Transcription profiling of Atlantic cod exposed to alkylphenols and produced water
Ontology highlight
ABSTRACT:
ORGANISM(S): Gadus morhua
SUBMITTER: Kai Kristoffer Lie
PROVIDER: E-TABM-676 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:In this study, both male and female sexually regressed largemouth bass (Micropterus salmoides) (LMB) were fed a nominal concentration of 3.0 mg dieldrin/kg in feed for 60 days. A third group of male LMB was fed both 3.0 mg dieldrin/kg dieldrin and 0.7 mg E2/kg in feed. E2 was used as a model compound to elicit estrogenic effects via ER signaling.
2011-04-17 | GSE27963 | GEO
Project description:Background: Previously, we reported that perfluorooctanoic acid (PFOA) promotes liver cancer in manner similar to that of 17β-estradiol (E2) in rainbow trout. Also, other perfluoroalkyl acids (PFAAs) are weakly estrogenic in trout and bind the trout liver estrogen receptor (ER). Objectives: The primary objective of this study was to determine whether multiple PFAAs enhance hepatic tumorigenesis in trout, an animal model that represents human insensitivity to peroxisome proliferators. Methods: A two-stage chemical carcinogenesis model was employed in trout to evaluate PFOA, perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), perfluorooctane sulfonate (PFOS) and 8:2 fluorotelomer alcohol (8:2FtOH) as complete carcinogens or promoters of aflatoxin B1 (AFB1)- and/or N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced liver cancer. A custom trout DNA microarray was used to assess hepatic transcriptional response to these dietary treatments in comparison to E2 and the classic peroxisome proliferator clofibrate (CLOF). Results: Incidence, multiplicity and size of liver tumors in trout fed diets containing E2, PFOA, PFNA and PFDA were significantly higher compared to AFB1-initiated animals fed control diet, whereas PFOS caused a minor increase in liver tumor incidence. E2 and PFOA also enhanced MNNG-initiated hepatocarcinogenesis. Pearson correlation analyses, unsupervised hierarchical clustering and principal components analyses showed that the hepatic gene expression profiles for E2 and PFOA, PFNA, PFDA and PFOS were overall highly similar, though distinct patterns of gene expression were evident for each treatment, particularly for PFNA. Conclusions: Overall, these data suggest that multiple PFAAs can promote liver cancer and that the mechanism of promotion may be similar to that for E2. A total of 40 samples were analyzed using a a dye-swap, reference sample hybridization protocol. Rainbow trout were exposed to the following experimental treatments via the diet for two weeks (number in parenthesis is assigned group #): (1) Control; (2) 5 mg/kg diet estradiol (E2); (3) 2000 mg/kg diet perfluorooctanoic acid (PFOA); (4) 2000 mg/kg diet perfluorononanoic acid (PFNA); (5) 2000 mg/kg diet perfluorodecanoic acid (PFDA); (6) 200 mg/kg diet perfluorooctane sulfonate; (7) 2000 mg/kg 8:2 fluorotelomer alcohol (FTOH); and (8) 2000 mg/kg diet clofibrate. A total of 40 total hepatic mRNA samples were analyzed using a dye-swap, reference sample hybridization protocol. A reference RNA pool was made by combining equal amounts of RNA from all control RNA samples, with one exception. A separate time-matched reference pool was utilized for group 6 samples (PFOS treatment). Five hybridizations were performed for each treatment group in the following pattern: Replicate A Cy5/Reference Cy3; Replicate A Cy3/Reference Cy 5; Replicate B Cy5/Reference Cy3; Replicate B Cy3/Reference Cy5; Replicate C Cy5/Reference Cy3. Thus, the experiment consisted of three biological replicates, for two of which were replicated technically.
2011-08-01 | E-GEOD-31085 | biostudies-arrayexpress
Project description:This study examines whether maternal low ω6:ω3 ratio diet and offspring seaweed (SW) supplementation can improve offspring immunity and performance by elucidating the effects on piglet serum proteome. A total of 16 sows were given either a standard (CR, 13:1) or low ω6:ω3 ratio diet (LR, 4:1) during pregnancy and lactation and their male weaned piglets were supplemented with SW powder (4 g/kg, SW) or not (CT) in a 21-day post-weaning (PW) diet. Four PW piglet groups were then identified based on dam and piglet treatment, namely CRCT, CRSW, LRCT, and LRSW (n = 10 each). Piglet serum collected at weaning and d21 PW were analyzed (n = 5 each) using TMT-based quantitative proteomics and validated by appropriate assays.
2023-04-17 | PXD032327 | Pride
Project description:Understanding pathogen recognition and mechanisms in Atlantic cod are of significant importance for both basic research on wild populations and health management in aquaculture. A microarray approach was utilized to search for effects of viral (poly I:C/ polyinosinic acid:polycytidylic acid), bacterial (LPS/lipopolysaccharide) and polyclonal activator (PHA-L/phytohaemoagglutinin) stress in Atlantic cod head kidney cells. LPS cell activation increased mRNA expression of chemokine/Interleukin 8 (CXCL8/IL-8); interleukin -1? (IL-1?); cyclooxygenase 2 (COX2); leukocyte derived chemotaxin 2 (LECT2); LOC100698154, encoding a protein with unknown function; carboxyl-esterase 2 (CES2) and environmental biomarker cytochrome P450 1A (CYP1A). Mitogen activated protein kinase p38 (p38MAPK) and cathepsin F (CTSF) were downregulated by LPS. The antiviral responses induced by double stranded RNA (Poly I:C) clearly increased transcription of Toll like receptor 3 (TLR3) and interferon stimulating gene 15 (ISG15). The PHA response seemed to be more non-specific. Special for the PHA induction were the increase in Major histocompatibility complex class I (MHCI). CC chemokine type 2 (CK2) mRNA expression was increased by PHA, LPS and poly I:C, while p38MAPK and LECT2 was downregulated by PHA. Oxidative stress related genes like catalase and glutaredoxin (GLRX2) and the anti-apoptotic gene Bcl-2 showed no transcriptional changes compared to control in any of the treatments. Especially Poly I:C, but also LPS, induced leukotriene B4 (LTB4) and leukotriene B5 (LTB5) synthesis, while small amounts of prostaglandine E2 (PGE2) seemed to be constitutively produced in untreated cells, a production that was slightly elevated when exposing cells for LPS. This study reveals distinct signatures of bacteria and virus transcriptional responses in cod head kidney cells. In addition, the novel finding that Cyp1a was upregulated during the antibacterial response indicates a connection between immunity and aryl hydrocarbon receptor (AhR) activation in Atlantic cod.
2012-03-21 | E-MTAB-1058 | biostudies-arrayexpress
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:Using scaling from PhysB model
Blood flow in L/hr
Compartments in Kg
Baseline as ~0.003nM Free E2 in Blood_venous
E2 biosynthesis rate constant = 2
E2 biosynthesis species = 1nM
CLeh = 5
CLint = metabolic model
T:P = 0.286
2018-02-02 | MODEL1711210002 | BioModels
Project description:Human artificial chromosomes (HACs) have unique characteristics as gene-delivery vector, e.g., episomal transmission and transfer of multiple, large transgenes. Here, we demonstrate the advantages of HAC vectors for reprogramming mouse embryonic fibroblasts (MEFs) to induced pluripotent stem (iPS) cells. Two HAC vectors (iHAC1 and iHAC2) were constructed. Both carried four reprogramming factors, and iHAC2 also encoded a p53-knockdown construct (see Kazuki et al 2011). The iHAC1 partially reprogrammed MEFs, and the iHAC2 efficiently reprogrammed MEFs. Global gene expression showed that the iHACs, unlike other vectors, generated relatively uniform iPS cells. We established iHAC-free iPS cells by isolating cells that spontaneously lost the iHAC2. Analyses of pluripotent markers, teratomas, and chimeras confirmed that these iHAC-free iPS cells were pluripotent. Moreover, iHAC-free iPS cells with a re-introduced HAC encoding Herpes Simplex Virus Thymidine Kinase were eliminated by Ganciclovir treatment; therefore, the HAC safeguard system functioned in iPS cells. Thus, the HAC vector could generate uniform, integration-free iPS cells with a safeguard system. Total RNA from mouse embryonic fibroblasts, two control ES cells (TT2 and B6ES), retrovirus vector-derived iPS cells (20D17), and twelve HAC-derived iPS clones were hybridized to the Agilent Whole Mouse Genome microarrays.
2011-10-15 | E-GEOD-29441 | biostudies-arrayexpress
Project description:Using scaling from PhysB model
Blood flow in L/hr
Compartments in Kg
Baseline as ~0.013nM free E2 in plasma_venous
E2 biosynthesis rate constant = 2
E2 biosynthesis species = 1nM
CLeh = 5
CLint = 1scaled by liver weight
B:P = 0.286
IV bolus = 250/h (delivers in 2-3mins)
Added ER{gonads}
2018-02-02 | MODEL1711210001 | BioModels
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) or triadimefon (175 mg/kg/day) for 6, 24 or 336 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 15 liver samples were analyzed. Five biological replicates each for the controls, 225 mg/kg/day myclobutanil, and 175 mg/kg/day triadimefon.
2008-04-09 | E-GEOD-10408 | biostudies-arrayexpress
Project description:In this study, both male and female sexually regressed largemouth bass (Micropterus salmoides) (LMB) were fed a nominal concentration of 3.0 mg dieldrin/kg in feed for 60 days. A third group of male LMB was fed both 3.0 mg dieldrin/kg dieldrin and 0.7 mg E2/kg in feed. E2 was used as a model compound to elicit estrogenic effects via ER signaling. There were four samples analyzed for 1) control males 2) control females 3) males fed 3 mg/kg dieldrin 4) females fed 3.0 mg/kg dieldrin, and 5) males fed 3.0 mg/kg dieldrin + 0.7 mg/kg E2. There was a total of 20 microarrays and sample processed.
2011-04-17 | E-GEOD-27963 | biostudies-arrayexpress