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PubMed2003

Exposure to the environmental estrogen bisphenol A differentially modulated estrogen receptor-alpha and -beta immunoreactivity and mRNA in male mouse testis.

We examined the effects of bisphenol A (0.5 microg/ml or 50 microg/ml) in the drinking water on estrogen receptor (ER) alpha and beta proteins and mRNA in the testis of young mice following 8-weeks of oral administration of bisphenol A utilizing immunohistochemistry and semiquantitative reverse transcription polymerase chain reaction amplification (RT-PCR). ER beta was clearly localized in the nuclei of spermatogonia and/or spermatocytes. ER beta immunopositive cell numbers per testis section were significantly decreased in the 50 microg/ml bisphenol A-treated group compared with control and the 0.5 microg/ml bisphenol A-treated group. The number of ER alpha positive cells in the testis was significantly lower than ER beta positive cells in control group. ER alpha immunopositive cell numbers per testis section were markedly increased in the 50 microg/ml bisphenol A-treated group compared with the control and the 0.5 microg/ml bisphenol A-treated group. ER beta mRNA expression was significantly decreased in the 50 microg/ml bisphenol A-treated group compared with the control and the 0.5 microg/ml bisphenol A-treated group. In contrast, ER alpha mRNA expression was markedly increased in the 50 microg/ml bisphenol A-treated group compared with the control and the 0.5 microg/ml bisphenol A-treated group. The existence of ER alpha and beta in the testis suggests that estrogens directly affect germ cells during testicular development and spermatogenesis, and differential modulation of ER alpha and beta in the testis could be involved in the effects of bisphenol A.

Animals↗
PubMed1998

DNA adducts in mouse testis and lung after inhalation exposure to 1,3-butadiene.

1,3-Butadiene is a widely used industrial chemical and also an environmental contaminant. Recent findings have shown that butadiene can also be a male germ cell mutagen. In this study, DNA adduct formation in testis and lung has been explored by using N7-alkylated guanines as a marker of biological effective dose. The adducts measured were the four structurally different guanine N7-adducts alkylated by butadienemonoepoxide, the main metabolite of 1,3-butadiene. This study demonstrates the dose-dependent adduct formation in lung and testis. At lower exposures (50 and 200 ppm) the adduct levels were about the same in the two organs, but at 500 ppm the adduct level was significantly (p < 0.03) higher in testis than in lung. The enantiomeric composition of the adducts detected was also different. In lung, all 4 possible adducts were present (S-C-1" dominating, 49%), but in testis only two out of four adducts were detected (S-C-2" being the most abundant adduct, 71%). These novel observations indicate that the DNA repair is different in these two organs studied and that heritable genetic effects observed may be mediated through the DNA adducts.

Alkylation↗
PubMedDate not supplied

Ginseng intestinal metabolite-I (GIM-I) reduces doxorubicin toxicity in the mouse testis.

The protective effect of ginseng intestinal metabolite-I (GIM-I) against doxorubicin-induced testicular toxicity was investigated in 5-week-old ICR male mice. GIM-I was administered orally to mice at a dose of 50 mg/kg daily for 4 weeks. From the second week, doxorubicin was coadministered intraperitoneally to the animals at a dose of 3 mg/kg once a week for 3 weeks (a total of 9 mg/kg). The body weight, spermatogenic activities (Sertoli cell, repopulation, and epididymal indices), and serum levels of lactate dehydrogenase (LDH) and creatine phosphokinase (CPK) were significantly decreased by doxorubicin treatment (P<0.01), while the combined treatment of GIM-I with doxorubicin resulted in parameters similar to the control. In the testes of doxorubicin-treated animals, almost all of the germ cells disappeared and were replaced by fibrinoid debris in the seminiferous tubules. Germ cell injury was significantly attenuated by GIM-I coadministration. The mRNA for phospholipid hydroperoxide glutathione peroxidase (PHGPx), a testis-specific antioxidant, was greatly decreased by doxorubicin treatment, and less decreased with GIM-I coadministration. These findings indicate that GIM-I may be partially protective against doxorubicin-induced testicular toxicity.

Administration, Oral↗
PubMed2002

Pleiotropic activity of hepatocyte growth factor during embryonic mouse testis development.

The hepatocyte growth factor (HGF) is a pleiotropic cytokine whose action is mediated by c-met, a glycoproteic receptor with tyrosine kinase activity which transduces its multiple biological activities including cell proliferation, motility and differentiation. During embryonic development HGF acts as a morphogenetic factor as previously demonstrated for metanephric and lung development. Recently, culturing male genital ridges, we demonstrated that HGF is able to support in vitro testicular cord formation. In the present paper we report the expression pattern of the HGF gene during embryonic testis development and the multiple roles exerted by this factor during the morphogenesis of this organ. Northern blot analysis reveals a positive signal in urogenital ridges isolated from 11.5 days post coitum (dpc) embryos and in testes isolated from 13.5 and 15.5 dpc male embryos. On the contrary HGF mRNA is undetectable in ovaries isolated from 13.5 and 15.5 dpc embryos. Moreover, we demonstrate that HGF is synthesized and secreted by the male gonad and is biologically active. These data indicate a male specific biological function of HGF during embryonic gonadal development. This hypothesis is supported by the in vitro demonstration that HGF acts as a migratory factor for male mesonephric cells which is a male specific event. In addition we demonstrate that during testicular development, HGF acts as a morphogenetic factor able to reorganize dissociated testicular cells which, under HGF stimulation, form a tridimensional network of cord-like structures. Finally, we demonstrate that HGF induces testicular cell proliferation in this way being responsible for the size increase of the testis. All together the data presented in this paper demonstrate that HGF is expressed during the embryonic development of the testis and clarify the multiple roles exerted by this factor during the morphogenesis of the male gonad.

Animals↗
PubMed2002

Detection of glycine receptor/Cl- channel beta subunit transcripts in mouse testis.

The sperm glycine receptor/Cl- channel (GlyR) is important to the initiation of the mammalian sperm acrosome reaction by the egg zona pellucida, but its presence in spermatogenic cells has not been demonstrated. Reverse transcriptase-polymerase chain reaction studies confirmed that GlyR beta subunit transcripts similar to those of the neuronal GlyR beta subunit are present in the testis of Swiss Webster mice. In situ hybridisation analysis demonstrated that GlyR beta subunit mRNAs were expressed within the germ cells of seminiferous tubules in those mice.

Animals↗
PubMed2003

Cisplatin-induced pulse of germ cell apoptosis precedes long-term elevated apoptotic rates in C57/BL/6 mouse testis.

Chemotherapeutic doses of cisplatin impair spermatogenesis and ultimately cause azoospermia and infertility in some men. The mechanism by which cisplatin damages testicular germ cells is poorly understood. Cisplatin's impact is first detected hours after exposure in the formation of DNA cross-links followed by weeks of testicular damage. Here, we report in 11-week-old male mice an early and massive rise of germ cell apoptosis after a single intraperitoneal (i.p.) injection of either 5 or 10 mg/kg cisplatin. For the lower dose, a roughly 9-fold peak increase in the apoptotic index over the control level is observed at 36 h, and for the higher dose, a 24-fold rise is seen at 24 h. At these peak levels, the lower dose produced a higher ratio of apoptotic early spermatocytes to apoptotic spermatogonia than did the higher dose. In addition to this early wave of germ cell die-off, our data show that while the post-wave apoptotic rates for both dose regimes diminish, at 12 days the apoptotic rates appear significantly higher (5 mg/kg) than controls. In summary, our findings show two events set in motion by acute cisplatin exposure: (1) a previously unreported massive apoptotic die-off of germ cells followed by (2) an elevated apoptotic rate possibly reflecting long-term or permanent damage to the seminiferous tubule.

Animals↗
PubMed1993

Erythroid transcription factor GATA-1 is abundantly transcribed in mouse testis.

The transcription factor GATA-1 is a fundamental regulator of genes in haematopoietic cell lineages and belongs to a family of factors that bind to the consensus sequence WGATAR. The GATA motif was originally identified in cis-regulatory regions of globin and other erythroid-specific genes, but the range of genes controlled by the GATA factors has since expanded. Members of the GATA transcription factor family share a conserved zinc-finger DNA-binding domain, but the expression profile of each GATA factor is distinct. Here we show that a testis form of murine (m)GATA-1 messenger RNA is transcribed from a promoter located 5' to the erythroid first exon, and the remaining exons (which encode the mGATA-1 protein) are used in common by both testis and erythroid transcripts. We use an anti-mGATA-1 monoclonal antibody to show that the factor expressed in erythroid cells is the same as that found in the seminiferous tubules of murine testis. The GATA-1-expressing cells in 10-week-old testis were found only in contact with the basement membrane of seminiferous tubules, suggesting that GATA-1 regulates genes during the earliest stages of spermatogenesis.

Aging↗
PubMed2003

FLIP is expressed in mouse testis and protects germ cells from apoptosis.

Apoptosis control in adult testis is crucial to achieve normal spermatogenesis. In this study c-FLIP, an apoptosis-modulating protein, was investigated. In Western blot and immunohistochemical analyses, the 55 KDa c-FLIP long isoform (c-FLIP(L)) was found to be expressed strongly in spermatocytes and spermatids, at low levels in spermatogonia and at almost undetectable levels in Sertoli cells. This expression pattern was confirmed by Northern blot analyses. Further experiments carried out on GC-1spg germ cell line revealed that reducing c-FLIP(L) expression increases Fas-dependent apoptosis. Conversely, restoring c-FLIP(L) expression reduces this response to control levels. Caspase-10 expression was found to match c-FLIP(L) expression pattern; further, caspase-10 activation upon anti-Fas treatment inversely correlated with c-FLIP(L) expression. Finally, TUNEL staining of seminiferous tubules incubated with anti-Fas antibody showed that apoptosis occurs mostly in basally located germ cells, indicating that such cells, expressing low levels of c-FLIP(L), are sensitive to Fas-mediated apoptosis. These data indicate for the first time that c-FLIP(L) might control germ cell apoptosis and caspase activity in the adult testis.

Animals↗
PubMed1997

Sequences 5' of the basement membrane laminin beta 1 chain gene (LAMB1) direct the expression of beta-galactosidase during development of the mouse testis and ovary.

The murine LAMB1 gene encoding laminin beta 1 is expressed in the developing male and female gonads and mesonephros. To identify the cis-acting elements regulating the expression of LAMB1, murine transgenic lines were generated by fusing regions of the LAMB1 gene to the Eschericia coli lacZ gene. The p3.9LAM beta gal construct contained approximately 4 kb of 5' flanking sequence and directed beta-galactosidase expression in many different organs including the kidney, mammary gland, and the male and female genital systems, the focus of this report. In male embryos, between gestational ages E 14.5 and birth beta-galactosidase was transiently expressed in the prospermatogonia cells of the testis and in the differentiating epithelial cells in the ductus deferens, ductus epididymis, and seminal vesicles. In female embryos, beta-galactosidase was not detected in the ovary until about 1 week after birth; at this time, beta-galactosidase was expressed by oocytes of primary and secondary follicles. In contrast, transgenic mice carrying the first 0.7 kb of LAMB1 fused to the lacZ gene expressed beta-galactosidase only in the prospermatogonia cells of the testis. Thus, the cis-acting element(s) necessary for the expression of the LAMB1 gene in prospermatogonia cells are located in the first 0.7 kb of LAMB1 5' flanking sequence; element(s) required for expression of the LAMB1 gene in oocytes and epithelial cells of the mesonephric ducts, mesonephric tubules, the ductus deferens, ductus epididymis, and seminal vesicles are located with 4 kb 5' of the transcription initiation site.

Animals↗
PubMed1988

Estrogen induced effects on mouse testis and epididymal spermatozoa.

The effects of estradiol benzoate (E2B) at a dose of 200 micrograms/kg body weight/day for 7 and 15 days were investigated on epididymal sperm parameters and morphology of testis in adult mice. The data revealed a decline in cauda epididymal sperm count and percentage motility with duration of estrogen administration. The decreased sperm motility was correlated with reduced sperm enzymes as evidenced by biochemical and cytochemical studies. The depletion of cauda epididymal sperm population in treated mice was related to inhibition of spermatogenic activity in testis as compared to control. Thus, the estrogen treatment to mice manifests maturational changes in epididymal spermatozoa as a result of androgen deprivation.

Acid Phosphatase↗
PubMed1994

Mouse testis Pdha-2 promoter upstream sequences confer tissue-and temporal-specific activity in transgenic mice.

Spermatogenesis is a complex process requiring the coordinate expression of a number of testis-specific genes. One of these, Pdha-2, codes for the murine testis-specific isoform of the E1 alpha subunit of the pyruvate dehydrogenase complex. To elucidate the mechanisms regulating its expression in vivo, we have begun to investigate the Pdha-2 promoter in transgenic mice. In this paper, a construct containing 3.0 kb of promoter and upstream sequences is reported to be sufficient for directing the testis-specific expression of a CAT reporter gene in mice harbouring the transgene. Similarly to the endogenous Pdha-2, the CAT gene is expressed in testis in a stage-specific manner. However, the 3.0-kb Pdha-2 promoter is not active in somatic tissue suggesting that repressor elements may be present within these sequences.

3T3 Cells↗
PubMed1995

A model for understanding gene regulation during spermatogenesis: the mouse testis Pdha-2 promoter.

Spermatogenesis is a complex process requiring the coordinate expression of a number of testis-specific genes. How these genes are regulated during spermatogenesis is poorly understood. However, the elucidation of these mechanisms has significant implications for both medicine and the primary livestock industry. The delineation of this process is of particular interest and, in this study, Pdha-2, a gene which codes for the murine testis-specific isoform of the E1 alpha subunit of the pyruvate dehydrogenase complex, has been used as a model. This review focuses on current knowledge about its expression and regulation during spermatogenesis.

Animals↗
PubMed2000

Spermatogonial stem cell enrichment by multiparameter selection of mouse testis cells.

The spermatogonial stem cell initiates and maintains spermatogenesis in the testis. To perform this role, the stem cell must self replicate as well as produce daughter cells that can expand and differentiate to form spermatozoa. Despite the central importance of the spermatogonial stem cell to male reproduction, little is known about its morphological or biochemical characteristics. This results, in part, from the fact that spermatogonial stem cells are an extremely rare cell population in the testis, and techniques for their enrichment are just beginning to be established. In this investigation, we used a multiparameter selection strategy, combining the in vivo cryptorchid testis model with in vitro fluorescence-activated cell sorting analysis. Cryptorchid testis cells were fractionated by fluorescence-activated cell sorting analysis based on light-scattering properties and expression of the cell surface molecules alpha6-integrin, alphav-integrin, and the c-kit receptor. Two important observations emerged from these analyses. First, spermatogonial stem cells from the adult cryptorchid testis express little or no c-kit. Second, the most effective enrichment strategy, in this study, selected cells with low side scatter light-scattering properties, positive staining for alpha6-integrin, and negative or low alphav-integrin expression, and resulted in a 166-fold enrichment of spermatogonial stem cells. Identification of these characteristics will allow further purification of these valuable cells and facilitate the investigation of molecular mechanisms governing spermatogonial stem cell self renewal and hierarchical differentiation.

Animals↗
PubMedDate not supplied

Effects of calcium channel blockers on the spermatogenesis and gene expression in peripubertal mouse testis.

Treatment of Ca(2+) channel blockers (CCB) to relieve hypertension causes reversible male infertility, suggesting deregulation of Ca(2+) homeostasis in testis is closely related with male infertility. To investigate the possible toxicity of therapeutic application of CCB in childhood, the effect of nifedipine and ethosuximide, an L-type and T-type CCB, respectively, on the spermatogenesis and testicular gene expression was examined. Following the intraperitoneal injection of either drug for 7 days to 18 days on old mice, the paired testes weights were significantly lower in mice treated with nifedipine (> or = 10 mg/kg/day) or ethosuximide (100 mg/kg/day) than vehicle controls. In mice given high drug dosing (100 mg/kg), seminiferous tubules showed immaturity with spermatogenic arrest at elongating spermatid stage and poorly developed lumen. Unexpectedly, the expression of activator isoform of transcription factor cAMP-responsive element modulator (CREM) mRNA increased together with transition protein 2 and protamine 2 mRNA in drug-treated mice testes, suggesting that CCB may deregulate expression of activator isoform of CREM in male germ cells and that spermatogenic defect following CCB treatment may attribute to ectopic expression of CREM-dependent gene battery in testis. Therapeutic application of CCB in childhood should be cautious because of their potential to cause spermatogenic defect and altered gene expression in testis.

Animals↗