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At least 1,099 records · Page 61Linked to original sources
PubMed2003

Consequences of xenoestrogen exposure on male reproductive function in spottail shiners (Notropis hudsonius).

There is limited information on the physiological consequences associated with exposure to xenoestrogens under field conditions. The objectives of this study were to determine the presence of estrogenic chemicals in the St. Lawrence River and their effects on male reproduction in the spottail shiner (Notropis hudsonius). Hepatic vitellogenin (VTG) mRNA levels in immature shiners indicate extensive estrogenic contamination spanning almost 50 km both upstream and downstream from the island of Montreal. Stages of spermatogenesis were assessed in fish captured at sites having varying levels of estrogenic contamination. In control fish, 95% had testis of either stage IV (50%) or stage V (45%) of spermatogenesis. At Ile Dorval, where VTG mRNA levels are moderate, fish had testes of stage III (38%) and IV (45%) and only 15% of fish were at spermatogenic stage V. In contrast, at Ilet Vert and Ile Beauregard, located in the sewage effluent plume from the City of Montreal and where hepatic VTG mRNA levels are high in fish, none of the fish were at stage V and 8% of fish at Ilet Vert were at stage II of development. Sperm concentration and various motility parameters were significantly lower in shiners from Ilet Vert as compared with those from Iles de la Paix (reference). Histological analyses of testes revealed that more than one-third of the fish captured at sites with the highest estrogenic contamination displayed intersex, a condition in which ovarian follicles were developing within the testis. These data indicate that there is significant estrogenic contamination in the St. Lawrence River that is associated with impaired reproductive function in male fish.

Animals↗
PubMed2005

Absence asymmetry: the evolution of monorchid beetles (Insecta: Coleoptera: Carabidae).

Asymmetrical monorchy, or the complete absence of one testis coupled with the presence of its bilateral counterpart, is reported for 174 species of the carabid beetle tribes Abacetini, Harpalini, and Platynini (Insecta: Coleoptera: Carabidae) based on a survey of over 820 species from throughout the family. This condition was not found in examined individuals of any other carabid beetle tribes, or of other adephagan beetle families. One monorchid taxon within Platynini exhibits symmetrical vasa deferentia at the beginning of the pupal stadium, suggesting that developmental arrest of the underdeveloped vas deferens takes place in pupation. The point at which development of the testis is interrupted is unknown. Complete absence of one organ of a bilateral pair--absence asymmetry--is rarely found in any animal clade and among insects is otherwise only known for testes in the minute-sized beetles of the family Ptiliidae, ovaries in Scarabaeinae dung beetles, and ovaries of some aphids. Based on current phylogenetic hypotheses for Carabidae, testis loss has occurred independently at least three times, and up to five origins are possible, given the variation within Abacetini. Clear phylogenetic evidence for multiple independent origins suggests an adaptive or functional cause for this asymmetry. A previously posited taxon-specific hypothesis wherein herbivory in the tribe Harpalini led to testis loss is rejected. Optimal visceral packing of the beetle abdomen is suggested as a general explanation. Specifically, based on the function of various organ systems, we hypothesize that interaction of internal organs and pressure to optimize organ size and space usage in each system led to the multiple origins and maintenance of the monorchid condition. Testes are the only redundant and symmetrically paired structures not thought to be developmentally linked to other symmetrical structures in the abdomen. Among all possible organs, they are the most likely--although the observed frequency is very small--to bypass constraints that maintain bilateral symmetry, resulting in absence asymmetry. However, based solely on our observations of gross morphology of internal organs, no function conclusively explains the ontogenetic loss of one testis in these taxa. Unlike the analogous absence asymmetry of organs in other animal groups, no dramatic body-form constraint--e.g., snakes and lung loss, ptiliid beetles' small body-size and relatively giant sperm--or adaptive scenario of improved locomotory performance--e.g., birds and ovary loss due to flight constraints-applies to these carabid beetles. We tentatively suggest that testis loss is driven wholly by an interaction among the internal organs of these beetles, possibly due to selective pressure to maximize the comparatively large accessory glands found in these taxa. However, as the ordering of these evolutionary events of testis loss and accessory gland size increase is not known, large accessory glands might have secondarily evolved to compensate for a decreased testicular output.

Adaptation, Physiological↗
PubMed2005

BRCTx is a novel, highly conserved RAD18-interacting protein.

The BRCT domain is a highly conserved module found in many proteins that participate in DNA damage checkpoint regulation, DNA repair, and cell cycle control. Here we describe the cloning, characterization, and targeted mutagenesis of Brctx, a novel gene with a BRCT motif. Brctx was found to be expressed ubiquitously in adult tissues and during development, with the highest levels found in testis. Brctx-deficient mice develop normally, show no pathological abnormalities, and are fertile. BRCTx binds to the C terminus of hRAD18 in yeast two-hybrid and immunoprecipitation assays and colocalizes with this protein in the nucleus. Despite this, Brctx-deficient murine embryonic fibroblasts (MEFs) do not show overt sensitivity to DNA-damaging agents. MEFs from Brctx-deficient embryos grow at a similar rate to wild-type MEF CD4/CD8 expressions, and the cell cycle parameters of thymocytes from wild-type and Brctx knockout animals are indistinguishable. Intriguingly, the BRCT domain of BRCTx is responsible for mediating its localization to the nucleus and centrosome in interphase cells. We conclude that, although highly conserved, Brctx is not essential for the above-mentioned processes and may be redundant.

Amino Acid Sequence↗
PubMed1998

Multiple roles for the Wilms' tumour suppressor gene, WT1 in genitourinary development.

Wilms' tumour is a childhood kidney cancer, and a classic example of cancer arising through disrupted development (Armstrong et al., 1992). It is one of the most common solid paediatric malignancies, affecting one in 10000 children. The genetics of Wilms' tumour is complicated, with several different genes or chromosomal regions being implicated (Armstrong et al., 1992). However, the gene we know most about is the Wilms' tumour predisposition gene, WT1 (Bickmore et al., 1992; Bruening and Pelletier, 1996). It is now clear that mutations in this gene in humans can lead to abnormalities of the kidneys and gonads, as well as to the eponymous tumour. Also, as discussed below, WT1 is essential for kidney, testis and ovary development, as revealed in knockout mice.

Animals↗
PubMed2004

Human endocrine gland-derived vascular endothelial growth factor: expression early in development and in Leydig cell tumors suggests roles in normal and pathological testis angiogenesis.

Angiogenesis is essential for tumor growth and metastasis. A new human angiogenic mitogen, endocrine gland-derived vascular endothelial growth factor (EG-VEGF), has been recently identified; its expression pattern is restricted to endocrine glands, with the highest expression in testis. We used in situ hybridization and newly generated monoclonal antibodies to investigate the expression of EG-VEGF in normal human prenatal and adult testis and in 48 human testicular tumors of different subtypes. We found that EG-VEGF was expressed from 14 wk until birth in human fetal testis. In the adult testis, EG-VEGF was strongly expressed only in Leydig cells. In testicular tumors, EG-VEGF was expressed specifically in Leydig cell tumors, whereas germ cell-derived neoplasms, including carcinoma in situ, seminoma, and nonseminomatous germ cell tumors, were negative for this antigen. In contrast, VEGF, another powerful angiogenic factor, was expressed in seminoma, but very weakly in Leydig cell tumors. Interestingly, we found that Leydig cell tumors presented vessel surface density 3.2-fold higher than seminoma. These findings argue that human EG-VEGF may play a role in angiogenesis both during the early endocrine development of testis and in the adult testis as well as in Leydig cell tumor growth.

Adult↗
PubMed2001

Cell-autonomous and somatic signals control sex-specific gene expression in XY germ cells of Drosophila.

When XX germ cells develop in a testis they become spermatogenic. Thus, somatic signals determine the sex of genetically female germ cells. In contrast, XY germ cells experimentally transferred to an ovary do not differentiate oogenic cells. Because such cells show some male characteristics when analyzed in adults, it was assumed that XY germ cells autonomously become spermatogenic. Recently, however, evidence showing that a female soma feminizes XY germ cells was reported. The conclusion was drawn that the sex determination of XY germ cells is dictated by the sex of the soma. We monitored the fate of XY germ cells placed in a female environment throughout development. Here we report that such germ cells respond to both cell-autonomous and somatic sex-determining signals, depending on the developmental stage. Analyzing the expression of sex-specific molecular markers, we first detected autonomous male-specific gene expression in XY germ cells embedded in female embryos and larvae. At later stages, however, we found that sex-specific regulation of gene expression within XY germ cells is influenced by somatic gonadal cells. After metamorphosis, XY germ cells developing in a female soma start expressing female-specific and male-specific markers. Transcription of female-specific genes is maintained, while that of male-specific genes is later repressed. We show that in such XY germ cells, the female-specific gene Sex-lethal (Sxl) is activated. Within the germline, Sxl expression is required for the activation of a further female-specific gene and the repression of male-specific genes. We thus report for the first time the existence of downstream targets of the gene Sxl in the germline.

Animals↗
PubMed1988

Trifluoroethanol and its oxidative metabolites: comparison of in vivo and in vitro effects in rat testis.

Trifluoroethanol (TFE) and trifluoroacetaldehyde (TFALD) produced a reduction in testis weight 3 days after a single oral dose of 10 mg/kg. In contrast, administration of trifluoroacetic acid (TFAA) caused no observable testicular effects. Reduction in testis weight was accompanied by morphological changes, involving specific damage to pachytene and dividing spermatocytes, and round spermatids. In an in vitro Sertoli/germ cell co-culture system, only TFALD was found to produce dose-related effects at concentrations of 10(-3) and 10(-4) M. There was increased germ cell loss from the cultures, particularly loss of pachytene and dividing spermatocytes, accompanied by leakage of the pachytene spermatocyte marker enzyme, lactate dehydrogenase-X. TFE and TFAA did not produce these effects in the culture system at concentrations equimolar with TFALD. These results suggest that TFALD may play a critical role in the development of the testis lesion seen with TFE in vivo. The effects seen both in vivo and in vitro were remarkably similar to those previously reported for another substituted alcohol and its metabolites, ethylene glycol monomethyl ether. It is postulated that the two series of compounds may have a similar mode of action on rat testis.

Acetaldehyde↗
PubMed2004

Cloning of a full-length cDNA of human testis-specific spermatogenic cell apoptosis inhibitor TSARG2 as a candidate oncogene.

A novel human gene full-length cDNA sequence-TSARG2 was identified from a human testis cDNA library using the SRG2 gene (GenBank Accession No. ), which was significantly up-regulated in cryptorchidism, as an electronic probe. TSARG2 was 1223 bp in length. The putative protein encoded by this gene was 305 amino acids with a theoretical molecular weight of 34,751 and isoelectric point of 9.85. The sequence shared no significant homology with any known protein in databases except SRG2. Northern blot analysis revealed that 1.7 kb TSARG2 transcript was detected selectively in human testis. Furthermore, results of in situ hybridization assay confirmed that TSARG2 was expressed in seminiferous tubules, more precisely in spermatogonia and spermatocyte. No mutation was found by PCR-SSCP in 122 cases of azoospermia, severe oligzoospermia, and cryptorchidism. The green fluorescence produced by pEGFP-C1/TSARG2 was detected on the nucleus of COS7 cells after 24h post-transfection. The pcDNA3.1(-)/TSARG2 plasmid was constructed and introduced into MCF7 cells by liposome transfection. TSARG2 can accelerate MCF7 cells to traverse the S-phase and enter the G2-phase compared with the control without transfection of TSARG2, which suggested that this gene plays an important role in the development of cryptorchid testis and is a testis-specific apoptosis candidate oncogene.

Amino Acid Sequence↗
PubMed1999

Temperature-dependent sex determination: upregulation of SOX9 expression after commitment to male development.

In mammals, birds and reptiles the morphological development of the gonads appear to be conserved. This conservation is evident despite the different sex determining switches employed by these vertebrate groups. Mammals exhibit chromosomal sex determination (CSD) where the key sex determining switch is the Y-linked gene, SRY. Although SRY is the trigger for testis determination in mammals, it is not conserved in other vertebrate groups. However, a gene closely related to SRY, the highly conserved transcription factor, SOX9, plays an important role in the testis pathway of mammals and birds. In contrast to the CSD mechanism evident in mammals and birds, many reptiles exhibit temperature dependent sex determination (TSD) where the egg incubation temperature triggers sex determination. Here we examine the expression of SOX9 during gonadogenesis in the American alligator, (Alligator mississippiensis), a reptile that exhibits TSD. Alligator SOX9 is expressed in the embryonic testis but not in the ovary. However, the timing of SOX9 upregulation in the developing testis is not consistent with a role for this gene in the early stages of alligator sex determination. Since SOX9 upregulation in male embryos coincides with the structural organisation of the testis, SOX9 may operate farther downstream in the vertebrate sex differentiation pathway than previously postulated.

Alligators and Crocodiles↗
PubMed1997

[Male pseudohermaphroditism].

Male pseudohermaphroditism is a condition of sex differentiation disorders in which the gonads are tests, but the genital ducts and/or external genitalia are incompletely masculinized. This syndrome is caused by a failure of the sequential process in embryonal development of the testis. In the presence of functioning testis the Müllerian ducts regress, while the mesonephric ducts and urogenital sinus differentiate into the internal and external male genitalia. Male pseudohermaphroditism is classified to subtypes according to etiological factors: (1) testicular unresponsiveness to hCG and LH; (2) defect in testosterone biosynthesis; (3) end-organ resistance to androgen; (4) defects in the intracellular metabolism of testosterone; (5) aberrations in testicular organogenesis; (6) defects in anti-Müllerian hormone.

Dihydrotestosterone↗
PubMed1988

[A case of Kallmann's syndrome].

A 13-year-old boy visited our hospital with the chief complaint of right undescended testis and retardation of secondary sexual characteristics. Central hyposmia and sensorineural hearing loss were found. The plasma levels of luteinizing hormone (LH) and follicle stimulating hormone (FSH) were low and the reaction to LH-releasing hormone (RH) test was poor. After repeated LH-RH tests, a good response in plasma levels of LH and FSH was observed. The diagnosis of Kallmann's syndrome was made from the above findings. The testicular biopsy specimen from him showed immature testis without any developed Leydig or Sertoli cells. To induce secondary sexual characteristics, 2000 I.U. of human chorionic gonadotropin (hCG) was administered to him twice a week for 3 months. The administration of hCG resulted in elevation of plasma testosterone level, swelling of testes, increase of pubic hair and spurt of height.

Adolescent↗
PubMed1998

Distribution of PNP 14 (beta-synuclein) in neuroendocrine tissues: localization in Sertoli cells.

Phosphoneuroprotein (PNP 14) is abundant in the central nervous system and is localized at nerve endings but not in synaptic vesicles. In this study, we examined the presence of PNP 14 in various endocrine tissues of the rat. PNP 14 was not detected in the endocrine cells of the intestine, testes, or adrenal gland, but it was present in axon terminals in both the medulla of the adrenal gland and the anterior pituitary gland. When testes were stained with PNP 14-specific antibodies by an indirect immunofluorescence method, PNP 14 was found in Sertoli cells of the testes, associated with fibrillar structures. PNP 14 was also detected in cultured Sertoli cells with a fibrillar pattern in the cytoplasm and around the nuclei. The fibrillar structure did not resemble actin stress fibers, microtubules, or intermediate filaments. The amount of PNP 14 in the testis changed with development. It increased markedly during the first 4 weeks after birth and then decreased. During the first 4 weeks after birth, spermatogonia undergo two rounds of meiosis. It is possible, therefore, that PNP 14 might be a factor related to meiosis.

Animals↗
PubMed2004

Differential expression of estrogen receptors (ERalpha/ERbeta) in testis of mature and immature pigs.

High affinity estrogen receptors (ERs) mediate estrogen action in male reproductive tissues. The objective of the present study was the immunolocalization of estrogen receptor alpha and estrogen receptor beta in immature and mature testes of pig, a species in which the role of estrogens on gonadal function is scarcely known. Testes from 3 and 18 month-old pigs were investigated. Immunohistochemistry was performed on paraffin embedded-tissues using both mouse anti-human monoclonal IgG ERalpha and IgG ERbeta 1 isoform. Western blot analysis demonstrated antibody specificity. ERalpha staining was not observed in immature testes, but it was detected in spermatogonia, spermatocytes and in the most Leydig cells of mature testes. ERbeta immunoreactivity was observed in spermatogonia and Leydig cells of immature gonads, while it was clearly detected in spermatogonia and in spermatocytes of adult pig testes. The differential ERalpha/ERbeta expression in germ and somatic cells of the gonads suggest a role of estrogens in function and in development of pig testis.

Animals↗
PubMedDate not supplied

[Environmental/occupational exposure and testicular tumors: is there a relationship?].

UNLABELLED: Although the incidence and mortality of testicular cancer are low (1), it is of interest because of its increasing incidence, its earlier onset and its geographical distribution. A part for cryptorchidism, the aetiology is unknown but previous studies have raised the hypothesis that exogenous hormones like endocrine disrupters may play a role in the development of testicular cancer. OBJECTIVE: The aim of this study is to identify possible risk factors of testicular cancer in relation to environmental and occupational exposure, of the subject himself and of his mother. In in particular the study attempts to evaluate exposure to endocrine disrupters during the critical period of the development of the testis. MATERIAL AND METHODS: This is an on going hospital case-control study conducted, at least, in six Romain hospital. Cases were recruited from hospital discharge records from 1995 to 2002. Controls were selected randomly form the orthopaedics' division. We are therefore collecting data with personal interviews from patients and their mother. Subjects are interviewed by phone (cases) or face-to-face (controls). We are interviewing also the mothers to received information on pregnancy. Estimate odds ratio (OR) and 95% confidence interval will be calculated, using a statistical software program specific for case-control studies. CONCLUSIONS: The study will contribute to clarify if the hypothesis that exposure to endocrine disrupters may be involved in the development of testicular cancer.

Case-Control Studies↗
PubMed2005

Clinical, hormonal and cytogenetic evaluation of 46,XX males and review of the literature.

The main factor influencing the sex determination of an embryo is the genetic sex determined by the presence or absence of the Y chromosome. However, some individuals carry a Y chromosome but are phenotypically female (46,XY females) or have a female karyotype but are phenotypically male (46,XX males). 46,XX maleness is a rare sex reversal syndrome affecting 1 in 20,000 newborn males. Molecular analysis of sex-reversed patients led to the discovery of the SRY gene (sex-determining region on Y). The presence of SRY causes the bipotential gonad to develop into a testis. The majority of 46, SRY-positive XX males have normal genitalia; in contrast SRY-negative XX males usually have genital ambiguity. A small number of SRY-positive XX males also present with ambiguous genitalia. Phenotypic variability observed in 46,XX sex reversed patients cannot be explained only by the presence or absence of SRY despite the fact that SRY is considered to be the major regulatory factor for testis determination. There must be some other genes either in the Y or other autosomal chromosomes involved in the definition of phenotype. In this article, we evaluate four patients with 46,XX male syndrome with various phenotypes. Two of these cases are among the first reported to be diagnosed prenatally.

Chromosome Aberrations↗
PubMed2005

Spermatogenesis and sperm transit through the epididymis in mammals with emphasis on pigs.

Starting from the period of testis differentiation, the Sertoli cell plays a pivotal role in the development of a functional testis. FSH is the major mitotic factor for Sertoli cells. Because the supporting capacity of Sertoli cells is relatively fixed for each species, their total number per testis, established just before puberty (approximately 4 months in pigs), dictates the potential for sperm production. In contrast to Sertoli cells that are still undifferentiated, mature Leydig cells are already present at birth in pigs. Spermatogenesis lasts from 30 to 75 days in mammals, and this time period is under the control of the germ cell genotype. In boars, each spermatogenic cycle and the entire spermatogenic process lasts 8.6-9.0 and approximately 40 days, respectively. The sperm transit through the epididymis takes approximately 10 days in pigs and this is within the range cited for most mammals. Germ cell loss occurs normally during spermatogenesis, mainly during the spermatogonial and meiotic phases. In pigs, significant germ cell loss also takes place during spermiogenesis. In mammals in general, including pigs, only 2-3 out of a possible 10 spermatozoa are produced from each differentiated type A1 spermatogonium. The high supporting capacity of Sertoli cells and the short duration of the spermatogenic cycle are the main factors responsible for the comparatively high spermatogenic efficiency of pigs.

Animals↗
PubMed1999

Effect of neonatal exposure to estrogenic compounds on development of the excurrent ducts of the rat testis through puberty to adulthood.

Neonatal exposure to diethylstilbestrol (DES) can alter the structure of the testicular excurrent ducts in rats. We characterized these changes according to dose and time posttreatment and established whether potent estrogens (ethinyl estradiol), environmental estrogens (genistein, octylphenol, bisphenol A, parabens), and tamoxifen induce such changes. Rats were administered these compounds neonatally and assessed at several time points during (day 10, or day 18 for some treatments) and after (days 18, 25, 35, and 75) the treatment period to detect any changes in testis weight, distension of the rete testis and efferent ducts, epithelial cell height in the efferent ducts, and immunoexpression of the water channel aquaporin-1 (AQP-1). Treatment with DES (10, 1, or 0.1 microg/injection; equivalent to 0.37, 0.037, or 0.0037 mg/kg/day, respectively) induced dose-dependent changes in testis weight and all parameters. These effects were most pronounced at days 18 and 25 and appeared to lessen with time, although some persisted into adulthood. Neonatal treatment with ethinyl estradiol (10 microg/injection; equivalent to 0.37 mg/kg/day) caused changes broadly similar to those induced by 10 mg DES. Administration of tamoxifen (2 mg/kg/day) caused changes at 18 days that were similar to those induced by 1 microg DES. Treatment with genistein (4 mg/kg/day), octylphenol (2 mg/injection; equivalent to 150 mg/kg/day), or bisphenol A (0.5 mg/injection; equivalent to 37 mg/kg/day) caused minor but significant (p<0.05) decreases in epithelial cell height of the efferent ducts at days 18 and/or 25. In animals that were followed through to 35 days and/or adulthood, these changes were no longer obvious; other parameters were either unaffected or were affected only marginally and transiently. Administration of parabens (2 mg/kg/day) had no detectable effect on any parameter at day 18. To establish whether these effects of estrogens were direct or indirect (i.e., resulting from reduced follicle-stimulating hormone/luteinizing hormone secretion), the above end points were assessed in animals in which gonadotropin secretion was suppressed neonatally by administration of a gonadotropin-releasing hormone antagonist. This treatment permanently reduced testis weight, but did not affect any of the other end points, apart from a minor transient reduction in efferent duct epithelial cell height at 18 days. This study suggests that structural and functional (expression of AQP-1) development of the excurrent ducts is susceptible to impairment by neonatal estrogen exposure, probably as a consequence of direct effects. The magnitude and duration of adverse changes induced by treatment with a range of estrogenic compounds was broadly comparable to their estrogenic potencies reported from in vitro assays.

Animals↗
PubMed1975

Effects of fetal decapitation on the structure and function of Leydig cells in rhesus monkeys (Macaca mulatta).

Fetal decapitation in utero has enabled us to study the role of fetal pituitary hormones in the development of the fetal testis. Testes from males decapitated near 80 days of gestational life and later delivered at 150 days were smaller than normal and about one-tenth the normal weight. The size of the seminiferous tubules was similar in both groups; however, the number of Leydig cells seemed reduced. In addition, the Leydig cells of the experimental group contained smaller mitochondria with reduced tubular cristae, fewer lipid droplets, and reduced agranular endoplasmic reticulum. Androgen production was inhibited. Measured by radioimmunoassay, the testosterone level in the umbilical vein was 329 +/- 82 pg/ml in six decapitates fetuses, 412 +/- 62 pg/ml in ten normal fetuses. The level in the umbilical artery was 328 +/- 56 pg/ml in five decapitated fetuses, 658 +/- 140 pg/ml in normal fetuses. These studies suggest that chronic deprivation of fetal pituitary hormones inhibits the growth and development of the testis in general and of the Leydig cells in particular.

Androgens↗