Adult rat Sertoli cells secrete a factor or factors which modulate Leydig cell function

1987 ◽  
Vol 114 (3) ◽  
pp. 459-467 ◽  
Author(s):  
V. Papadopoulos ◽  
P. Kamtchouing ◽  
M. A. Drosdowsky ◽  
M. T. Hochereau de Reviers ◽  
S. Carreau
Keyword(s):  
Cyclic Amp ◽  
Sertoli Cell ◽  
Leydig Cell ◽  
Sertoli Cells ◽  
Leydig Cells ◽  
Cell Function ◽  
Cell Interaction ◽  
Adult Rats ◽  
Adult Rat ◽  
Stimulating Factor

ABSTRACT Production of testosterone and oestradiol-17β by Leydig cells from adult rats was stimulated by LH or dibutyryl cyclic AMP (10 and 2·5-fold respectively). The addition of spent medium from normal, hemicastrated or γ-irradiated rat seminiferous tubule cultures, as well as from Sertoli cell cultures, to purified Leydig cells further enhanced both basal (44 and 53% for testosterone and oestradiol-17β respectively) and LH-stimulated (56 and 18%) steroid output. Simultaneously, a decrease (20–30%) in intracellular cyclic AMP levels was observed. This stimulating factor (or factors) secreted by the Sertoli cells is different from LHRH, is of proteinic nature and has a molecular weight ranging between 10 000 and 50 000; its synthesis is not controlled by FSH nor by testosterone. This factor(s) involved in rat Leydig cell steroidogenesis, at a step beyond the adenylate cyclase, does not require protein synthesis for testosterone formation whereas it does for oestradiol-17β production. It should be noted that a germ cell–Sertoli cell interaction modulates the synthesis of this factor(s). J. Endocr. (1987) 114, 459–467

Cultured Sertoli cell-mediated FSH stimulatory effect on Leydig cell steroidogenesis

1985 ◽  
Vol 248 (2) ◽  
pp. E176-E181
Author(s):  
M. Benahmed ◽  
J. Reventos ◽  
E. Tabone ◽  
J. M. Saez
Keyword(s):  
Sertoli Cell ◽  
Leydig Cell ◽  
Sertoli Cells ◽  
Leydig Cells ◽  
Cell Function ◽  
Cell Activity ◽  
Defined Medium ◽  
Cell Number ◽  
Two Parameters ◽  
Leydig Cell Function

To determine the precise role of Sertoli cells in the stimulating effects of follicle stimulating hormone (FSH) on Leydig cell activity, porcine purified Leydig and Sertoli cells were cultured separately or together in a chemically defined medium in the absence or presence of porcine, FSH 50 ng/ml. Leydig cell activity was evaluated using two parameters: human chorionic gonadotropin (hCG) binding sites; and hCG-stimulated cAMP production and testosterone secretion. First, it was found that FSH increases Leydig cell activity in crude Leydig cell preparations (40–60% of Leydig cells), whereas it exerts no effect on purified Leydig cells (greater than 90% of Leydig cells). Second, FSH stimulates the activity of Leydig cells cocultured with Sertoli cells, whereas it remains without effect on purified Leydig cells cultured alone. This stimulating effect of FSH on Leydig cell activity is dependent on the Sertoli cell number in the coculture. These data 1) show that the stimulating effect of FSH on Leydig cell function is mediated by Sertoli cells and 2) support the concept of local control of Leydig cell function originating from Sertoli cells.

Increase in Leydig cell responsiveness in the unilaterally cryptorchid rat testis and its relationship to the intratesticular levels of testosterone

1984 ◽  
Vol 102 (3) ◽  
pp. 319-327 ◽  
Author(s):  
R. M. Sharpe ◽  
I. Cooper ◽  
D. G. Doogan
Keyword(s):  
Leydig Cell ◽  
Leydig Cells ◽  
Venous Blood ◽  
Cell Interaction ◽  
Adult Rats ◽  
Similar Reduction ◽  
Testosterone Production ◽  
Lh Releasing Hormone ◽  
Unilateral Cryptorchidism

ABSTRACT Adult rats were made unilaterally cryptorchid (UCD) and 6–7 weeks later Leydig cells were isolated from the scrotal and abdominal testes and their capacity to secrete testosterone in vitro was compared. Basal testosterone production by Leydig cells from the abdominal testes of UCD rats was lowered, compared with cells from the contralateral scrotal testes, whilst their responsiveness to both human chorionic gonadotrophin and an LH releasing hormone agonist was enhanced two- to threefold (P< 0·001) compared both with cells from the contralateral scrotal testes and with cells isolated from untreated rats of the same age. In the UCD rats, concentrations of testosterone in testicular interstitial fluid (IF) were reduced (P< 0·001) by 70–90% in abdominal, compared with scrotal, testes. A similar reduction was evident in the levels of testosterone in spermatic venous blood, and both this decrease and that in IF levels of testosterone varied according to the degree of testicular involution. The ontogeny of the above changes was investigated. After induction of unilateral cryptorchidism, the weight of the abdominal compared with the scrotal testis declined slowly, such that by day 5 there was only a 25% reduction in weight compared with a 70% reduction by day 40. In contrast, the levels of testosterone in IF from abdominal testes declined rapidly, such that by day 5 an 80% reduction was attained, compared with scrotal testes, with little further change by day 40. Hormone-stimulated testosterone production by Leydig cells isolated from the abdominal testes was unchanged or marginally reduced over the first 3 days compared with cells from the scrotal testes, but by day 5 there was a significant increase in responsiveness; this increase was of smaller magnitude than that evident at day 40. These results suggest a possible association between the fall in intratesticular levels of testosterone induced by unilateral cryptorchidism and the Leydig cell hypertrophy and hyper-responsiveness that occurs in the same testes. The implications with respect to altered Sertoli–Leydig cell interaction are discussed. J. Endocr. (1984) 102, 319–327

scholarly journals THE EFFECT OF CHRONIC EXPOSURE OF NICOTINE INHALATION TO THE COUNT OF SPERMATOGONIA, SERTOLI CELLS AND LEYDIG CELLS OF YOUNG WHITE RAT WISTAR STRAIN

2019 ◽  
Vol 26 (2) ◽  
Author(s):  
Aril Rizaldi ◽  
Doddy M Soebadi ◽  
Soetojo Soetojo
Keyword(s):  
Cell Count ◽  
Sertoli Cell ◽  
Leydig Cell ◽  
Sertoli Cells ◽  
Chronic Exposure ◽  
Leydig Cells ◽  
Control Group ◽  
Nicotine Exposure ◽  
Control Group Design ◽  
Wistar Strain

Objective: To analyze the difference in the number of spermatogonia, leydig cells and sertoli cells in young age of  white mice Wistar strain after inhalation of chronic nicotine exposure. Material & Method: Laboratory experimental study with post test only control group design, measurement of spermatogonium, leydig cell, sertoli cell in 5 groups of young male Wistar strain, negative control group and treatment group given nicotine exposure 0.5 mg, 1 mg, 2 mg, and 4 mg/kg body weight/day for 30 days. Results: A significant reduction in spermatogonium was found in the group given nicotine 0.5 mg/kgBW/day (p=0.048), 1 mg/kgBW/day (p=0.002), 2 mg/kgBW/day (p=0.002) and 4 mg/kgBW/day (p=0.000) when compared to the control group. Significant decreases were also seen in the group receiving 4 mg of nicotine exposure compared with 0.5 mg (p=0.018). Significant decrease in sertoli cell count was seen only in the nicotine group of 4 mg/kgBW/day compared with the control group (p=0.047). A significant decrease in leydig cell count was found in the nicotine 2 mg/kgBW/day (p=0.037) and nicotine group 4 mg/kgBW/day (p=0.023) when compared with the control group. Significant decreases were also found in the 4 mg/kgBW/day group compared to the 0.5 mg/kgBW/day group (p=0.004). In this study there were also a decrease in the number of spermatogonia, sertoli cells, and leydig cells in the increased dose of nicotine given although not statistically significant. Conclusion: Chronic exposure of nicotine per inhalation may decrease the number of spermatogonia, sertoli cells, and leydig cells. The higher the dose of nicotine given the greater the decrease in the number of spermatogonium cells, sertoli cells, and leydig cells that occur. This proves that nicotine is one of the causes of infertility in men.

Ethan-1,2-dimethanesulphonate reduces testicular oxytocin content and seminiferous tubule movements in the rat

1987 ◽  
Vol 112 (2) ◽  
pp. 311-NP ◽  
Author(s):  
H. D. Nicholson ◽  
R. T. S. Worley ◽  
S. E. F. Guldenaar ◽  
B. T. Pickering
Keyword(s):  
Leydig Cell ◽  
Seminiferous Tubule ◽  
Leydig Cells ◽  
Contractile Activity ◽  
Histological Study ◽  
Interstitial Cells ◽  
Seminiferous Tubules ◽  
Adult Rats ◽  
Adult Rat

ABSTRACT An oxytocin-like peptide is present in the interstitial cells of the testis, and testicular concentrations of oxytocin have been shown to increase seminiferous tubule movements in vitro. We have used the drug ethan-1,2-dimethanesulphonate (EDS), which depletes the Leydig cell population of the adult rat testis, to examine further the relationships between the Leydig cell, testicular oxytocin and tubular movements. Adult rats were injected i.p. with a single dose of EDS (75 mg/kg) or of vehicle (25% dimethyl sulphoxide). Histological study 3 and 10 days after treatment with EDS showed a reduction in the number of interstitial cells, and levels of oxytocin immunoreactivity were undetectable by radioimmunoassay. Immunostaining revealed very few oxytocin-reactive cells. Spontaneous contractile activity of the seminiferous tubules in vitro was also dramatically reduced, but could be restored by the addition of oxytocin to the medium. Four weeks after EDS treatment, the interstitial cells were similar to those in the control animals both in number and in immunostaining; immunoassayable oxytocin was present and tubular movements were normal. The EDS effect, seen at 3 and 10 days, was not altered by daily treatment with testosterone. However, repopulation of the testes with oxytocin-immunoreactive cells was not seen until 6 weeks in the testosterone-treated animals. We suggest that the Leydig cells are the main source of oxytocin immunoreactivity in the testis and that this oxytocin is involved in modulating seminiferous tubule movements and the resultant sperm transport. The results also imply that testosterone does not play a major role in controlling tubular activity in the mature rat. J. Endocr. (1987) 112, 311–316

scholarly journals Spermatogonial behavior in rats during radiation-induced arrest and recovery after hormone suppression

Reproduction ◽  
2013 ◽  
Vol 146 (4) ◽  
pp. 363-376 ◽  
Author(s):  
Amanda V Albuquerque ◽  
Fernanda R C L Almeida ◽  
Connie C Weng ◽  
Gunapala Shetty ◽  
Marvin L Meistrich ◽  
...  
Keyword(s):  
Sertoli Cell ◽  
Leydig Cell ◽  
Sertoli Cells ◽  
Leydig Cells ◽  
Gradual Increase ◽  
Immunohistochemical Analysis ◽  
Type A ◽  
Kit Ligand ◽  
Kit Receptor ◽  
Radiation Induced

Ionizing radiation has been shown to arrest spermatogenesis despite the presence of surviving stem spermatogonia, by blocking their differentiation. This block is a result of damage to the somatic environment and is reversed when gonadotropins and testosterone are suppressed, but the mechanisms are still unknown. We examined spermatogonial differentiation and Sertoli cell factors that regulate spermatogonia after irradiation, during hormone suppression, and after hormone suppression combined with Leydig cell elimination with ethane dimethane sulfonate. These results showed that the numbers and cytoplasmic structure of Sertoli cells are unaffected by irradiation, only a few type A undifferentiated (Aund) spermatogonia and even fewer type A1 spermatogonia remained, and immunohistochemical analysis showed that Sertoli cells still produced KIT ligand (KITLG) and glial cell line-derived neurotrophic factor (GDNF). Some of these cells expressed KIT receptor, demonstrating that the failure of differentiation was not a result of the absence of the KIT system. Hormone suppression resulted in an increase in Aund spermatogonia within 3 days, a gradual increase in KIT-positive spermatogonia, and differentiation mainly to A3 spermatogonia after 2 weeks. KITL (KITLG) protein expression did not change after hormone suppression, indicating that it is not a factor in the stimulation. However, GDNF increased steadily after hormone suppression, which was unexpected since GDNF is supposed to promote stem spermatogonial self-renewal and not differentiation. We conclude that the primary cause of the block in spermatogonial development is not due to Sertoli cell factors such (KITL\GDNF) or the KIT receptor. As elimination of Leydig cells in addition to hormone suppression resulted in differentiation to the A3 stage within 1 week, Leydig cell factors were not necessary for spermatogonial differentiation.

Effects of FSH on Leydig cell morphology and function in the hypogonadal mouse

1992 ◽  
Vol 135 (3) ◽  
pp. 517-NP ◽  
Author(s):  
P. J. O'Shaughnessy ◽  
M. K. Bennett ◽  
I. S. Scott ◽  
H. M. Charlton
Keyword(s):  
Leydig Cell ◽  
Sertoli Cells ◽  
Leydig Cells ◽  
Cell Function ◽  
Reductase Activity ◽  
Fold Increase ◽  
Paracrine Factors ◽  
Androgen Synthesis ◽  
Congenital Deficiency ◽  
Stimulation Of

ABSTRACT The hypogonadal (hpg) mouse has a congenital deficiency in gonadotrophin-releasing hormone and the gonads consequently lack exposure to endogenous gonadotrophins during development. To determine the effect of FSH on Leydig cell function in these animals adult hpg mice were injected twice daily with FSH (2 μg injections) or LH (40 ng injections, the presumed LH contamination of FSH used). Following FSH treatment there was a clear stimulation of the seminiferous epithelium and in animals injected with FSH plus [3H]thymidine, the incorporation of label was largely confined to the germ cells with no apparent uptake by the Sertoli cells. In FSH-treated testes the Leydig cells contained numerous large lipid droplets, similar to the unstimulated hpg testis. There was no evidence of the interstitial hyperplasia which is observed following injection of high doses of LH (2 pg twice daily). There was no change in basal androgen content of the testis in vivo following FSH treatment but injection of a maximal dose of human chorionic gonadotrophin (hCG), 1 h before death, markedly increased testicular androgen content only in the FSH-treated group. Testicular androgen production in vitro was significantly increased following FSH treatment both under basal conditions (FSH-treated, 17·4 pmol/testis; control, 1·46 pmol/testis) and during stimulation by hCG (FSH-treated, 940 pmol/testis; control, 81 pmol/testis). Associated with the increased androgen production following FSH treatment there were significant increases in the activities of three steroidogenic enzymes; cholesterol side-chain cleavage (186-fold increase over control), 17α-hydroxylase (103-fold increase) and 17-ketosteroid reductase (177-fold increase). The fourth enzyme involved in androgen synthesis, 3β-hydroxysteroid dehydrogenase, shows relatively high activity in the control hpg testis and was only increased by sixfold following FSH treatment. There was no effect of FSH on 5α-reductase activity. Results show that FSH causes a marked stimulation of the steroidogenic capacity of the hpg testis. Leydig cells do not contain FSH receptors and it is assumed that FSH acts through paracrine factors released by the Sertoli cells. Journal of Endocrinology (1992) 135, 517–525

FSH regulates cultured Leydig cell function via Sertoli cell proteins: An in vitro study

1985 ◽  
Vol 132 (2) ◽  
pp. 729-734 ◽  
Author(s):  
M. Benahmed ◽  
C. Grenot ◽  
E. Tabone ◽  
P. Sanchez ◽  
A.M. Morera
Keyword(s):  
Sertoli Cell ◽  
Leydig Cell ◽  
Cell Function ◽  
In Vitro Study ◽  
Vitro Study ◽  
Leydig Cell Function

Testicular serotonin is related to mast cells but not to Leydig cells in the rat

1995 ◽  
Vol 146 (1) ◽  
pp. 15-21 ◽  
Author(s):  
R Aguilar ◽  
F Antón ◽  
C Bellido ◽  
E Aguilar ◽  
F Gaytan
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Leydig Cell ◽  
Leydig Cells ◽  
Interstitial Fluid ◽  
Ventral Prostate ◽  
Adult Rats ◽  
Cell Numbers ◽  
Oestradiol Benzoate ◽  
Testicular Capsule

Abstract Testicular serotonin (5HT) concentrations were determined by HPLC in the testes of rats treated neonatally with oestradiol benzoate (EB) and in adult rats treated with the Leydig cell cytotoxic ethylene dimethane sulphonate (EDS). 5HT concentrations were related to mast cell numbers. EB-treated rats showed an accumulation of mast cells in the testes at 35 and 70 days of age and increased 5HT concentrations in both the interstitial fluid and the testicular capsule, whereas no increases in 5HT concentrations or in the number of mast cells were found for the ventral prostate of these animals. On the contrary, 5HT concentrations were not related to the number of Leydig cells. In EB-treated rats, in which Leydig cells were nearly absent at 35 days of age, 5HT concentrations were significantly increased. Furthermore, EDS-treated rats did not show significant changes in 5HT concentrations, in spite of the elimination of Leydig cells. These data suggest that mast cells are a major source of serotonin in the rat testis. Journal of Endocrinology (1995) 146, 15–21

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