scholarly journals Spermatogonial behavior in rats during radiation-induced arrest and recovery after hormone suppression

Reproduction ◽  
2013 ◽  
Vol 146 (4) ◽  
pp. 363-376 ◽  
Author(s):  
Amanda V Albuquerque ◽  
Fernanda R C L Almeida ◽  
Connie C Weng ◽  
Gunapala Shetty ◽  
Marvin L Meistrich ◽  
...  
Keyword(s):  
Sertoli Cell ◽  
Leydig Cell ◽  
Sertoli Cells ◽  
Leydig Cells ◽  
Gradual Increase ◽  
Immunohistochemical Analysis ◽  
Type A ◽  
Kit Ligand ◽  
Kit Receptor ◽  
Radiation Induced

Ionizing radiation has been shown to arrest spermatogenesis despite the presence of surviving stem spermatogonia, by blocking their differentiation. This block is a result of damage to the somatic environment and is reversed when gonadotropins and testosterone are suppressed, but the mechanisms are still unknown. We examined spermatogonial differentiation and Sertoli cell factors that regulate spermatogonia after irradiation, during hormone suppression, and after hormone suppression combined with Leydig cell elimination with ethane dimethane sulfonate. These results showed that the numbers and cytoplasmic structure of Sertoli cells are unaffected by irradiation, only a few type A undifferentiated (Aund) spermatogonia and even fewer type A1 spermatogonia remained, and immunohistochemical analysis showed that Sertoli cells still produced KIT ligand (KITLG) and glial cell line-derived neurotrophic factor (GDNF). Some of these cells expressed KIT receptor, demonstrating that the failure of differentiation was not a result of the absence of the KIT system. Hormone suppression resulted in an increase in Aund spermatogonia within 3 days, a gradual increase in KIT-positive spermatogonia, and differentiation mainly to A3 spermatogonia after 2 weeks. KITL (KITLG) protein expression did not change after hormone suppression, indicating that it is not a factor in the stimulation. However, GDNF increased steadily after hormone suppression, which was unexpected since GDNF is supposed to promote stem spermatogonial self-renewal and not differentiation. We conclude that the primary cause of the block in spermatogonial development is not due to Sertoli cell factors such (KITL\GDNF) or the KIT receptor. As elimination of Leydig cells in addition to hormone suppression resulted in differentiation to the A3 stage within 1 week, Leydig cell factors were not necessary for spermatogonial differentiation.

Adult rat Sertoli cells secrete a factor or factors which modulate Leydig cell function

1987 ◽  
Vol 114 (3) ◽  
pp. 459-467 ◽  
Author(s):  
V. Papadopoulos ◽  
P. Kamtchouing ◽  
M. A. Drosdowsky ◽  
M. T. Hochereau de Reviers ◽  
S. Carreau
Keyword(s):  
Cyclic Amp ◽  
Sertoli Cell ◽  
Leydig Cell ◽  
Sertoli Cells ◽  
Leydig Cells ◽  
Cell Function ◽  
Cell Interaction ◽  
Adult Rats ◽  
Adult Rat ◽  
Stimulating Factor

ABSTRACT Production of testosterone and oestradiol-17β by Leydig cells from adult rats was stimulated by LH or dibutyryl cyclic AMP (10 and 2·5-fold respectively). The addition of spent medium from normal, hemicastrated or γ-irradiated rat seminiferous tubule cultures, as well as from Sertoli cell cultures, to purified Leydig cells further enhanced both basal (44 and 53% for testosterone and oestradiol-17β respectively) and LH-stimulated (56 and 18%) steroid output. Simultaneously, a decrease (20–30%) in intracellular cyclic AMP levels was observed. This stimulating factor (or factors) secreted by the Sertoli cells is different from LHRH, is of proteinic nature and has a molecular weight ranging between 10 000 and 50 000; its synthesis is not controlled by FSH nor by testosterone. This factor(s) involved in rat Leydig cell steroidogenesis, at a step beyond the adenylate cyclase, does not require protein synthesis for testosterone formation whereas it does for oestradiol-17β production. It should be noted that a germ cell–Sertoli cell interaction modulates the synthesis of this factor(s). J. Endocr. (1987) 114, 459–467

scholarly journals THE EFFECT OF CHRONIC EXPOSURE OF NICOTINE INHALATION TO THE COUNT OF SPERMATOGONIA, SERTOLI CELLS AND LEYDIG CELLS OF YOUNG WHITE RAT WISTAR STRAIN

2019 ◽  
Vol 26 (2) ◽  
Author(s):  
Aril Rizaldi ◽  
Doddy M Soebadi ◽  
Soetojo Soetojo
Keyword(s):  
Cell Count ◽  
Sertoli Cell ◽  
Leydig Cell ◽  
Sertoli Cells ◽  
Chronic Exposure ◽  
Leydig Cells ◽  
Control Group ◽  
Nicotine Exposure ◽  
Control Group Design ◽  
Wistar Strain

Objective: To analyze the difference in the number of spermatogonia, leydig cells and sertoli cells in young age of  white mice Wistar strain after inhalation of chronic nicotine exposure. Material & Method: Laboratory experimental study with post test only control group design, measurement of spermatogonium, leydig cell, sertoli cell in 5 groups of young male Wistar strain, negative control group and treatment group given nicotine exposure 0.5 mg, 1 mg, 2 mg, and 4 mg/kg body weight/day for 30 days. Results: A significant reduction in spermatogonium was found in the group given nicotine 0.5 mg/kgBW/day (p=0.048), 1 mg/kgBW/day (p=0.002), 2 mg/kgBW/day (p=0.002) and 4 mg/kgBW/day (p=0.000) when compared to the control group. Significant decreases were also seen in the group receiving 4 mg of nicotine exposure compared with 0.5 mg (p=0.018). Significant decrease in sertoli cell count was seen only in the nicotine group of 4 mg/kgBW/day compared with the control group (p=0.047). A significant decrease in leydig cell count was found in the nicotine 2 mg/kgBW/day (p=0.037) and nicotine group 4 mg/kgBW/day (p=0.023) when compared with the control group. Significant decreases were also found in the 4 mg/kgBW/day group compared to the 0.5 mg/kgBW/day group (p=0.004). In this study there were also a decrease in the number of spermatogonia, sertoli cells, and leydig cells in the increased dose of nicotine given although not statistically significant. Conclusion: Chronic exposure of nicotine per inhalation may decrease the number of spermatogonia, sertoli cells, and leydig cells. The higher the dose of nicotine given the greater the decrease in the number of spermatogonium cells, sertoli cells, and leydig cells that occur. This proves that nicotine is one of the causes of infertility in men.

Cultured Sertoli cell-mediated FSH stimulatory effect on Leydig cell steroidogenesis

1985 ◽  
Vol 248 (2) ◽  
pp. E176-E181
Author(s):  
M. Benahmed ◽  
J. Reventos ◽  
E. Tabone ◽  
J. M. Saez
Keyword(s):  
Sertoli Cell ◽  
Leydig Cell ◽  
Sertoli Cells ◽  
Leydig Cells ◽  
Cell Function ◽  
Cell Activity ◽  
Defined Medium ◽  
Cell Number ◽  
Two Parameters ◽  
Leydig Cell Function

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.

Age-related changes in human Leydig cell status

2020 ◽  
Vol 35 (12) ◽  
pp. 2663-2676
Author(s):  
Valentina Mularoni ◽  
Valentina Esposito ◽  
Sara Di Persio ◽  
Elena Vicini ◽  
Gustavo Spadetta ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Sertoli Cell ◽  
Leydig Cell ◽  
Leydig Cells ◽  
Cell Number ◽  
Organ Donors ◽  
Steroidogenic Enzymes ◽  
Age Related ◽  
Age Range

Abstract STUDY QUESTION What are the consequences of ageing on human Leydig cell number and hormonal function? SUMMARY ANSWER Leydig cell number significantly decreases in parallel with INSL3 expression and Sertoli cell number in aged men, yet the in vitro Leydig cell androgenic potential does not appear to be compromised by advancing age. WHAT IS KNOWN ALREADY There is extensive evidence that ageing is accompanied by decline in serum testosterone levels, a general involution of testis morphology and reduced spermatogenic function. A few studies have previously addressed single features of the human aged testis phenotype one at a time, but mostly in tissue from patients with prostate cancer. STUDY DESIGN, SIZE, DURATION This comprehensive study examined testis morphology, Leydig cell and Sertoli cell number, steroidogenic enzyme expression, INSL3 expression and androgen secretion by testicular fragments in vitro. The majority of these endpoints were concomitantly evaluated in the same individuals that all displayed complete spermatogenesis. PARTICIPANTS/MATERIALS, SETTING, METHODS Testis biopsies were obtained from 15 heart beating organ donors (age range: 19–85 years) and 24 patients (age range: 19–45 years) with complete spermatogenesis. Leydig cells and Sertoli cells were counted following identification by immunohistochemical staining of specific cell markers. Gene expression analysis of INSL3 and steroidogenic enzymes was carried out by qRT-PCR. Secretion of 17-OH-progesterone, dehydroepiandrosterone, androstenedione and testosterone by in vitro cultured testis fragments was measured by LC-MS/MS. All endpoints were analysed in relation to age. MAIN RESULTS AND THE ROLE OF CHANCE Increasing age was negatively associated with Leydig cell number (R = −0.49; P < 0.01) and concomitantly with the Sertoli cell population size (R= −0.55; P < 0.001). A positive correlation (R = 0.57; P < 0.001) between Sertoli cell and Leydig cell numbers was detected at all ages, indicating that somatic cell attrition is a relevant cellular manifestation of human testis status during ageing. INSL3 mRNA expression (R= −0.52; P < 0.05) changed in parallel with Leydig cell number and age. Importantly, steroidogenic capacity of Leydig cells in cultured testis tissue fragments from young and old donors did not differ. Consistently, age did not influence the mRNA expression of steroidogenic enzymes. The described changes in Leydig cell phenotype with ageing are strengthened by the fact that the different age-related effects were mostly evaluated in tissue from the same men. LIMITATIONS, REASONS FOR CAUTION In vitro androgen production analysis could not be correlated with in vivo hormone values of the organ donors. In addition, the number of samples was relatively small and there was scarce information about the concomitant presence of potential confounding variables. WIDER IMPLICATIONS OF THE FINDINGS This study provides a novel insight into the effects of ageing on human Leydig cell status. The correlation between Leydig cell number and Sertoli cell number at any age implies a connection between these two cell types, which may be of particular relevance in understanding male reproductive disorders in the elderly. However aged Leydig cells do not lose their in vitro ability to produce androgens. Our data have implications in the understanding of the physiological role and regulation of intratesticular sex steroid levels during the complex process of ageing in humans. STUDY FUNDING/COMPETING INTEREST(S) This work was supported by grants from Prin 2010 and 2017. The authors have no conflicts of interest. TRIAL REGISTRATION NUMBER N/A.

248. Oestrogen receptor beta is involved in the regulation of Leydig cell number in the mouse

2005 ◽  
Vol 17 (9) ◽  
pp. 99
Author(s):  
M. Gould ◽  
H. D. Nicholson
Keyword(s):  
Leydig Cell ◽  
Sertoli Cells ◽  
Leydig Cells ◽  
Oestrogen Receptor ◽  
Physiological Role ◽  
Plasma Testosterone ◽  
Testis Weight ◽  
Wild Type ◽  
Significant Difference ◽  
Receptor Beta

Recent evidence suggests that oestrogen plays a physiological role in the testis. Both oestrogen receptor alpha and oestrogen receptor beta (ERb) are present in the testis and administration of oestrogen has been shown to inhibit the development of Sertoli, Leydig and germ cells. This study investigates the effect of ERb on the testis using ERb knockout mice (bERKO). Adult male bERKO mice (n=8) and their wild-type littermates (n=7) were killed at 11 weeks postpartum. One testis from each animal was fixed in Bouin’s fluid and embedded. Each testis was fractionated and thick sections cut and stained with PAS. The optical disector method was used to count the number of Leydig cells, Sertoli cells, spermatogonia, spermatocytes and spermatids in each testis. Trunk blood was collected and plasma testosterone concentrations measured by radioimmunoassay. No significant differences in body or testis weight were seen between the bERKO or wild-type mice. Similar numbers of Sertoli cells, spermatogonia, spermatocytes and spermatids were also observed between the two groups. The number of Leydig cells was significantly increased in bERKO mice compared with their wild-type littermates (P < 0.05). Despite the increased number of Leydig cells in the bERKO mice there was no significant difference in plasma testosterone concentrations in this group compared to the wild-type mice. Oestrogen has been reported to inhibit proliferation of adult-type Leydig cells and to inhibit steroidogenesis. This study suggests that the regulation of Leydig cell proliferation may be mediated by ERb. The presence of normal circulating testosterone concentrations in bERKO mice suggests that the effects of oestrogen on steroidogenesis are not brought about by ERbeta.

scholarly journals Role of gonadotrophins in regulating numbers of Leydig and Sertoli cells during fetal and postnatal development in mice

Reproduction ◽  
2001 ◽  
pp. 227-234 ◽  
Author(s):  
PJ Baker ◽  
PJ O'Shaughnessy
Keyword(s):  
Cell Volume ◽  
Postnatal Development ◽  
Leydig Cell ◽  
Sertoli Cells ◽  
Leydig Cells ◽  
Normal Values ◽  
Fold Increase ◽  
Adult Mice ◽  
Number Of Cells

The role of the gonadotrophins in regulating numbers of Leydig and Sertoli cells during fetal and postnatal development was examined using normal mice and hypogonadal (hpg) mice, which lack circulating gonadotrophins. The disector method was used to determine the number of cells from day 16 of gestation until adulthood. The numbers of Leydig cells did not change significantly between day 16 of gestation and day 5 after parturition in normal mice and were not significantly different from numbers in hpg mice at any age up to day 5 after parturition. There was a 16-fold increase in the number of Leydig cells in normal mice between day 5 and day 20 after parturition, followed by a further doubling of number of cells between day 20 and adulthood. The number of Leydig cells in hpg testes did not change between day 5 and day 20 after parturition but doubled between day 20 and adulthood so that the number of cells was about 10% of normal values from day 20 onwards. Leydig cell volume was constant in normal animals from birth up to day 20 and then showed a 2.5-fold increase in adult animals. Leydig cell volume was normal in hpg testes at birth but decreased thereafter and was about 20% of normal volume in adult mice. The number of Sertoli cells increased continuously from day 16 of gestation to day 20 after gestation in normal mice and then remained static until adulthood. The number of Sertoli cells in hpg testes was normal throughout fetal life but was reduced by about 30% on day 1 (day of parturition). Thereafter, Sertoli cells proliferated at a slower rate but over a longer period in the hpg testis so that on day 20 after parturition the number of Sertoli cells was about 50% of normal values, whereas in adult mice the number was 65% of normal. The number of gonocytes did not change between day 16 of gestation and day 1 and did not differ between normal and hpg testes. The number of gonocytes increased nine-fold in normal testes but only three-fold in hpg testes between day 1 and day 5 after parturition. Gonocytes differentiated into spermatogonia in both normal and hpg testes between day 5 and day 20 after parturition. These results show: (i) that fetal development of both Sertoli and Leydig cells is independent of gonadotrophins; (ii) that normal differentiation and proliferation of the adult Leydig cell population (starting about day 10 after parturition) is dependent on the presence of gonadotrophins; and (iii) that the number of Sertoli cells after birth is regulated by gonadotrophins, although proliferation will continue, at a lower rate and for longer, in the absence of gonadotrophins.

scholarly journals Microscopic morphology and testis morphometry of captivity-bred Adult bullfrogs (Lithobates catesbeianus Shaw, 1802)

2009 ◽  
Vol 52 (6) ◽  
pp. 1461-1472 ◽  
Author(s):  
Jaqueline Carlos ◽  
Sérgio Luis Pinto da Matta
Keyword(s):  
Young Adult ◽  
Adult Male ◽  
Leydig Cell ◽  
Sertoli Cells ◽  
Rainy Season ◽  
Leydig Cells ◽  
Lithobates Catesbeianus ◽  
Nuclear Diameter ◽  
The Mean ◽  
Microscopic Morphology

The aim of this work was to study the testicular morphometry of captivity-bred adult bullfrogs. Fifteen young adult male were studied, in the rainy season and a lengthy photoperiod. The GSI was established at 0.15%. The nuclear diameter of germinative and Leydig cells, the nucleolus diameter of Sertoli cells and the area of cysts and tubules were determined and the mean number of ISPC, IISPC and SPT per cyst and the mean number of cysts per tubule was estimated. The nucleoplasmatic proportion of the nucleus of the Leydig cell was 76.22%, indicating less cytoplasmic activity. Eight generations of spermatogonia were found. The spermatogenesis efficiency in meiosis and in mitosis was 63 and 49%, respectively. The spermatogenesis of bullfrog fited in the pattern of other captivity Anurans, with differences as the morphology of Sertoli and Leydig cells nuclei.

Some histochemical and ultrastructural observations on the early foetal pig testis

Development ◽  
1986 ◽  
Vol 95 (1) ◽  
pp. 261-277
Author(s):  
C. J. A. H. V. van Vorstenbosch ◽  
C. M. J. E. van Rossum-Kok ◽  
B. Colenbrander ◽  
C. J. G. Wensing
Keyword(s):  
Endoplasmic Reticulum ◽  
Leydig Cell ◽  
Sertoli Cells ◽  
Leydig Cells ◽  
Tunica Albuginea ◽  
Hydroxysteroid Dehydrogenase ◽  
Mesenchymal Cells ◽  
Mitochondrial Complex ◽  
Sustentacular Cells

Testes of foetal pigs between 26 to 35 days post coitum (p.c.) were investigated histochemically and ultrastructurally. Diaphorase and Δ5-3β-hydroxysteroid dehydrogenase activities were studied using, respectively, NADH and pregnenolone and dihydroxy androsterone as substrates. Ultrastructurally, attention was focused on the development of mesenchymal cells and on the sustentacular cells in the primitive sex cords in an attempt to detect the origin of Ley dig cells. Histochemically there is a concentration of activity toward the interstitium with increasing age. Also the reactions increase in intensity. Ultrastructurally no evidence for Leydig cell development from Sertoli cells could be observed. Mesenchymal cells between the sex cords show a development toward Leydig cells. This is absent in mesenchymal cells in the future tunica albuginea. Before 30 days p.c. no ‘true’ Leydig cells can be observed morphologically. The role of the rough endoplasmic reticulum/mitochondrial complex, which is present in many mesenchymal and sustentacular cells, is discussed.

scholarly journals Effect of FSH on testicular morphology and spermatogenesis in gonadotrophin-deficient hypogonadal mice lacking androgen receptors

Reproduction ◽  
2010 ◽  
Vol 139 (1) ◽  
pp. 177-184 ◽  
Author(s):  
P J O'Shaughnessy ◽  
A Monteiro ◽  
G Verhoeven ◽  
K De Gendt ◽  
M H Abel
Keyword(s):  
Germ Cell ◽  
Leydig Cell ◽  
Sertoli Cells ◽  
Leydig Cells ◽  
Androgen Receptors ◽  
Round Spermatid ◽  
Cell Number ◽  
Cell Numbers ◽  
No Formation ◽  
Testicular Morphology

FSH and androgen act to stimulate and maintain spermatogenesis. FSH acts directly on the Sertoli cells to stimulate germ cell number and acts indirectly to increase androgen production by the Leydig cells. In order to differentiate between the direct effects of FSH on spermatogenesis and those mediated indirectly through androgen action, we have crossed hypogonadal (hpg) mice, which lack gonadotrophins, with mice lacking androgen receptors (AR) either ubiquitously (ARKO) or specifically on the Sertoli cells (SCARKO). These hpg.ARKO and hpg.SCARKO mice were treated with recombinant FSH for 7 days and testicular morphology and cell numbers were assessed. In untreated hpg and hpg.SCARKO mice, germ cell development was limited and did not progress beyond the pachytene stage. In hpg.ARKO mice, testes were smaller with fewer Sertoli cells and germ cells compared to hpg mice. Treatment with FSH had no effect on Sertoli cell number but significantly increased germ cell numbers in all groups. In hpg mice, FSH increased the numbers of spermatogonia and spermatocytes, and induced round spermatid formation. In hpg.SCARKO and hpg.ARKO mice, in contrast, only spermatogonial and spermatocyte numbers were increased with no formation of spermatids. Leydig cell numbers were increased by FSH in hpg and hpg.SCARKO mice but not in hpg.ARKO mice. Results show that in rodents 1) FSH acts to stimulate spermatogenesis through an increase in spermatogonial number and subsequent entry of these cells into meiosis, 2) FSH has no direct effect on the completion of meiosis and 3) FSH effects on Leydig cell number are mediated through interstitial ARs.

Testicular gonadotrophins and their receptors in human cryptorchidism as revealed by immunohistochemistry and radioreceptor assay

1986 ◽  
Vol 111 (1) ◽  
pp. 128-132 ◽  
Author(s):  
Outi Hovatta ◽  
I. Huhtaniemi ◽  
T. Wahlström
Keyword(s):  
Sertoli Cell ◽  
Sertoli Cells ◽  
Leydig Cells ◽  
Radioreceptor Assay ◽  
Human Testis ◽  
Immunoperoxidase Technique ◽  
Fsh Receptor ◽  
Lh Receptor ◽  
And Control ◽  
Testicular Macrophages

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.

Sign in / Sign up

Export Citation Format

Share Document