Development of a new Leydig cell population after the destruction of existing Leydig cells by ethane dimethane sulphonate in rats: an autoradiographic study

Teerds, K. J.; Rooij, Dirk G. de; Rommerts, F. F. G.; Wensing, C. J. G.

doi:10.1677/joe.0.1260229

Cited by 49 publications

(41 citation statements)

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“…Some studies reported Leydig cell proliferation in rat testis after selective Leydig cell destruction by ethylene dimethane sulfonate [13,14,15,16]. Leydig cell proliferation was shown with normal endocrinological function after 3 weeks of destruction [14,15,16].…”

Section: Discussionmentioning

confidence: 99%

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The Effect of Testicular Torsion Duration on Testicular Steroidogenesis in the Rat Model

Kurt¹,

Yazıcı²,

Gevher³

et al. 2016

Urol Int

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Background: Testicular torsion is an emergency condition in which spermatogenesis may be irreversibly damaged. There have been controversial results about the effect of testicular torsion on steroidogenesis. We aimed at investigating the effect of testicular torsion on steroidogenesis. Material and Methods: A total of 40 adult male rats were divided into 4 groups. Left testicles were removed in all groups. Right testicles were torsioned and remained in the torsion position for 1, 3 and 5 h in study groups, whereas no torsion was performed in control. Serum luteinizing hormone (LH) and total testosterone (TT) levels were measured on the 3rd and 30th days of surgery and orchiectomy was performed on the 30th day of testicular torsion for histopathological evaluation. Results: TT levels of study groups were significantly lower than that of the control group on the 3rd day of torsion. LH of study groups was higher than that of the control group, but the difference was significant only in the 5 h-torsion group. The total number of Leydig cells increased in 1- and 3-h groups, whereas it decreased in the 5-hour group. Conclusion: Testosterone production and Leydig cell functions significantly decreased after 5 h torsion in the rat model. The duration of torsion less than 5 h yielded partial dysfunction on steroidogenesis.

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Section: Discussionmentioning

confidence: 99%

“…Leydig cell proliferation was shown with normal endocrinological function after 3 weeks of destruction [14,15,16]. Increase in LH was proposed to be important for Leydig cell differentiation and proliferation [13,17].…”

Section: Discussionmentioning

confidence: 99%

The Effect of Testicular Torsion Duration on Testicular Steroidogenesis in the Rat Model

Kurt¹,

Yazıcı²,

Gevher³

et al. 2016

Urol Int

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“…Other data indicate that testicular macrophages also play an important role in regulating LC regeneration in EDS-treated rats (Gaytan et al, 1994a,b). While the initial recruitment and proliferation of LC precursors occurs in the absence of LH and is presumed to be paracrine mediated, it appears that the final differentiation of these precursors into adult LCs is an LH-dependent process (Teerds et al, 1988(Teerds et al, , 1989a(Teerds et al, , 1990a.…”

Section: The Adult Lcmentioning

confidence: 99%

Rodent Leydig Cell Tumorigenesis: A Review of the Physiology, Pathology, Mechanisms, and Relevance to Humans

Cook

Klinefelter

Hardisty

et al. 1999

Critical Reviews in Toxicology

175

122

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Leydig cells (LCs) are the cells of the testis that have as their primary function the production of testosterone. LCs are a common target of compounds tested in rodent carcinogenicity bioassays. The number of reviews on Leydig cell tumors (LCTs) has increased in recent years because of its common occurrence in rodent bioassays and the importance in assessing the relevance of this tumor type to humans. To date, there have been no comprehensive reviews to identify all the compounds that have been shown to induce LCTs in rodents or has any review systematically evaluated the epidemiology data to determine whether humans were at increased risk for developing LCTs from exposure to these agents. This review attempts to fill these deficiencies in the literature by comparing the cytology and ontogeny of the LC, as well as the endocrine and paracrine regulation of both normal and tumorigenic LCs. In addition, the pathology of LCTs in rodents and humans is compared, compounds that induce LC hyperplasia or tumors are enumerated, and the human relevance of chemical-induced LCTs is discussed. There are plausible mechanisms for the chemical induction of LCTs, as typified by agonists of estrogen, gonadotropin releasing hormone (GnRH), and dopamine receptors, androgen receptor antagonists, and inhibitors of 5alpha-reductase, testosterone biosynthesis, and aromatase. Most of these ultimately involve elevation in serum luteinizing hormone (LH) and/or LC responsiveness to LH as proximate mediators. It is expected that further work will uncover additional mechanisms by which LCTs may arise, especially the role of growth factors in modulating LC tumorigenesis. Regarding human relevance, the pathways for regulation of the hypothalamo-pituitary-testis (HPT) axis of rats and humans are similar, such that compounds that either decrease testosterone or estradiol levels or their recognition will increase LH levels. Hence, compounds that induce LCTs in rats by disruption of the HPT axis pose a risk to human health, except for possibly two classes of compounds (GnRH and dopamine agonists). Because GnRH and prolactin receptors are either not expressed or are expressed at very low levels in the testes in humans, the induction of LCTs in rats by GnRH and dopamine agonists would appear not to be relevant to humans; however, the potential relevance to humans of the remaining five pathways of LCT induction cannot be ruled out. Therefore, the central issue becomes what is the relative sensitivity between rat and human LCs in their response to increased LH levels; specifically, is the proliferative stimulus initiated by increased levels of LH attenuated, similar, or enhanced in human vs. rat LCs? There are several lines of evidence that suggest that human LCs are quantitatively less sensitive than rats in their proliferative response to LH, and hence in their sensitivity to chemically induced LCTs. This evidence includes the following: (1) the human incidence of LCTs is much lower than in rodents even when corrected for detection bias; (2) several ...

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“…But the cells showed strong adherence in primary culture and grew into typical epithelioid-like cells, probably because of the simplified procedure and shortened operation time. In addition, the macrophages and Leydig cells located in the testicular interstitium experience complex paracrine effects that promote cell growth and development and hormone synthesis [14,15], and the formation of new Leydig cells in adult male animals was derived from mesenchymal cells when the original Leydig cell population was destroyed [16,17]. Moreover, adult Leydig cells and mesenchymal cells per testis increased linearly from birth to postpuberty with a ratio of 2:1 respectively, indicating there were considerable mesenchymal cells in adult animals [18].…”

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confidence: 99%

Research on the Isolation of Mouse Leydig Cells Using Differential Digestion with a Low Concentration of Collagenase

et al. 2011

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Abstract. The aim of this study was to establish a novel method for isolating and purifying Leydig cells from mice testes. Testes of postpuberal mice were harvested and digested in a low concentration of collagenase NB4 for 15 min 2 times. Cells obtained were cultured in low glucose DMEM with 10% FBS. Immunofluorescence was used to detect the expression of Leydig cell biomarkers including 3β-hydroxysteroid dehydrogenase, cholesterol side-chain cleaving enzyme (CYP11A1) and 17α-hydroxylase/17,20-lyase (CYP17A1). It was found that the purity of the isolated Leydig cells was 69.6 ± 4.16%. After 7 days in primary culture, it increased to 90%. The testosterone synthase spectrum could be detected at the primary culture. In conclusion, the application of a low concentration of collagenase for differential digestion allows isolation of large quantities of viable Leydig cells. Key words: Differential digestion, Isolation and purification, Leydig cells (J. Reprod. Dev. 57: [433][434][435][436] 2011) eydig cells exist in the testicular interstitium and are the primary cells that synthesize and secrete testosterone in adult male animals. Qualified isolation of Leydig cells is very important for primary culture, which lays the foundation for and play a key role in all research in this field.However, at present, the steps for Leydig cell isolation and purification, including centrifugal elutriation and continuous or uncontinuous gradient of Percoll, are not only complex but also have strict requirements. As Leydig cells are particularly sensitive to mechanical intrusion [1], the long procedures of these protocols seriously damages the isolated cells and does not guarantee the long-term culture viability or continued secretion of androgens [2,3]; even primary cultures show significant cell aging and apoptosis [4][5][6][7]. Some researchers have also adopted the whole interstitial cell culture method to obtain Leydig cells [8,9]. However, Leydig cells comprise only 18% of the total interstitial cell components, while macrophages, which have a stronger proliferative capacity, account for 12% [10]. Consequently, Leydig cells obtained using the whole interstitial cell culture method may be competitively eliminated by dominant impure cells in the process of culture, resulting low culture purity.In this study, we modified this method by using a low concentration (0.03%) of NB4 collagenase to develop a new isolation method that causes less damage to the Leydig cells. This study was dedicated to improving the method for isolating viable, high-purity Leydig cells.In this procedure, two steps with a low concentration of NB4 collagenase were used to digest and isolate the mouse Leydig cells. With this method, there were about 1.0 × 10 5 cells that could be collected from each testis. The purity of the Leydig cells was 69.6 ± 4.2%. Cells were stained with trypan blue, and their survival rates were above 90%. The isolated cells had a uniform epithelial-like shape (Fig. 1A). After totally spreading, the Leydig cells had an irregular poly...

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Development of a new Leydig cell population after the destruction of existing Leydig cells by ethane dimethane sulphonate in rats: an autoradiographic study

Cited by 49 publications

References 0 publications

The Effect of Testicular Torsion Duration on Testicular Steroidogenesis in the Rat Model

The Effect of Testicular Torsion Duration on Testicular Steroidogenesis in the Rat Model

Rodent Leydig Cell Tumorigenesis: A Review of the Physiology, Pathology, Mechanisms, and Relevance to Humans

Research on the Isolation of Mouse Leydig Cells Using Differential Digestion with a Low Concentration of Collagenase

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