leydig cell size was not changed within 2 h of injection (89.73 +/- 3.02 micron 2) but had increased significantly by 12 h (114.76 +/- 3.57 micron 2). Leydig cell size continued to increase until 24 h when a maximum cross-sectional area of 186.30 +/- 4.72 micron 2 was measured. This area was significantly greater than that recorded after 1 week of daily hCG treatment (143.18 +/- 6.25 micron 2, P less than 0.05). At 48 and 72 h Leydig cell size decreased slightly and was not significantly different from that seen after chronic hCG treatment. A single injection of 100 IU hCG induced a biphasic serum testosterone response with peaks in serum testosterone at 2 h and 72 h, the intervening nadir suggesting a period of in vivo refractoriness. A corresponding period of Leydig cell refractoriness in vitro was also demonstrated 12 h following a single injection of 100 IU hCG and persisted for 48 h. Further injections of hCG on day 2 or 3 did not induce a second biphasic serum testosterone pattern or the accompanying period of refractoriness, indicating that Leydig cell refractoriness is a temporary phenomenon which cannot be maintained during persistent stimulation with hCG. The absence of further refractory periods to hCG during recurrent stimulation may be related to the trophic action of the hormone on Leydig cells.

Animals↗

PubMed1981

The heterogeneity of Leydig cells from mouse and rat testes--evidence for a Leydig cell cycle?

A method for purifying Leydig cells by centrifugation of testes cells on continuous density gradients of Percoll has been investigated. The distribution of Leydig cells in the separated bands of cells obtained and their receptor content and testosterone production after addition of lutropin (LH) has been measured. In agreement with previous work (Schumacher, Schäfer, Holstein & Hilz 1978) it was found that highly pure mouse Leydig cells (average density 1.070 g/ml) could be prepared by this method. These cells responded to LH and produced high amounts of testosterone (1 - 4 microgram/10(6) cells/2 h), and bound [125]hCG specifically (25 - 64 fmols hCG bound/10(6)). Similarly from rat testes, Leydig cells (average density 1.072 g/ml) were purified. These cells also responded to LH and produced 5 - 25 ng testosterone/10(6) cells/2 h and bound [125]hCG specifically (3 - 18 fmols hCG bound/10(6)cells). Two other bands of nucleated cells of lower density (approximately 1.045 and 1.052 g/ml) were formed on the gradients from both mouse and rat testes. Both these bands of cells were found to contain Leydig cells which bound [125]hCG specifically but little or not stimulation of testosterone production could be demonstrated. Fractionation of the gradients after separation of the cells into small aliquots demonstrated that fractions containing up to 100% Leydig cells could be isolated which were not stimulated to produce testosterone after addition of LH. It is concluded that in both the adult rat and mouse testes, Leydig cells of different densities and steroidogenic responsiveness to LH exist. The data obtained in this and other studies suggest that Leydig cells in the rat and mouse testes are not a homogeneous population and that they may be undergoing a continuous cycle of activity which involves changes in density and steroidogenic capacity.

Animals↗

PubMedDate not supplied

Stimulation of the proliferation and differentiation of Leydig cell precursors after the destruction of existing Leydig cells with ethane dimethyl sulphonate (EDS) can take place in the absence of LH.

In hypophysectomized rats, 2 days after the administration of the cytotoxic drug ethane dimethyl sulphonate (EDS), the proliferative activity of Leydig cell precursors increased six-fold. Thus, factors other than LH act locally to stimulate the proliferation of precursor cells after EDS. Twenty-six days after EDS administration, neither cells with the morphological characteristics of Leydig cells nor histochemical enzyme activities, such as 3 beta-HSD and alpha-naphtyl esterase, could be detected in testis tissue. In hypophysectomized rats treated daily with hCG (100 iu) for 7 days, starting at 26 days after EDS, the number of Leydig cells was increased to 48 +/- 11 cells (per 1000 Sertoli cells), which is approximately 4.5% of the intact control level. 3 beta-HSD and alpha-naphtyl esterase activity could be detected, and plasma testosterone levels had increased 15-fold compared with the hypophysectomized controls. These results show that proliferation and some differentiation of precursor cells along the Leydig cell lineage can occur independent of LH, but the final stages of the differentiation process require hCG stimulation.

Animals↗

PubMed1992

Testicular Leydig cells in vitro secrete only inhibin alpha-subunits, whereas Leydig cell tumors can secrete bioactive inhibin.

The secretion of inhibin and inhibin-related proteins by testicular Leydig cells was studied by estimation of inhibin immunoreactivity and bioactivity in spent media of preparations of immature and mature rat Leydig cells and of tumor Leydig cells. Immature and mature rat Leydig cells expressed inhibin alpha-subunit mRNA and secreted immunoreactive inhibin. The immunoreactive material did not contain inhibin bioactivity as measured by an in vitro rat pituitary bioassay system. Results of pulse labeling with [35S]methionine followed by immunoprecipitation indicated that the inhibin-related proteins secreted by the immature Leydig cell preparations are 26 kDa and 44 kDa molecules. Mature rat Leydig cells only secreted the 44 kDa inhibin-related protein. Tumor Leydig cells (rat H540 and mouse MA10) secreted immunoreactive and bioactive inhibin, which could be immunoneutralized by an antibody against inhibin. In the culture medium of some H540 tumor Leydig cells 26 kDa and 42 kDa inhibin-related proteins and 30 kDa inhibin were detected. In culture medium of other H540 tumor Leydig cells, not secreting bioactive inhibin, only 26 kDa and 42 kDa inhibin-related proteins were found. No activin bioactivity was detected in culture media of immature rat Leydig cells, H540 and MA10 tumor Leydig cells. It is concluded that normal Leydig cells secrete inhibin alpha-subunits, while Leydig cell tumors can also secrete bioactive inhibin. Neither normal Leydig cells nor Leydig cell tumors produce activin.

Activins↗

PubMed1990

An enzymatic method for the isolation of mouse Leydig cells.

Mouse Leydig cells were obtained by dispersion of testes of adult animals (aged 6-15 months) with a neutral protease from B. polymxa (dispase; EC 3.4.24.4). The crude Leydig cell suspension was purified by centrifugation on a discontinuous Percoll gradient using a special centrifugation procedure similar to elutriation. The crude cell suspension obtained from 50 testes could be processed in one run. The combination of these two methods yielded 320000 +/- 53000 Leydig cells/testis (n = 554 testes). The purity of the Leydig cell fraction was greater than or equal to 95% (nucleated cells) based on morphological and histochemical (staining for naphthyl esterase) identification. The purified Leydig cells showed an excellent ultrastructural appearance. More than 98% excluded trypan blue. In the presence of NADPH, testosterone biosynthesis was increased only 1.15 +/- 0.1-fold yielding a "quality factor" of 34.8. Maximal hCG doses induced 10(6) purified Leydig cells to produce 5 nmol testosterone/hr. (40-fold stimulation in comparison to basal values). The Leydig cells showed 43100 +/- 2500 LH/hCG receptors and an association constant of Ka = 1.95 x 10(9) M-1. Due to the reproducibility of the method, to the yield as well as to the morphological and functional state of the purified Leydig cells at least 25% of laboratory animals could be saved.

Animals↗

PubMed1981

Primary cultures of Leydig cells from rat, mouse and pig: advantages of porcine cells for the study of gonadotropin regulation of Leydig cell function.

Primary cultures of interstitial cells were prepared from the testis of mice, rats, and pigs. The cells were grown in a defined medium supplemented with low (0.1%) serum and insulin, transferrin and epidermal growth factor. Comparisons of the interstitial cell cultures from the three species were made for plating efficiency, cell survival, maintenance of hCG receptors and maintenance of steroidogenic responsiveness to hCG. The porcine cultures had a higher plating efficiency and higher hCG receptor levels per cell than Leydig cells from either rodent. Additionally, the porcine cells showed an increase in testosterone (T) production with hCG stimulation throughout their lifespan in culture while the rodent cultures showed a decrease in T stimulation with time with no stimulation by day 6 in culture. These data indicate that species differences exist in hCG receptor concentrations per cell, the maintenance of hCG receptors and steroidogenic response in culture. The initial high survival, purity and continued functional response of porcine interstitial cell cultures make them a superior system for the study of gonadotropin regulation of Leydig cell function.

Animals↗

PubMed1991

Hormonal control of Leydig cell differentiation.

Leydig cell progenitors contain significant concentrations of androgen receptors. When the metabolism of DHT to 3 alpha-DIOL is blocked, DHT stimulates testosterone production by Leydig cell progenitors, most probably via an androgen receptor dependent mechanism. Rapid metabolism by 3 alpha-HSD may limit the potency of exogenous DHT to stimulate differentiation of Leydig cell progenitors in vitro. Insulin-like growth factor-I enhances androgen production by purified immature Leydig cells. The elevated sensitivity of immature Leydig cells versus adult Leydig cells to IGF-I stimulation indicates that this peptide hormone has a role in their differentiation during puberty.

Androgens↗

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↗