Immunocytochemical localization of hFSH as an index of Sertoli cell function in the human testis

1987 ◽  
Vol 116 (3) ◽  
pp. 333-338 ◽  
Author(s):  
Doug J. Yoon ◽  
Mircea Golimbu ◽  
Roger Schinella ◽  
Bruce Stein ◽  
Charles A. Sklar ◽  
...  

Abstract. The FSH receptor in the human testis has not been well characterized in vivo. Using an immunoperoxidase technique we have attempted the immunocytochemical localization of FSH in testicular tissue from patients with a variety of disorders including oligo- or azoospermia (N = 6), cryptorchidism (N = 3), and prostatic carcinoma (N = 3). Specific staining for hFSH was observed inside the seminiferous tubule, generally near the basal membrane in all except the cryptorchid patients. Specific staining was also localized in the luminal area of the seminiferous tubule. In most cases, FSH-positive cells were also found in the interstitium, with a minority of the cells being macrophages. The latter were more prevalent in the undescended testes and in orchiectomy specimens from patients with prostatic cancer. The pattern of FSH localization observed in this study probably represents receptorbound hormone, and may reflect damage to the Sertoli cell and its tight junctions. Further study of the changes in receptor distribution as an indication of Sertoli cell malfunction, may be helpful in our understanding of human testicular disorders.

2007 ◽  
Vol 76 (2) ◽  
pp. 223-229 ◽  
Author(s):  
P. Massányi ◽  
N. Lukáč ◽  
J. Zemanová ◽  
A. V. Makarevich ◽  
P. Chrenek ◽  
...  

The aim of this study was to describe the effects of nickel (NiCl2) on murine testicular structure. Experimental animals were injected intraperitoneally with a single dose of 20 mg NiCl2 per kg of body mass (group A, n = 5) and 40 mg NiCl2 per kg b. m. (group B, n = 5). The group without injection (n = 5) was the control (C). Animals were killed 48 hours after administration of nickel. The body mass of animals, the mass of testes and the testes : body mass ratio were not significantly affected. In both experimental groups a significant (p < 0.001) decrease of germinal epithelium in comparison with control group was observed. The relative volume of the interstitium was increased but not significantly in both experimental groups. An increase in the relative volume of the lumen was registered in both experimental groups in comparison with the control group. The qualitative analysis detected a dilatation of blood vessels in the interstitium, undulation of the basal membrane and several empty spaces in the germinal epithelium. The diameter (n = 150) of the seminiferous tubule was markedly (p < 0.05) decreased in both experimental groups (A, B) compared to control group. The height of the germinal epithelium showed a significant decrease (p < 0.05 - 0.001) after nickel administration. Evaluation of the lumen diameter in the seminiferous tubule showed a significant increase in both experimental groups. The data of the perimeter of seminiferous tubules corresponded with those of the seminiferous tubule diameter. TUNEL assay detected a higher frequency of localized apoptosis in the interstitium of nickel-administered animals compared to control group. Our findings clearly suggest a negative effect of nickel on the structure as well as on the function of the seminferous epithelium at the site of spermatozoa production.


1986 ◽  
Vol 111 (1) ◽  
pp. 128-132 ◽  
Author(s):  
Outi Hovatta ◽  
I. Huhtaniemi ◽  
T. Wahlström

Abstract. The localisation of endogenous FSH and LH was studied in 4 inguinal adult human testes by the immunoperoxidase technique utilising antisera against the β-subunits of human FSH and LH. The content of available FSH and LH receptors was determined by radioreceptor assay. The Sertoli cells and about 10% of cells in the intersitium the Leydig cells, possibly the testicular macrophages, were similarly FSH-positive in cryptorchidism and control testes. The FSH receptor levels per testis were significantly lower in cryptorchidism than in control testes. Also the localisation of LH in Leydig cells in cryptorchidism was similar to the control testes, but the LH receptor level was significantly lower. These data bring further evidence for Leydig and Sertoli cell malfunction in the inguinal human testis.


1997 ◽  
Vol 21 (8) ◽  
pp. 1409-1417 ◽  
Author(s):  
Qianlong Zhu ◽  
David H. Van Thiel ◽  
Judith S. Gavaler
Keyword(s):  

1979 ◽  
Vol 90 (3) ◽  
pp. 544-551 ◽  
Author(s):  
E. Nieschlag ◽  
E. J. Wickings ◽  
J. Mauss

ABSTRACT In order to detect any possible Leydig cell dysfunction associated with male infertility, the endocrine capacity of the testes was investigated in vivo and in vitro in 21 infertile men. Plasma testosterone was determined before and after 3 days of hCG stimulation. Testicular tissue obtained by bilateral biopsies was subjected to (1) histological examination, (2) determination of basal testosterone concentration and (3) incubation with hCG. Patients were grouped according to histology. In vitro basal and stimulated testicular testosterone was similar in patients with normal histology, Sertoli-cell-only syndrome and spermatogenic arrest. Tissue from patients with Leydig cell hyperplasia showed 3-fold higher basal testosterone levels and a greater response to hCG. All patients had plasma testosterone levels and responses to hCG in the normal range. There was no significant correlation between the data obtained in vivo and in vitro, indicating that testosterone determinations in peripheral blood do not necessarily reflect the intratesticular situation. There was no evidence for gross abnormality in Leydig cell function accompanying disturbed spermatogenesis.


1995 ◽  
Vol 108 (3) ◽  
pp. 917-925
Author(s):  
N. Gerard ◽  
A. Corlu ◽  
B. Kneip ◽  
H. Kercret ◽  
M. Rissel ◽  
...  

We have identified a liver-regulating protein involved in cell contact-mediated regulation of Sertoli cell function by primary spermatocytes in rat testis. Liver-regulating protein was studied using monoclonal antibody L8 prepared from rat primitive biliary epithelial cells. This molecule was located in vivo at the interface of Sertoli cells and spermatocytes, and expressed in a stage-dependent manner (expression peaked on leptotene-zygotene spermatocytes). In vitro, the liver-regulating protein was found on Sertoli cell, spermatocyte and early spermatid membranes. Immunoaffinity procedures revealed two peptides of 85 and 73 kDa for Sertoli cells, while spermatocytes and spermatids displayed a single smaller peptide of 56 kDa. The involvement of the liver-regulating protein in cell interaction-mediated regulation of Sertoli cell was assessed in vitro by tracing Sertoli cell transferrin and inhibin secretion, as well as mRNA synthesis in spermatocyte-Sertoli cell cocultures and in rat liver biliary epithelial cell-Sertoli cell cocultures, performed in the presence or absence of monoclonal antibody L8. Inhibition of the spermatocyte- and liver biliary epithelial cell-stimulated secretion of transferrin and inhibin by Sertoli cells was observed in the presence of antibody, whereas spermatocyte adhesiveness was unchanged. Using northern blot analysis, the steady state levels of transferrin mRNA decreased when the anti-liver-regulating protein antibody was added to the Sertoli cell-spermatocyte cocultures or to the Sertoli cell-liver biliary epithelial cell cocultures. The data demonstrate the role of the liver-regulating protein in cell-cell contact-mediated regulation of Sertoli function by primary spermatocytes and the important implications of this cell contact-dependent control in testicular activity.


2017 ◽  
Vol 29 (7) ◽  
pp. 1369 ◽  
Author(s):  
Renata S. Tavares ◽  
Joana M. D. Portela ◽  
Maria I. Sousa ◽  
Paula C. Mota ◽  
João Ramalho-Santos ◽  
...  

Besides known factors that may cause male infertility, systemic diseases such as diabetes mellitus may further exacerbate a decline in male fertility. This metabolic disease, clinically characterised by a hyperglycaemic phenotype, has devastating consequences in terms of human health, with reproductive dysfunction being one of the associated clinical complications. Nonetheless, the mechanisms responsible for such alterations are still poorly understood due to the multiplicity of factors involved in the induced pathophysiological changes. With this in mind, we focused on the main mediator of diabetes-associated alterations and performed an in vitro approach to address the effects of high glucose conditions on spermatogenesis, avoiding other confounding in vivo factors. Mouse (5 days post partum) testis fragments were cultured on agar gel stands at a gas–liquid interface with either 5, 25 or 50 mM D-glucose for 3 weeks. Stereological analysis revealed that high D-glucose levels increased Sertoli cell number (P < 0.05) and decreased tubular luminal area (P < 0.01), suggesting an impairment of this somatic cell type. Moreover, higher proliferative activity in a TM4 Sertoli cell line exposed to high D-glucose was found (P < 0.05) without compromising cell viability (P > 0.05), further suggesting altered Sertoli cell maturation. Overall, high D-glucose concentrations may lead to impairment of Sertoli cell function, which, given their significant role in spermatogenic control, may compromise male fertility.


1990 ◽  
Vol 34 (5-6) ◽  
pp. 254-259 ◽  
Author(s):  
A. Tsatsoulis ◽  
S.M. Shalet ◽  
I.D. Morris ◽  
D.M. de Kretser

2021 ◽  
Vol 31 (1) ◽  
Author(s):  
Marion Lapoirie ◽  
Frederique Dijoud ◽  
Hervé Lejeune ◽  
Ingrid Plotton

Abstract Background Androgens are well known to be necessary for spermatogenesis. The purpose of this study was to determine Sertoli cell responsiveness to androgens according to age from birth to puberty. Results Testicular tissue samples were studied in a population of 84 control boys classified into seven groups according to age: group 1 (1–30 days), group 2 (1–3 months), group 3 (3–6 months), group 4 (0.5–3 years), group 5 (3–6 years), group 6 (6–12 years), and group 7 (12–16 years). We compared these data with those of 2 situations of pathology linked to androgens: 1/premature secretion of testosterone: 4 cases of Leydig cell tumor (LCT) in childhood; and 2 /defect of androgen receptors (AR): 4 cases of complete form of insensitivity to androgen syndrome (CAIS). In control boys, AR immunoreactivity (ir) in Sertoli cells appeared between 4.6 and 10.8 years of age, Anti-Mullerian Hormone (AMH) ir in Sertoli cells disappeared between 9.2 and 10.2 years of age. Connexin 43 (Cx43) ir in Sertoli cells and histological features of the onset of spermatogenesis appeared between 10.8 and 13,8 years of age. Cx43 ir was significantly higher in 12–16 year-olds than in younger boys. In case of CAIS, no spermatogenesis was observed, both AR and Cx43 ir were undetectable and AMH ir was elevated in Sertoli cells even at pubertal age. In the vicinity of LCTs, spermatogenesis occurred and both AR and Cx43 ir were strongly positive and AMH ir in Sertoli cells was low for age. Conclusions Androgen action on Sertoli cells is required for onset of spermatogenesis and premature androgen secretion by LCT can induce spermatogenesis in the vicinity of the tumor. AR ir appeared earlier than onset of spermatogenesis, with large interindividual variability. The timing and mechanisms of Sertoli cell responsiveness to androgens are important issues for understanding the induction of spermatogenesis at puberty.


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