Steroid metabolism by a tumour of the specific gonadal stroma in a child

1982 ◽  
Vol 99 (4) ◽  
pp. 624-629 ◽  
Author(s):  
Alicia Barmach de Niepomniszcze ◽  
Marco A. Rivarola ◽  
Héctor E. Chemes ◽  
César Bergadá

Abstract. A study of steroid metabolism by a tumour of the specific gonadal stroma was carried out in a 10 year old boy. Tumours developed in the two testes from multiple foci, and clinically, no signs of sexual development were evident. Four testicular enzymes necessary for testosterone biosynthesis were estimated in the child, in two adult controls, and in three pre-pubertal boys with male pseudohermaphroditism but normal tests of Leydig cell function. 17α-Hydroxylase and 17β-hydroxysteroid dehydrogenase were similar in the five controls and in the gonad with the tumour, while 17,20-desmolase and 3β-hydroxysteroid dehydrogenase were grossly deficient in the child with the tumour. These enzyme deficiencies might explain the absence of peripheral virilization in a boy with a tumour of Leydig and Sertoli cells.

1978 ◽  
Vol 46 (4) ◽  
pp. 593-603 ◽  
Author(s):  
WALTER J. MEYER ◽  
BRUCE S. KEENAN ◽  
LUIZ DE LACERDA ◽  
I. PARK JAMES ◽  
HOWARD E. JONES ◽  
...  

2007 ◽  
Vol 19 (5) ◽  
pp. 664 ◽  
Author(s):  
S. Haeussler ◽  
R. Claus

The glucocorticoid (GC)–cortisol receptor (GCR)–11β-hydroxysteroid dehydrogenase 2 (11β-HSD2) system is involved in the regulation of Leydig cell function and spermatogenesis in mature animals. Herein, we describe the expression of the GCR and 11β-HSD2 and the occurrence of apoptosis during fetal development. Male fetuses were collected from Weeks 6, 10, 13, and 15 of pregnancy and from neonates. The testes were used for the immunocytochemical staining of GCR, 11β-HSD2 and for terminal deoxyribonucleotidyl transferase-mediated dUTP–digoxigenin nick end-labelling (TUNEL) staining of apoptosis. Apoptosis did not occur in any Leydig cells, but approximately 30% expressed GCR and 11β-HSD2. The number of GCR-positive cells was similar at all stages, but the number of 11β-HSD2-positive cells tended to be higher at Weeks 6 and 15. Steroid synthesis was also higher compared with Weeks 10 and 13. Apoptosis occurred in only a few germ cells. Nearly all germ cells were GCR positive at Weeks 10 and 13, when 11β-HSD2 was also increased. The total number of 11β-HSD2-positive germ cells was approximately 30%. Thus, elevated GCR expression coincided with the differentiation of gonocytes to spermatogonia and their migration to the basal lamina.


1975 ◽  
Vol 6 (2) ◽  
pp. 95-99 ◽  
Author(s):  
R. Scholler ◽  
M. Roger ◽  
P. Leymarie ◽  
M. Castanier ◽  
J.E. Toublanc ◽  
...  

1992 ◽  
Vol 8 (3) ◽  
pp. 73-83 ◽  
Author(s):  
Herv� Lejeune ◽  
Mourad Skalli ◽  
Pierre G. Chatelain ◽  
Odile Avallet ◽  
Jos� M. Saez

1985 ◽  
Vol 248 (2) ◽  
pp. E176-E181
Author(s):  
M. Benahmed ◽  
J. Reventos ◽  
E. Tabone ◽  
J. M. Saez

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.


1974 ◽  
Vol 77 (1_Suppl) ◽  
pp. S61
Author(s):  
R. Mies ◽  
D. Heesen ◽  
W. Winkelmann

1985 ◽  
Vol 132 (2) ◽  
pp. 729-734 ◽  
Author(s):  
M. Benahmed ◽  
C. Grenot ◽  
E. Tabone ◽  
P. Sanchez ◽  
A.M. Morera

1999 ◽  
Vol 17 (1) ◽  
pp. 173-173 ◽  
Author(s):  
Peter Meidahl Petersen ◽  
Aleksander Giwercman ◽  
Steen W. Hansen ◽  
Jørgen G. Berthelsen ◽  
Gedske Daugaard ◽  
...  

PURPOSE: To elucidate the biologic association between germ cell neoplasia and testicular dysfunction, through investigation of Leydig cell function and semen quality in men with carcinoma-in-situ (CIS) of the testis. PATIENTS AND METHODS: We examined two groups of men, unilaterally orchidectomized for testicular cancer. Biopsy of the contralateral testis had showed CIS in a group of 24 patients and no evidence of CIS in the other group of 30 patients. Semen quality and serum levels of testosterone, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) were compared in these two groups of men after orchidectomy but before further treatment for testicular cancer. RESULTS: Significantly higher LH levels (median, 8.1 IU/L v 4.8 IU/L; P < .001) and generally lower testosterone levels (median, 12.5 nmol/L v 15.5 nmol/L; P = .13) were found in the CIS group. The proportion of patients with Leydig cell dysfunction was higher in the group of patients with CIS (11 of 24) than in the group of patients without (two of 30) (P = .01). Sperm concentration and total sperm count were significantly lower (P < .001) in patients with CIS (median, 0.03 × 106/mL and 0.10 × 106, respectively) than in patients without (median, 9.1 × 106/mL and 32 × 106, respectively), whereas the levels of FSH were significantly higher (P < .001) in the former group of men (median, 19.6 IU/L v 9.0 IU/L). CONCLUSION: Not only spermatogenesis but also Leydig cell function is impaired in testes with CIS. This impairment could be due to common factors in the pathogenesis of germ cell neoplasm and testicular dysfunction. Alternatively, CIS cells may have a negative impact on Leydig cell function.


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