Transcriptional Profiling of Adult Male Rat Liver and Testis following 14 Day Myclobutanil Exposure
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE139098 | GEO | 2020/12/15
REPOSITORIES: GEO
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Project description:Transcriptional Profiling of Adult Male Rat Liver and Testis following 14 Day Myclobutanil Exposure
| PRJNA578380 | ENA
Project description:The modes of triazole reproductive toxicity have been characterized by an observed increased in serum testosterone and reduced insemination and fertility indices. The key events involved in the disruption in testosterone homeostasis and reduced fertility remain unclear. Gene expression analysis was conducted on liver and testis from Wistar Han IGS rats fed myclobutanil (M: 500, 2000 ppm), propiconazole (P: 500, 2500 ppm), or triadimefon (T: 500, 1800 ppm) from gestation day six to postnatal day 92. Pathway-based analysis highlighted key biological processes affected by all three triazoles in the liver including fatty acid catabolism, steroid metabolism, and xenobiotic metabolism. Triadimefon induced a distinctive expression profile of genes involved in liver sterol biosynthesis. There were no common pathways modulated by all three triazoles in the testis. Within the pathways identified in the liver, specific genes involved in phase I-III metabolism (Aldh1a1, Cyp1a1, Cyp2b2, Cyp3a1, Slco1a4, Udpgtr2), fatty acid metabolism (Cyp4a10, Pc, Ppap2b), and steroid metabolism (Srd5a1, Ugt1a1, Ugt2a1) were affected by all three triazoles. These modulated genes are part of a network of lipid and testosterone homeostasis pathways regulated by the constitutive androstane (CAR) and pregnane X (PXR) receptors. Gene expression profiles from this study indicate triazoles activate CAR and PXR; increase fatty acid catabolism, sterol biosynthesis, and steroid metabolism in the liver; constituting a plausible series of key events contributing to the observed disruption in testosterone homeostasis. Experiment Overall Design: A total of 34 testis samples were analyzed. Seven biological replicates for control, 4 biological replicates for mid dose myclobutanil, 5 biological replicates for high dose myclobutanil, 4 biological replicates for mid dose propiconazole, 5 biological replicates for high dose propiconazole, 4 biological replicates for mid dose triadimefon, and 5 biological replicates for high dose triadimefon.
2008-04-09 | E-GEOD-10412 | biostudies-arrayexpress
Project description:Purpose: The objective of this study was to identifiy if a low dose of BaP would alter gene expression profiles and key pathways in the liver and testis of adult male tilapia Methods: The liver and testis tissue from the BaP-treated or control groups fish were collected and then total RNA was extracted, RNA integrity (RIN) was evaluated (RIN >7) for Illumina RNA-Seq library construction and Sequencing. Gene read mapping was performed with TopHat and differential expression analysis (DE) was conducted using exact test with R package EdgeR (p < 0.05; fold change > ± 1.5 were considered as significant). Pathway analysis was performed using the gene set enrichment analysis (GSEA) and subnetwork enrichment analysis (SNEA) applying the Mann-Whitney test with an alpha level of p < 0.05 to identify the biological mechanism that underlie the BaP effects in male tilapia. Results: RNA-Seq analysis using EdgeR showed a larger number of altered genes in liver than in testis as a result of BaP exposure. In liver, 1444 genes were significantly differentially expressed, while in the testis only 309 showed any changes using a p < 0.05 and fold change > ± 1.5 Conclusions: Low dose of BaP can alter genes and molecular pathways in the liver and testis in male adult tilapia, and these changes could be associated with biological endpoints disruption.
2018-07-06 | GSE116687 | GEO
Project description:The modes of triazole reproductive toxicity have been characterized by an observed increased in serum testosterone and reduced insemination and fertility indices. The key events involved in the disruption in testosterone homeostasis and reduced fertility remain unclear. Gene expression analysis was conducted on liver from Sprague Dawley rats dosed with myclobutanil (300 mg/kg/day), propiconazole (300 mg/kg/day), or triadimefon (175 mg/kg/day) for 72 hours. Pathway-based analysis highlighted key biological processes affected by all three triazoles in the liver including fatty acid catabolism, steroid metabolism, and xenobiotic metabolism. Within the pathways identified in the liver, specific genes involved in phase I-III metabolism and fatty acid metabolism were affected by all three triazoles. These modulated genes are part of a network of lipid and testosterone homeostasis pathways regulated by the constitutive androstane (CAR) and pregnane X (PXR) receptors. Gene expression profiles from this study indicate triazoles activate CAR and PXR; increase fatty acid catabolism and steroid metabolism in the liver; constituting a plausible series of key events contributing to the observed disruption in testosterone homeostasis. Experiment Overall Design: A total of 12 liver samples were analyzed. Three biological replicates each for the controls, 300 mg/kg/day myclobutanil, 300 mg/kg/day propiconazole, and 175 mg/kg/day triadimefon.
2008-04-08 | E-GEOD-10409 | biostudies-arrayexpress
Project description:Provided later Pregnant Fisher 344 rats will be purchased from Charles River Laboratories, Inc. and delivered to CIIT on gestational day (GD) 7 (GD0 = day first vaginal plug positive). At gestational day 12 (GD12), the dams will be exposed once/day until GD20 to 50 mg/kg dibutyl phthalate (DBP) in corn oil vehicle via oral gavage. Each dose group will contain 4-6 vehicle control or phthalate treated dams. Groups of animals will be sacrificed at GD20, postnatal day (PND) 35, and PND90 for endpoint analysis. At GD20, treated and control animals will be examined for various endpoints including body weight, testicular histopathology, gene expression profile via microarray analysis, and anogenital distance (AGD). AGD (at parturition; PND1) and nipple number/location (at PND14 and day of sacrifice) will be determined on animals in the postnatal groups. At PND35 or 90, one male from each in utero corn oil vehicle or DBP exposed group will receive a second gavage of either corn oil or 500 mg/kg DBP. 6 hours after the second gavage, the following endpoints will be examined: 1) testis histopathology; 2) spermatid head quantification (PND90 only); 3) testis and body weights; 5) genome-wide gene expression (via microarray); and 6) germ cell apoptosis (TUNEL assay).
2008-11-24 | E-GEOD-13550 | biostudies-arrayexpress
Project description:The current study investigates the direct effects of in utero vinclozolin exposure on the developing rat testis transcriptome. Vinclozolin is a commonly used fungicide in agriculture and is an endocrine disruptor with anti-androgenic activity. Previous studies have demonstrated that exposure to vinclozolin during embryonic gonadal sex determination induces epigenetic modifications of the germ line and transgenerational adult onset disease states that include spermatogenic cell defects, prostate disease, kidney disease, and tumor development. An investigation of the molecular actions of vinclozolin was initiated through an analysis of direct actions on the F1 generation embryonic testis development. Microarray analyses were performed to compare control and vinclozolin treated testis transcriptomes at embryonic day 13, 14 and 16. A total of 576 differentially expressed genes were identified and the major cellular functions and pathways associated with these altered transcripts were examined. The sets of regulated genes at the different development periods were found to be transiently altered and distinct. Interestingly, genes previously shown to be regulated during normal male sex determination were not altered by vinclozolin treatment. Categorization by major known functions of all 576 genes altered by in utero vinclozolin exposure demonstrates transcription, signaling, cytoskeletal and extra cellular matrix associated transcripts are highly represented. Specific cellular process and pathway analyses suggest the involvement of Wnt and calcium signaling, vascular development and epigenetic mechanisms as potential mediators of the direct F1 generation actions of vinclozolin. For Samples 1-12: We used microarrays to determine genes expressed differentially between control and in utero Vinclozolin treated E13, E14, and E16 rat testis. For Samples 13-16: We used microarrays to determine genes expressed differentially between control and in vitro Vinclozolin treated E13 cultured rat testis. For Samples 17-20: We used microarrays to determine genes expressed differentially between control and in vitro Flutamide treated rat E13 cultured testis.
2010-02-14 | GSE20245 | GEO
Project description:The current study investigates the direct effects of in utero vinclozolin exposure on the developing rat testis transcriptome. Vinclozolin is a commonly used fungicide in agriculture and is an endocrine disruptor with anti-androgenic activity. Previous studies have demonstrated that exposure to vinclozolin during embryonic gonadal sex determination induces epigenetic modifications of the germ line and transgenerational adult onset disease states that include spermatogenic cell defects, prostate disease, kidney disease, and tumor development. An investigation of the molecular actions of vinclozolin was initiated through an analysis of direct actions on the F1 generation embryonic testis development. Microarray analyses were performed to compare control and vinclozolin treated testis transcriptomes at embryonic day 13, 14 and 16. A total of 576 differentially expressed genes were identified and the major cellular functions and pathways associated with these altered transcripts were examined. The sets of regulated genes at the different development periods were found to be transiently altered and distinct. Interestingly, genes previously shown to be regulated during normal male sex determination were not altered by vinclozolin treatment. Categorization by major known functions of all 576 genes altered by in utero vinclozolin exposure demonstrates transcription, signaling, cytoskeletal and extra cellular matrix associated transcripts are highly represented. Specific cellular process and pathway analyses suggest the involvement of Wnt and calcium signaling, vascular development and epigenetic mechanisms as potential mediators of the direct F1 generation actions of vinclozolin. For Samples 1-12: We used microarrays to determine genes expressed differentially between control and in utero Vinclozolin treated E13, E14, and E16 rat testis. For Samples 13-16: We used microarrays to determine genes expressed differentially between control and in vitro Vinclozolin treated E13 cultured rat testis. For Samples 17-20: We used microarrays to determine genes expressed differentially between control and in vitro Flutamide treated rat E13 cultured testis. For Samples 1-12: RNA samples from two control groups are compared to two Vinclozolin treated groups for each E13, E14, E16 testis. For Samples 13-16: RNA samples from two control groups of E13 cultured testis are compared to two Vinclosolin treated groups of E13 cultured testis. For Samples 17-20: RNA samples from two control groups of E13 cultured testis are compared to two Flutamide treated groups of E13 cultured testis.
2010-02-24 | E-GEOD-20245 | biostudies-arrayexpress
Project description:We determined global gene changes in immature ovaries and testes in response to an in utero exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure. Microarray analysis was performed using testes and ovaries of the dioxin-exposed dams’ offspring. One hundred and thirteen genes were differentially expressed in ovaries and 56 genes in testes of 14 and 5 days-old, respectively. Real-time PCR was used to validate and extend data using RNA extracted from 5 to 145-day old rat testes and 3 to 25-day old rat ovaries. A single gene of the classic dioxin battery, i.e., the repressor of the aryl hydrocarbon receptor (Ahrr) was found altered in testes. In contrast, several of them including Cyp1a1, Cyp1b1, Nqo1, and Ahrr were found up-regulated in ovary, pituitary (a different endocrine organ) and liver. In addition to Ahrr, we identified 6 genes targeted by dioxin in both gonads, including the chemokines Cxcl4, Ccl5. Ccl5 gene expression levels were also regulated in pituitary and liver, so as pituitary Cxcl4. Four genes targeted by TCDD in testis and meeting stringent criteria were further surveyed. It included 2 genes with no previous reported function in testis, Art2b, Gzmf, Hpgds and Fgf13. Fgf13 was down-regulated in testis, and pituitary but not in ovary or liver. Interestingly, Art2b and Gzmf were up-regulated in testis, liver and pituitary but not ovary. Finally, Hpgds was unique in that expressed in various tissues it was regulated by TCDD in the gonads but not in the other tissues studied.
2011-10-12 | GSE32890 | GEO
Project description:The modes of triazole reproductive toxicity have been characterized by an observed increased in serum testosterone and reduced insemination and fertility indices. The key events involved in the disruption in testosterone homeostasis and reduced fertility remain unclear. Gene expression analysis was conducted on liver and testis from Wistar Han IGS rats fed myclobutanil (M: 500, 2000 ppm), propiconazole (P: 500, 2500 ppm), or triadimefon (T: 500, 1800 ppm) from gestation day six to postnatal day 92. Pathway-based analysis highlighted key biological processes affected by all three triazoles in the liver including fatty acid catabolism, steroid metabolism, and xenobiotic metabolism. Triadimefon induced a distinctive expression profile of genes involved in liver sterol biosynthesis. There were no common pathways modulated by all three triazoles in the testis. Within the pathways identified in the liver, specific genes involved in phase I-III metabolism (Aldh1a1, Cyp1a1, Cyp2b2, Cyp3a1, Slco1a4, Udpgtr2), fatty acid metabolism (Cyp4a10, Pc, Ppap2b), and steroid metabolism (Srd5a1, Ugt1a1, Ugt2a1) were affected by all three triazoles. These modulated genes are part of a network of lipid and testosterone homeostasis pathways regulated by the constitutive androstane (CAR) and pregnane X (PXR) receptors. Gene expression profiles from this study indicate triazoles activate CAR and PXR; increase fatty acid catabolism, sterol biosynthesis, and steroid metabolism in the liver; constituting a plausible series of key events contributing to the observed disruption in testosterone homeostasis. Experiment Overall Design: A total of 35 liver samples were analyzed. Seven biological replicates for the controls, 5 biological replicates for mid dose myclobutanil and 5 biological replicates for high dose mylcobutanil. There are 5 biological replicates for mid dose propiconazole, 4 biological replicates for high dose propiconazole, 5 biological replicates for mid dose triadimefon, and 4 biological replicates for triadimefon.
2008-04-09 | E-GEOD-10411 | biostudies-arrayexpress
Project description:To investigate the molecular mechanisms associated with initial dose-related events that are linked to the development of liver tumours: liver growth; cell proliferation; changes in histopathology such as hypertrophy
2009-10-28 | GSE18753 | GEO