Effects of pure FSH and LH preparations on the number and function of Leydig cells in immature hypophysectomized rats

Teerds, K. J.; Closset, J.; Rommerts, F. F. G.; Rooij, Dirk G. de; Stocco, DM; Colenbrander, B.; Wensing, C. J. G.; Hennen, Georges

doi:10.1677/joe.0.1200097

Cited by 104 publications

(36 citation statements)

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“…FSH and LH are known to stimulate Sertoli cells to accelerate spermatogenesis and Leydig cells to secret testosterone, respectively, but both LH and FSH have also been reported to stimulate proliferation of Leydig cells [17,18]. Therefore, the elevated levels of FSH and LH have been thought to be the cause of the hyperplasia of Leydig cells in Klinefelter syndrome.…”

Section: Discussionmentioning

confidence: 99%

Leydig Cell Hyperplasia in an ENU-induced Mutant Mouse with Germ Cell Depletion

et al. 2008

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Abstract.Repro22 is an N-ethyl-N-nitrosourea (ENU)-induced mutation in mice showing depletion of both male and female germ cells. In the present study, we investigated the male phenotypes of the mutant mouse at the adult stage. The repro22/repro22 homozygous mice showed reduced body weights as well as markedly reduced testis weights. Histological examination of the testes at 4 and 10 months of age showed no germ cells in the seminiferous tubules of the affected testis while a number of Sertoli cells were observed in the tubules. In addition to the germ cell depletion, the testes of the affected mouse contained expanded intertubular spaces that were filled by Leydig cell-like interstitial cells. These interstitial cells were confirmed to be Leydig cells by immunohistochmical staining using anti-3β-HSD antibody. The estimated number of Leydig cells in the affected testes at 10 months of age increased approximately 2 fold compared with those of normal testes. Furthermore, the plasma testosterone levels of the affected mice at 10 months of age were significantly higher than those of the normal mice. These findings indicated that the repro22/repro22 mouse developed hyperplasia of Leydig cells that was presumably caused by the absence of germ cells in the seminiferous tubules. Key words: ENU mutagenesis, Germ cell, Infertility, Leydig cell, Mouse, Testosterone (J. Reprod. Dev. 54: [225][226][227][228] 2008) nfertility is a major health problem worldwide that influences more than 10% of couples, and approximately 50% of cases of infertility are caused by male factors. In particular, Sertoli cellonly syndrome, a form of non-obstructive azoospermia, is the most serious male infertility, as patients with this disorder show germ cell depletion and are untreatable using assisted reproduction techniques. Although a significant portion of male infertilities is believed to be caused by autosomal recessive mutations [1], the genetic factors that underlay most nonsyndromic male infertilities have not yet been identified, with a few exceptions [2,3]. Mutant mice established by gene targeting technology, chemical mutagenesis and spontaneous mutations [4][5][6][7], showing various features of infertility are expected to be useful animal models for investigating the pathogenesis and genetic factors of human infertilities. However, only a limited number of mouse models for Sertoli cell-only syndrome or germ cell depletion have been reported [8][9][10][11]. Repro22 is a mutation in mice recently produced by N-ethyl-Nnitrosourea (ENU)-induced mutagenesis at The Jackson Laboratory, showing depletion of germ cells in both the male and female. In the present study, we investigated male phenotypes of the mutant mouse at the adult stage and found that the mutant mouse showed Leydig cell hyperplasia and an elevated plasma testosterone level in addition to germ cell depletion. Materials and MethodsThe mice bearing the repro22 mutation were produced and provided by the ReproGenomics Program at The Jackson Laboratory. The mice have a mixed g...

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Section: Discussionmentioning

confidence: 99%

Leydig Cell Hyperplasia in an ENU-induced Mutant Mouse with Germ Cell Depletion

et al. 2008

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“…Androgen also appears to be essential for adult Leydig cell function, at least in the mouse (Murphy et al, 1994;O'Shaughnessy et al, 2002;Eacker et al, 2008) and there is evidence, going back a number of years, that FSH may also play a role in Leydig cell function. The first data showed that purified or recombinant FSH would stimulate Leydig cell function in hypophysectomised rats (Chen et al, 1976;Kerr & Sharpe, 1985;Teerds et al, 1989;Vihko et al, 1991) and this has, since, been confirmed in the hypogonadal mouse (O'Shaughnessy et al, 1992;Sadate-Ngatchou et al, 2004a). In the testis, receptors for FSH are only found in the Sertoli cells (Heckert and Griswold, 2002) and the effects of FSH must be mediated by a factor or factors released by the Sertoli cells which act on the Leydig cells.…”

Section: Adult Leydig Cellsmentioning

confidence: 96%

Role of androgen and gonadotrophins in the development and function of the Sertoli cells and Leydig cells: Data from mutant and genetically modified mice

O’Shaughnessy

Morris

Huhtaniemi

et al. 2009

Molecular and Cellular Endocrinology

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“…The testosterone 15 , FSH 16 and LH 17 were assayed using ELISA kits purchased from DRG International, Inc, BIOCODE-HYCEL and Elabscience Co., respectively.…”

Section: Determination Of Testosterone Fsh and Lhmentioning

confidence: 99%

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2017

IJPSR

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ABSTRACT:The present study was designed to evaluate the protective effect of omega-3 against β-cyfluthrin (β-cyf)-induced neurotransmitters' impairment, oxidative damage, testicular toxicity and genotoxicity. Adult male Wistar rats were divided equally into four groups: Group (I): Control, Group (II): β-cyf (5 mg/kg body weight/day), Group (III): omega-3 (400 mg/kg body weight/da y) + β-cyf (5 mg/kg body weight/day), Group (IV): omega-3 (400 mg/kg body weight/day). β-cyf's treatment for 8 weeks inhibited the activities of AChE, DA, LDH, total ATPase and Na + /K + ATPase. Also, β-cyf resulted in an increase in oxidative stress as indicated by elevations in the levels of MDA and NO while, the levels of TAC, thiol content and TP were decreased in brain and testis. Sperm count, sperm motility and testosterone levels were reduced while, sperm abnormalities, FSH and LH levels were increased in β-cyf-treated group. Also, β-cyf administration led to a significant increase in TNFα, IL-6 and APP mRNA expressions. In addition, β-cyf caused histopathological alterations in brain and testis. The present results showed that omega-3 could improve all the measured parameters. In conclusion, omega-3 could exhibit protective effects against β-cyf induced neurological and testicular damage.

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Effects of pure FSH and LH preparations on the number and function of Leydig cells in immature hypophysectomized rats

Cited by 104 publications

References 36 publications

Leydig Cell Hyperplasia in an ENU-induced Mutant Mouse with Germ Cell Depletion

Leydig Cell Hyperplasia in an ENU-induced Mutant Mouse with Germ Cell Depletion

Role of androgen and gonadotrophins in the development and function of the Sertoli cells and Leydig cells: Data from mutant and genetically modified mice

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