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Anchoring ethinylestradiol induced gene expression changes with testicular morphology and reproductive function in the medaka

ABSTRACT: This study assessed the implications of a 14 day sub-chronic exposure of ethinylestradiol (EE2; 1.0 or 10.0 µg/L EE2) on male medaka fertility, testicular histology and testicular gene expression. The findings demonstrate that a 14 day exposure to EE2 induced impaired male reproductive capacity and time- and dose-dependent alterations in testicular morphology and gene expression. The average fertilization rate/day following the exposure for control, 1.0 and 10.0 µg/L EE2 was 91.3% (±4.4), 62.8% (±8.3) and 28.8% (±5.8), respectively. The testicular morphologic alterations observed include increased germ cell apoptosis, decreased germinal epithelium and thickening of the interstitium. The morphologic changes observed were highly associated with gene expression changes observed using a medaka-specific microarray. A pathway analysis of the differentially expressed genes emphasized genes and pathways associated with apoptosis, cell cycle and proliferation, collagen production/extracellular matrix organization, hormone signaling, male reproduction and protein ubiquitination among others.

ORGANISM(S): Oryzias latipes

PROVIDER: GSE44859 | GEO | 2013/03/06

SECONDARY ACCESSION(S): PRJNA192424

REPOSITORIES: GEO

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Anchoring ethinylestradiol induced gene expression changes with testicular morphology and reproductive function in the medaka

Project description:This study assessed the implications of a 14 day sub-chronic exposure of ethinylestradiol (EE2; 1.0 or 10.0 M-BM-5g/L EE2) on male medaka fertility, testicular histology and testicular gene expression. The findings demonstrate that a 14 day exposure to EE2 induced impaired male reproductive capacity and time- and dose-dependent alterations in testicular morphology and gene expression. The average fertilization rate/day following the exposure for control, 1.0 and 10.0 M-BM-5g/L EE2 was 91.3% (M-BM-14.4), 62.8% (M-BM-18.3) and 28.8% (M-BM-15.8), respectively. The testicular morphologic alterations observed include increased germ cell apoptosis, decreased germinal epithelium and thickening of the interstitium. The morphologic changes observed were highly associated with gene expression changes observed using a medaka-specific microarray. A pathway analysis of the differentially expressed genes emphasized genes and pathways associated with apoptosis, cell cycle and proliferation, collagen production/extracellular matrix organization, hormone signaling, male reproduction and protein ubiquitination among others. Six month old male medaka were exposed to ethinyl estradiol (EE2) for a 14 day time period. Treatment exposures were completed in triplicate including DMSO (vehicle control), 1.0 M-BM-5g/L EE2, and 10.0 M-BM-5g/L EE2. Fish were sampled for gene expression on days 1, 7 and 14 of exposure. Five male fish were placed in 2-liter beaker replicates for each treatment and sampling time point.

2013-03-06 | E-GEOD-44859 | biostudies-arrayexpress

Effects of in utero and lactational exposure to new generation green plasticizers on adult male rats: a comparative study with di(2-ethylhexyl) phthalate

Project description:Di(2-ethylhexyl) phthalate (DEHP), a widely used plasticizer, is a ubiquitous environmental pollutant and may act as an endocrine disruptor. Early life exposures to DEHP may result in anti-androgenic effects, impairing the development of the male reproductive tract. However, data on the long-lasting consequences of such DEHP exposures on adult male reproductive function are still rare and discrepant. Previously, we identified two novel plasticizers, 1,4 butanediol dibenzoate (BDB) and dioctyl succinate (DOS), as potential substitutes for DEHP that did not reproduce classically described endocrine disrupting phenotypes in prepubertal male offspring after maternal exposure. Here, we investigated the consequences of in utero and lactational exposure to BDB and DOS on adult male rat reproductive function in a comparative study with DEHP and a commercially available alternative plasticizer, 1,2-cyclohexane dicarboxylic acid diisononyl ester (DINCH). Timed pregnant Sprague-Dawley rats were gavaged with vehicle or a test chemical (30 or 300 mg/kg/day) from gestation day 8 to postnatal day 21. While DEHP exposure (300 mg/kg/day) significantly increased epididymal weight in the adult, exposure to DINCH, BDB or DOS did not affect reproductive organ weights, steroid levels or sperm quality. Using a toxicogenomic microarray approach, we found that adult testicular gene expression was affected by exposure to the higher dose of DEHP; transcripts such as Nr5a2, Ltf or Runx2 were significantly downregulated, suggesting that DEHP was targeting estrogen signaling. Lesser effects were observed after treatment with either DINCH or BDB. DOS exposure did not produce such effects, confirming its potential as a responsible substitute for DEHP. The data deposited correspond to testicular gene expression in 90 day-old Sprague-Dawley rats after exposure to CORN OIL and 30 or 300 mg/kg/day DEHP, DINCH, BDB or DOS from gestational day 8 to post-natal day 21

2018-02-14 | GSE110553 | GEO

Proteomic analysis after chronic exposure to 3 different low-dose of IR

Project description:Research describing alteration of Medaka proteome after chronic exposure (190 days) to low-doses (2.25, 21.01 or 204.3 mGy/day) ionizing radiation analyzing the whole-body.

2021-08-10 | PXD025741 | JPOST Repository

RNA-seq of the zebrafish (danio rerio) brain after developmental exposure to 17-ethinylestradiol

Project description:17-ethinylestradiol (EE2) is a synthetic estrogen commonly used as an active substance in oral contraceptives. It is frequently found in waste water effluent and raise concern due to its persistent nature. EE2 binds to estrogen receptors with similar affinity to oestradiol and acts as one of the most potent hormone mimics found in the environment. Estrogen is involved in many aspects of the development of the neuroendocrine system influencing both brain structure and behavior. We and others have reported a significant effect on non-reproductive behaviors in adult fish and in recent studies we found that developmental exposure to EE2 resulted in an anxiogenic phenotype as adults even after a long remediation period. In this study we aim to study possible mechanisms behind the behavior alterations of zebrafish developmentally exposed to EE2 by sequencing the whole brain transcriptome. Zebrafish embryos were exposed to 0, 2.14 and 7.34 ng/L EE2 from 1 day to 80 days post fertilization. After the exposure period a remediation period of 120 days followed before the fish were sampled. 3 male brains from the control group (0 ng/L) and the 2.14 ng/L group were sampled and 3 female brains from the control group (0 ng/L) and 7.34 ng/L were sampled.

2017-10-02 | E-MTAB-5173 | biostudies-arrayexpress

Expression data from mouse testis following chronic exposure to acrylamide via the drinking water

Project description:Acrylamide is a reproductive toxicant that has been detected in foods such as potato chips and breads. The consequences of chronic exposure to acrylamide in the human diet are unknown; however we previously reported that exposure to acrylamide at levels equivalent to human exposure produced high levels of genetic damage in early male germ cells of mice [Nixon et al. ToxSci 129(1), 135–145 (2012)]. In the present study, we examined changes in testicular gene expression in these mice to examine the potential mechanisms involved in acrylamide induced DNA damage in male germ cells and to provide a better understanding of the reproductive toxic effects of acrylamide in the male. Adult male mice were subjected to chronic acrylamide exposure via the drinking water at concentrations of 0, 0.001, 0.01, 0.1, 1 and 10 µg/ml for 1, 6 and 12 months. The testes were collected at each time point for RNA extraction and hybridization on an Illumina Sentrix Mouse ref-8 v2 Beadchip.

2014-06-01 | E-GEOD-47574 | biostudies-arrayexpress

Gene signaling pathways in liver of largemouth bass by a sub-chronic dietary exposure to EE2

Project description:The objective of this study was to investigate pathway signatures altered in the livers of female largemouth bass (LMB) and their potential links with biological responses by dietary exposure to 0.2 mg EE2/Kg (1% of their body weight) over two months using a transcriptomics approach. A high concentration of dietary 17alpha-ethinylestradiol (EE2) can activate key signaling pathways in response to oxidative damage may occur regardless of tumorigenesis and cancer. Female LMB received about 1.2g EE2/day/fish (from EE2-laced feed containing 0.2 mg EE2/Kg) for 60 days.

2014-08-31 | E-GEOD-59224 | biostudies-arrayexpress

17b-Trenbolone study

Project description:We investigated the genomic transcriptional response of female fathead minnows (Pimephales promelas) to an acute (4 day) exposure to 0.1 or 1.0 µg/L of, 17β-trenbolone (TB), the active metabolite of an anabolic androgenic steroid used as a growth promoter in cattle and a contaminant of concern in aquatic systems. Our objectives were to investigate the gene expression profile induced by TB, define biomarkers of exposure to TB, and increase our understanding of the mechanisms of adverse effects of TB on fish reproduction. In female gonad tissue, microarray analysis using a 22K oligonucleotide microarray (EcoArray Inc., Gainesville, FL) showed 99 significantly upregulated genes and 741 significantly downregulated genes in response to 1 µg TB/L. In particular, hydroxysteroid (17β) dehydrogenase 12a (hsd17b12a), zona pellucida glycoprotein 2.2 (zp2.2), and protein inhibitor of activated STAT, 2 (pias2) were all downregulated in gonad.

2009-01-01 | GSE12904 | GEO

High-fat or ethinyl-estradiol intake during pregnancy increases mammary cancer risk in several generations of offspring

Project description:Maternal exposures during pregnancy influence the risk of many chronic adult-onset diseases in the offspring. We investigated whether feeding pregnant rats a high fat (HF) or ethinyl-estradiol (EE2)-supplemented diet affects carcinogen-induced mammary cancer risk in daughters, granddaughters and great-granddaughters. Here we show that mammary tumorigenesis is higher in daughters and granddaughters of HF rat dams and in daughters, granddaughters and great-granddaughters of EE2 rat dams. Outcross experiments indicate that increased mammary cancer risk is transmitted to HF granddaughters equally through the female or male germlines, but it is only transmitted to EE2 granddaughters through the female germline. The effects of maternal EE2 exposure on offspring's mammary cancer risk are associated with alternations in the DNA methylation machinery and methylation patterns in mammary tissue of all three EE2 generations. We conclude that dietary and estrogenic exposures in pregnancy increase breast cancer risk in multiple generations of offspring, possibly through non-genetic means

2012-09-20 | GSE40251 | GEO

Gene expression profiles from livers of ethinylestradiol- and chlorpromazine-treated C57BL6/mice after 25 days

Project description:Toxicogenomics is used as a tool to identify mechanisms and markers of cholestasis in C57BL/6 mice treated by oral gavage using ethinylestradiol(EE2) and chlorpromazine (CPZ). A 25 day dose range finding study was performed, which resulted in no changes in clinical chemistry (serum cholesterol, total bile acids, and total bilirubin) or histopathology (hepatocyte vacuolization). Whole genome expression profiling of the liver was assessed after 25 days of repeated exposure with 10 mg/kg bw for CPZ and 3.70 mg/kg bw for EE2.

2017-08-10 | GSE47585 | GEO

Embryonic exposure to aluminium chloride blocks the onset of spermatogenesis through disturbing the dynamics of testicular tight junctions via upregulating Slc25a5 in offspring

Project description:Studies reveal neurotoxicity, hepatotoxicity, and developmental and reproductive toxicity in mice exposed to aluminium (Al). However, relatively few researches are conducted to clarify the mechanism of the impact of embryonic exposure to aluminium chloride (AlCl3) on the development of the reproductive system in male offspring. Here, pregnant mice were fed AlCl3 by gavage from day 12.5 of gestation. The results showed that embryonic AlCl3 exposure disrupted testicular development and spermatogenesis by damaging the testicular structure, reducing sperm counts, and altering the expression of the tight junction (TJ) proteins between Sertoli cells (SCs). Further in vitro studies showed that AlCl3 treatment stabilized the TJ proteins Occludin and ZO-1 expression by inhibiting the ERK signaling pathway to upregulate the Slc25a5 protein, which prompted ATP production to disrupt cytoskeletal protein homeostasis. Therefore, our study provided a new mechanism for AlCl3 exposure to interfere with testicular development and spermatogenesis and implied that Slc25a5 could be a target of AlCl3 affecting cell metabolism.

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