Combined effect of triparanol and human chorionic gonadotrophin on the ultrastructure of the adult Leydig cell

1971 ◽  
Vol 113 (2) ◽  
pp. 249-258 ◽  
Author(s):  
J. Russo
Keyword(s):  
Leydig Cell ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Combined Effect

Direct in-vivo detection of atypical hormonal expression of a Sertoli-Leydig cell tumour following stimulation with human chorionic gonadotrophin

1993 ◽  
Vol 39 (4) ◽  
pp. 491-495 ◽  
Author(s):  
Ilan Cohen ◽  
Menahem Shapira ◽  
Solomon Cuperman ◽  
Shmuel Goldberger ◽  
Annette Siegal ◽  
...  
Keyword(s):  
Leydig Cell ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Cell Tumour ◽  
In Vivo Detection ◽  
Leydig Cell Tumour

Studies on the testicular source of inhibin and its route of secretion in rams: failure of the Leydig cell to secrete inhibin in response to a human chorionic gonadotrophin/LH stimulus

1991 ◽  
Vol 130 (1) ◽  
pp. 107-114 ◽  
Author(s):  
A. J. Tilbrook ◽  
D. M. de Kretser ◽  
I. J. Clarke
Keyword(s):  
Leydig Cell ◽  
Leydig Cells ◽  
Jugular Vein ◽  
Plasma Concentrations ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Spermatic Vein ◽  
Jugular Veins ◽  
Testicular Vein ◽  
Peripheral Plasma

ABSTRACT To determine whether Leydig cells produce inhibin in the ram, Leydig cells were stimulated by administering human chorionic gonadotrophin (hCG) or raising the levels of endogenous LH by an injection of gonadotrophin releasing hormone (GnRH). Plasma concentrations of testosterone increased in the 72 h after either a single injection (P < 0·05) or two injections (P < 0·01) of hCG. Plasma concentrations of inhibin were not significantly influenced by either one or two injections of hCG. Administration of GnRH (1 μg) caused an 11-fold increase in plasma concentrations of LH but did not influence concentrations of inhibin in either the jugular or testicular veins (pampiniform plexus). In contrast, concentrations of testosterone were increased by about fourfold in both jugular (P < 0·01) and testicular (P < 0·05) veins. The concentrations of inhibin in the testicular vein were 1·3-fold higher than in the peripheral plasma (P < 0·05) both before and following treatment with GnRH whereas the concentrations of testosterone were 18- to 21-fold greater than in peripheral concentrations. In view of the difference in concentrations of inhibin between testicular and jugular veins, in a further experiment a sample was taken from the jugular vein, a vein located in the tunica vasculosa of the testis (testicular vein) and from a vein (spermatic vein) and lymph vessels located in the spermatic cord. The mean (± s.e.m.) concentrations of inhibin were highest in the testicular lymph (45·93±4·21 μg/l; P < 0·001) compared with the peripheral (4·14±0·31 μg/l), spermatic (8·0±1·17 μg/l) or testicular (6·4±0·82 μg/l) plasma. Plasma concentrations of inhibin were significantly higher in the spermatic vein than in the testicular vein (P < 0·05) and jugular vein (P < 0·01), and concentrations of inhibin in the testicular vein were significantly (P < 0·05) higher than in the jugular vein. There were no significant differences in the concentrations of testosterone in the spermatic vein, testicular vein or testicular lymph but the concentrations of testosterone in the peripheral plasma were significantly (P < 0·05) less than in the testicular plasma or lymph. These results suggest that, in the ram, the Leydig cell does not respond to hCG or endogenous LH by secreting inhibin or by influencing other cells within the testis to secrete inhibin within the time-frame of these experiments. The low testicular to jugular differences in the concentration of inhibin and the high concentrations of inhibin in the testicular lymph suggest that the lymph may be an important route of secretion of inhibin from the testis in the ram. Journal of Endocrinology (1991) 130, 107–114

Proliferation and differentiation of possible Leydig cell precursors after destruction of the existing Leydig cells with ethane dimethyl sulphonate: the role of LH/human chorionic gonadotrophin

1989 ◽  
Vol 122 (3) ◽  
pp. 689-NP ◽  
Author(s):  
K. J. Teerds ◽  
D. G. de Rooij ◽  
F. F. G. Rommerts ◽  
R. van den Hurk ◽  
C. J. G. Wensing
Keyword(s):  
Leydig Cell ◽  
Proliferative Activity ◽  
Leydig Cells ◽  
Precursor Cells ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Adult Rats ◽  
Proliferation And Differentiation ◽  
Endocrine Factors

ABSTRACT The influence of LH levels on the proliferation and differentiation of possible Leydig cell precursors was investigated in adult rats, after the destruction of the existing Leydig cells with the cytotoxic drug ethane dimethyl sulphonate (EDS). In rats bearing a testosterone implant which prevented the rise in plasma LH levels and kept them within the normal range after the destruction of the Leydig cells, the proliferative activity of possible Leydig cell precursors still increased seven- to eightfold 2 days after EDS administration. Apparently, in this situation, locally produced factors, and not LH, may play a role in the stimulation of proliferation. The proliferative activity of the possible precursor cells could be further stimulated by treating rats with daily injections of human chorionic gonadotrophin (hCG) following EDS administration. It was concluded that the proliferative activity of possible Leydig cell precursors is probably regulated by both paracrine and endocrine factors. Almost no Leydig cells were formed in the rats bearing a testosterone implant during the first 4 weeks after EDS administration. When these rats were treated with hCG, starting 28 days after administration of EDS, a substantial number of Leydig cells was found after 2 days, and these cells also showed 3β-hydroxysteroid dehydrogenase (3β-HSD) and α-naphtyl esterase (α-NE) activity. When hCG treatment was started at 14 or 21 days after EDS administration, some cells with the nuclear characteristics of Leydig cells were present after 2 days, but no 3β-HSD or α-NE activity could be detected. Finally, when hCG treatment was started directly after EDS administration, a considerable number of Leydig cells was found 14 days after EDS, and some of these cells already showed 3β-HSD and α-NE activity. It is concluded that precursor cells are able to develop into advanced precursor cells at normal LH levels, and that the rate of development of new Leydig cells strongly depends upon LH/hCG levels. Journal of Endocrinology (1989) 122, 689–696

Effects of hypophysectomy and human chorionic gonadotrophin on Leydig cell function in mature rats

1990 ◽  
Vol 126 (3) ◽  
pp. 367-NP ◽  
Author(s):  
D. M. Stocco ◽  
K. J. Teerds ◽  
M. van Noort ◽  
F. F. G. Rommerts
Keyword(s):  
Leydig Cell ◽  
Leydig Cells ◽  
Cell Function ◽  
Fold Increase ◽  
Specific Protein ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Cell Functions ◽  
Complete Restoration ◽  
Hypophysectomized Rats

ABSTRACT The biochemical activities involved in the maintenance of Leydig cell functions, and the effects of hypophysectomy and human chorionic gonadotrophin (hCG) on these functions are largely unknown. In the present study, adult hypophysectomized rats were used as a model to determine the effects of these treatments on a number of biochemical and morphological parameters. After 33 days of hypophysectomy, the morphology of the Leydig cells had been drastically altered. In addition, α-naphthol and β-naphthol esterase activity as well as the steroidogenic capacity of the Leydig cells were greatly reduced at this time. In contrast, the level of sterol carrier protein 2 (SCP2), a Leydig cell-specific protein, was affected by hypophysectomy much less than the other parameters measured. Two daily injections of hCG to rats hypophysectomized for 31 days resulted in no change in the morphology of the Leydig cells, or in their proliferative activity. Non-specific esterase activities were also unaffected by 2 days of treatment with hCG. However, two injections of hCG to rats hypophysectomized for 31 days resulted in nearly complete restoration of steroidogenic capacity, and a 3·5-fold increase in the level of SCP2. These findings indicate that hypophysectomy results in significant morphological and biochemical changes in Leydig cells, and that hCG is capable of restoring some of these capacities within a short time. Journal of Endocrinology (1990) 126, 367–375

The aging Leydig cell: VI. Response of testosterone precursors to gonadotrophin in men

1982 ◽  
Vol 100 (3) ◽  
pp. 455-461 ◽  
Author(s):  
E. P. Murono ◽  
H. R. Nankin ◽  
T. Lin ◽  
J. Osterman
Keyword(s):  
Young Adults ◽  
Leydig Cell ◽  
Young Men ◽  
Significant Rise ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Aged Population ◽  
Small Peak ◽  
Early Peak ◽  
Old Men

Abstract. The effects of a single im injection of human chorionic gonadotrophin (hCG) on circulating testosterone precursor levels at 0, 1–6, 24, 48 and 72 h were examined in normal young adults (mean age 34 years) and normal aged men (mean age 74 years). Basal 08.30–09.00 h concentrations of androstenedione and dehydroepiandrosterone were lower in aged men while progesterone levels were not significantly different from young men. A significant biphasic increase of circulating progesterone was observed in young men, characterized by an early peak at 2 h (33% above basal) and a secondary peak at 24 h (49% above basal). In old men there were no increases in circulating progesterone levels following hCG treatment during the early (1–6 h) or late (24–72 h) periods. There were not discernable increases in circulating dehydroepiandrosterone levels following hCG administration in both groups of men. Androstenedione levels in young men did not change during the first 6 h following hCG but increased significantly at 48 and 72 h, while in old men there was a small peak at 4 h (which was not statistically significant) and a secondary significant rise at 48 and 72 h. However, early and late stimulated absolute levels for androstenedione were lower in the aged population. Thus, there are differences in precursor concentrations in the basal state and in response to hCG in aged men.

THE PRECISION OF THE OVARIAN ASCORBIC ACID DEPLETION TEST FOR LUTEINIZING HORMONE

1963 ◽  
Vol 43 (1) ◽  
pp. 155-160
Author(s):  
Jørgen Falck Larsen ◽  
Christian Hamburger
Keyword(s):  
Ascorbic Acid ◽  
Luteinizing Hormone ◽  
Clinical Analysis ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin

ABSTRACT Various modifications of the Parlow test for luteinizing hormone (ovarian ascorbic acid depletion in rats) were tried. Human chorionic gonadotrophin was used instead of hypophyseal luteinizing hormone. The precision of the method was found to be so low, however, that the test could not be used for routine clinical analysis. The low precision found in this and other laboratories is thought to be due to the strains of rats used.

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