Stimulatory and inhibitory factors of Leydig cell steroidogenesis are secreted simultaneously by the rat seminiferous tubules and do not affect Leydig cell inhibin production in vitro

1994 ◽  
Vol 6 (6) ◽  
pp. 693 ◽  
Author(s):  
JR McFarlane ◽  
Kretser DM de ◽  
GP Risbridger
Keyword(s):  
Conditioned Medium ◽  
Leydig Cell ◽  
Leydig Cells ◽  
Seminiferous Tubules ◽  
Low Doses ◽  
Adult Rat ◽  
Testosterone Production ◽  
Significant Reversal ◽  
The Mean

The effect of conditioned medium from rat seminiferous tubules (at Stages VII-VIII and Stages IX-VI) cultured with or without follicle-stimulating hormone (FSH) on the production of testosterone and immunoactive inhibin by Leydig cells was examined. Low doses of conditioned medium from unstimulated tubules at Stages VII-VIII significantly (P < 0.05) increased the mean testosterone production to greater than 31 +/- 11% over that achieved with luteinizing hormone (LH) alone. At the highest dose, the conditioned medium significantly inhibited (P < 0.05) LH-stimulated testosterone production by 13 +/- 7%. Low doses of conditioned medium from unstimulated tubules at Stages IX-VI increased the mean testosterone production to 22 +/- 10%, whereas at higher doses, a significant reversal in the stimulation occurred although not to the same extent as that found with medium from tubules at Stages VII-VIII. Conditioned medium from FSH-stimulated tubules at Stages VII-VIII and Stages IX-VI, significantly increased testosterone production to 39 +/- 7% and 31 +/- 13% respectively. Immunoactive inhibin production by the Leydig cells remained unaffected by exposure to conditioned medium from FSH stimulated and unstimulated tubules at Stages VII-VIII and Stages IX-VI. The data demonstrate that tubule culture medium contains FSH-modulated activities which can specifically stimulate and inhibit testosterone synthesis by adult rat Leydig cells in vitro and therefore explains the contradictory reports in the literature.

Intragonadal regulation of immune system functions

1990 ◽  
Vol 2 (3) ◽  
pp. 263 ◽  
Author(s):  
MP Hedger ◽  
JX Qin ◽  
DM Robertson ◽  
Kretser DM de
Keyword(s):  
Immune System ◽  
Immune Responses ◽  
Germ Cell ◽  
Conditioned Medium ◽  
Leydig Cells ◽  
Seminiferous Tubules ◽  
Interstitial Tissue ◽  
Short Term ◽  
Adult Rat

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.

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 Mumps Virus Decreases Testosterone Production and Gamma Interferon-Induced Protein 10 Secretion by Human Leydig Cells

2003 ◽  
Vol 77 (5) ◽  
pp. 3297-3300 ◽  
Author(s):  
Ronan Le Goffic ◽  
Thomas Mouchel ◽  
Annick Ruffault ◽  
Jean-Jacques Patard ◽  
Bernard Jégou ◽  
...  
Keyword(s):  
Cell Cultures ◽  
Leydig Cell ◽  
Leydig Cells ◽  
Mumps Virus ◽  
Gamma Interferon ◽  
Testosterone Secretion ◽  
Testosterone Production

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.

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 Androgen profiles during pubertal Leydig cell development in mice

Reproduction ◽  
2010 ◽  
Vol 140 (1) ◽  
pp. 113-121 ◽  
Author(s):  
Xiufeng Wu ◽  
Ramamani Arumugam ◽  
Ningning Zhang ◽  
Mary M Lee
Keyword(s):  
Leydig Cell ◽  
Developmental Changes ◽  
Side Chain ◽  
Adult Rat ◽  
Testosterone Production ◽  
Chain Cleavage ◽  
Cleavage Enzyme ◽  
Species Specific

Postnatal Leydig cell (LC) development in mice has been assumed empirically to resemble that of rats, which have characteristic hormonal profiles at well-defined maturational stages. To characterize the changes in LC function and gene expression in mice, we examined reproductive hormone expression from birth to 180 days, and quantified in vivo and in vitro production of androgens during sexual maturation. Although the overall plasma androgen and LH profiles from birth through puberty were comparable to that of rats, the timing of developmental changes in androgen production and steroidogenic capacity of isolated LCs differed. In mice, onset of androgen biosynthetic capacity, distinguished by an acute rise in androstenedione and testosterone production and an increased expression of the steroidogenic enzymes, cytochrome P450 cholesterol side-chain cleavage enzyme and 17α-hydroxylase, occurred at day 24 (d24) rather than at d21 as reported in rats. Moreover, in contrast to persistently high testosterone production by pubertal and adult rat LCs, testosterone production was maximal at d45 in mice, and then declined in mature LCs. The murine LCs also respond more robustly to LH stimulation, with a greater increment in LH-stimulated testosterone production. Collectively, these data suggest that the mouse LC lineage has a delayed onset, and that it has an accelerated pace of maturation compared with the rat LC lineage. Across comparable maturational stages, LCs exhibit species-specific developmental changes in enzyme expression and capacity for androgen production. Our results demonstrate distinct differences in LC differentiation between mice and rats, and provide informative data for assessing reproductive phenotypes of recombinant mouse models.

Effects of clodronate-containing liposomes on testicular macrophages and Leydig cells in vitro

1997 ◽  
Vol 155 (1) ◽  
pp. 87-92 ◽  
Author(s):  
DE Brigham ◽  
G Little ◽  
YO Lukyanenko ◽  
JC Hutson
Keyword(s):  
Direct Effect ◽  
Dose Response ◽  
Leydig Cell ◽  
Leydig Cells ◽  
Direct Effects ◽  
Testosterone Production ◽  
Identical Response ◽  
Testicular Macrophages

We undertook the present studies to determine if clodronate-containing liposomes have direct effects on Leydig cells. Macrophages and Leydig cells were isolated and maintained separately in culture. Following treatment with clodronate-containing liposomes, macrophages were killed in a dose-response fashion over a range of 5-200 microliters liposomes. By comparison, a 500 microliters dose was required to kill Leydig cells, but this was not dependent upon clodronate since liposomes containing buffer elicited an identical response. The concentration of testosterone in medium from Leydig cells treated with clodronate-containing liposomes was significantly reduced compared with untreated cells. However, we subsequently found that liposomes can adsorb testosterone. Therefore, testosterone production was determined at various times following removal of liposomes from Leydig cells, thereby circumventing this complication. It was found that testosterone production was not altered by liposomes under these conditions. Finally, free clodronate had no effect on testosterone production, even at doses representing the amount present within the 500 microliters dose of liposomes. In summary, clodronate-containing liposomes killed testicular macrophages at a far smaller dose than required to kill Leydig cells. Most importantly, neither liposomes no free clodronate had a direct effect on testosterone production. Thus, clodronate-containing liposomes represent a valuable tool to study Leydig cell-macrophage interactions.

scholarly journals Adrenocorticotropic Hormone Directly Stimulates Testosterone Production by the Fetal and Neonatal Mouse Testis

Endocrinology ◽  
2003 ◽  
Vol 144 (8) ◽  
pp. 3279-3284 ◽  
Author(s):  
P. J. O’Shaughnessy ◽  
L. M. Fleming ◽  
G. Jackson ◽  
U. Hochgeschwender ◽  
P. Reed ◽  
...  
Keyword(s):  
Leydig Cell ◽  
Leydig Cells ◽  
Cell Function ◽  
Expressed Sequence Tag ◽  
Acth Stimulation ◽  
Testosterone Production ◽  
Testicular Cells ◽  
Testicular Steroidogenesis ◽  
Fetal Leydig Cells

Abstract Adult Leydig cell steroidogenesis is dependent on LH but fetal Leydig cells can function independently of gonadotropin stimulation. To identify factors that may be involved in regulation of fetal Leydig cells expressed sequence tag libraries from fetal and adult testes were compared, and fetal-specific genes identified. The ACTH receptor [melanocortin type 2 receptor (Mc2r)] was identified within this fetal-specific group. Subsequent real-time PCR studies confirmed that Mc2r was expressed in the fetal testis at 100-fold higher levels than in the adult testis. Incubation of fetal or neonatal testes with ACTH in vitro stimulated testosterone production more than 10-fold, although ACTH had no effect on testes from animals aged 20 d or older. The steroidogenic response of fetal and neonatal testes to a maximally stimulating dose of human chorionic gonadotropin was similar to the response shown to ACTH. The ED50 for ACTH, measured in isolated fetal and neonatal testicular cells, was 5 × 10−10m and the lowest dose of ACTH eliciting a response was 2 × 10−11m. Circulating ACTH levels in fetal mice were around 8 × 10−11m. Neither α-MSH nor γ-MSH had any effect on androgen production in vitro at any age. Fetal testosterone levels were normal in mice that lack circulating ACTH (proopiomelanocortin-null) indicating that ACTH is not essential for fetal Leydig cell function. Results show that both LH and ACTH can regulate testicular steroidogenesis during fetal development in the mouse and suggest that fetal Leydig cells, but not adult Leydig cells, are sensitive to ACTH stimulation.

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