Influence of the cryptorchid testis on the regeneration of rat Leydig cells after administration of ethane dimethane sulphonate

1987 ◽  
Vol 112 (2) ◽  
pp. 197-NP ◽  
Author(s):  
G. P. Risbridger ◽  
J. B. Kerr ◽  
D. M. de Kretser

ABSTRACT Leydig cells were selectively eliminated from the testis by treatment with the cytotoxin, ethane dimethane sulphonate. Rats were then made unilaterally cryptorchid and the morphological and functional response of the interstitial tissue in abdominal compared with scrotal testes was examined for up to 8 weeks. Regeneration of new Leydig cells occurred more rapidly in the interstitial tissue of abdominally cryptorchid testes compared with the interstitial tissue of contralateral scrotal testes. More rapid recovery of Leydig cells was coincident with significant increases in the bioactivity of a local factor(s), collected from interstitial fluid of cryptorchid testes, which stimulated testosterone production by isolated Leydig cells in vitro. These results support the theory that the production of a local factor(s) plays a role in the regeneration of Leydig cells and is affected by damage to the seminiferous epithelium. J. Endocr. (1987) 112, 197–204

1987 ◽  
Vol 113 (1) ◽  
pp. 89-96 ◽  
Author(s):  
R. M. Sharpe ◽  
I. Cooper

ABSTRACT Four hormones have been identified by various authors as possible paracrine regulators of testicular Leydig cells. The aim of this study was to evaluate their effects on purified adult rat Leydig cells under various conditions in vitro, and then to assess whether comparable effects occurred in vivo. In agreement with previous findings, an LHRH agonist (LHRH-A) exerted clear-cut effects on testosterone secretion by Leydig cells both in vitro and in vivo. On its own, LHRH-A stimulated testosterone production by Leydig cells for up to 24 h in culture but inhibited testosterone production stimulated by human chorionic gonadotrophin (hCG) between 24 and 72 h of culture. In-vivo, unilateral intratesticular injection of adult rats with 1 ng LHRH-A resulted 5 h later in a significant increase in testosterone concentrations in testicular interstitial fluid (IF). Vasopressin exerted effects in vitro which were similar to those of LHRH-A. On its own, vasopressin stimulated testosterone production for up to 5 h of culture, but not thereafter, while in the presence of hCG, vasopressin inhibited testosterone production beyond 24 h of culture. The initial stimulatory effect of vasopressin on testosterone production occurred with concentrations of 1 nmol/l and higher, but the magnitude of stimulation (threefold or less) was considerably less than that induced by LHRH-A (ninefold) over the same time period. In contrast to LHRH-A, unilateral intratesticular injection of vasopressin in high doses (20 and 2 ng) had no effect on IF testosterone levels 5 h later. When Leydig cells were cultured in the presence of testicular IF, to approximate in-vivo conditions, there was marked stimulation of testosterone production, but the effects of vasopressin and LHRH-A in the presence of IF were comparable to those observed in its absence. Neither morphine nor oxytocin at concentrations of 0·1 μmol/l had any effect on testosterone production under any of the conditions of culture, and unilateral intratesticular injection of oxytocin, morphine or naloxone was without effect on the IF levels of testosterone. It is concluded that opiates and oxytocin are probably not involved in the paracrine regulation of Leydig cells, whereas vasopressin may play such a role. However, as the stimulatory effects of vasopressin were small in relation to those of LHRH-A and were not evident in vivo, the physiological significance of the effects of vasopressin are uncertain. J. Endocr. (1987) 113, 89–96


2003 ◽  
Vol 77 (5) ◽  
pp. 3297-3300 ◽  
Author(s):  
Ronan Le Goffic ◽  
Thomas Mouchel ◽  
Annick Ruffault ◽  
Jean-Jacques Patard ◽  
Bernard Jégou ◽  
...  

ABSTRACT Mumps virus is responsible for sterility. Here, we show that the mumps virus infects Leydig cells in vitro and totally inhibits testosterone secretion and that ribavirin in mumps virus-infected Leydig cell cultures completely restores testosterone production. Moreover, we show that gamma interferon-induced protein 10 (IP-10) is highly expressed by mumps virus-infected Leydig cells and that ribavirin does not block IP-10 production.


1990 ◽  
Vol 2 (3) ◽  
pp. 263 ◽  
Author(s):  
MP Hedger ◽  
JX Qin ◽  
DM Robertson ◽  
Kretser DM de

Immune responses within the mammalian gonads, and in particular the testis, are deficient in spite of adequate lymphatic drainage and the presence of lymphocytes and MHC II+ macrophages. There is considerable evidence from in vivo and in vitro studies that this 'suppression' of the immune system may be due, at least in part, to localized inhibition or regulation of normal lymphocyte and/or macrophage functions within the gonads. In the testis, both steroidal and non-steroidal products of the Leydig cells, including androgens, endorphins, and inhibin-related proteins, have been implicated in mediating this activity. In turn, a number of immune cell cytokines affect steroidogenic cell function in vitro. The studies described in this paper indicated that [3H]-thymidine incorporation by adult rat thymocytes in vitro was inhibited by conditioned medium collected from short-term incubations of Percoll-purified adult rat Leydig cells, but stimulated by testicular interstitial fluid and by conditioned medium collected from short-term incubations of adult rat seminiferous tubules. The factors responsible for these effects on thymocyte function appeared to be of large molecular weight, as they were retained by ultrafiltration membranes with exclusion limits of 10,000 or 30,000 daltons. It is hypothesized that an 'immunosuppressive' mechanism, principally mediated by non-steroidal factors secreted by the steroidogenic cells of the gonadal interstitial tissue, exists within the gonads in order to prevent activation of the immune system by germ cell antigens and growth factors associated with germ cell proliferation and differentiation. This mechanism probably acts in parallel with normal antigen-specific tolerance mechanisms operating at the gonadal level. As immune responses to germ cells are believed to be a significant causative factor in infertility, particularly in men, this represents an important area for further study.


1984 ◽  
Vol 62 (9) ◽  
pp. 1166-1169 ◽  
Author(s):  
M. Bernier ◽  
W. Gibb ◽  
R. Collu ◽  
J. R. Ducharme

For this study, purified immature porcine Leydig cells in primary culture were used. After 2 days of culture, the cells were incubated with dexamethasone (5 × 10−9, 1 × 10−7 M) for various periods of time (3–45 h). The media were discarded and treatment was repeated with or without the addition of human chorionic gonadotropin (HCG, 10 mIU/mL) for 3 h. Dexamethasone (10−7 M) decreased testosterone production of HCG-treated cells (up to 40%) in a time-dependent fashion while the lower dose was ineffective. The effect of varying doses (10−8 and 10−6 M) of natural glucocorticoids (corticosterone, cortisol) or synthetic glucocorticoids (triamcinolone, triamcinolone acetonide, betamethasone, dexamethasone) and that of a synthetic progestin (R-5020) on cultured Leydig cells was also studied. After 18 h of preincubation, the various synthetic but not the natural steroids nor R-5020, were able to decrease testosterone production of control and HCG-treated cells by 20–40%. Of a number of other hormonal and nonhormonal substances studied at concentrations of 10−9 – 10−5 M, only lysine8-vasopressin at a concentration of 10−6 M was able to inhibit testosterone production by these cells. These results indicate that dexamethasone and other synthetic glucocorticoids, and to a lesser degree lysine8-vasopressin, may exert a direct inhibitory effect on testosterone production by purified porcine immature Leydig cells in vitro.


2002 ◽  
Vol 61 (4) ◽  
pp. 493-503 ◽  
Author(s):  
Emilce S. Diaz ◽  
Eliana Pellizzari ◽  
Silvina Meroni ◽  
Selva Cigorraga ◽  
Livia Lustig ◽  
...  

1984 ◽  
Vol 102 (3) ◽  
pp. 319-327 ◽  
Author(s):  
R. M. Sharpe ◽  
I. Cooper ◽  
D. G. Doogan

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


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