The present study investigated whether inhibition of deiodinase, the enzyme which converts thyroxine (T4) to the more biologically-active form, 3,5,3'-triiodothyronine (T3), would impact inflation of the posterior and/or anterior chamber of the swim bladder, processes previously demonstrated to be thyroid-hormone regulated. Two experiments were conducted using a model deiodinase inhibitor, iopanoic acid (IOP). In the first study, fathead minnow (Pimephales promelas) embryos were exposed to 0.6, 1.9, or 6.0 mg IOP/L or control water in a flow-through system until reaching 6 days post-fertilization (dpf) at which time posterior swim bladder inflation was assessed. To examine effects on anterior swim bladder inflation, a second study was conducted with 6 dpf larvae exposed to the same IOP concentrations until reaching 21 dpf. Fish from both studies were sampled for T4/T3 measurements, gene transcription analyses, and thyroid histopathology. In the embryo study, incidence and length of inflated posterior swim bladders were significantly reduced in the 6.0 mg/L treatment at 6 dpf. Incidence of inflation and length of anterior swim bladder in larval fish were significantly reduced in all IOP treatments at 14 dpf, but inflation recovered by 18 dpf. Throughout the larval study, whole body T4 concentrations were significantly increased and T3 concentrations were significantly decreased in all IOP treatments. Consistent with hypothesized compensatory responses, significant up-regulation of deiodinase-2 mRNA was observed in the larval study, and down-regulation of thyroperoxidase mRNA was observed in all IOP treatments in both studies. Taken together, these results support the hypothesized adverse outcome pathways linking inhibition of deiodinase activity to impaired swim bladder inflation. This dataset is associated with the following publication: Cavallin, J., G. Ankley, B. Blackwell, C. Blanksma, K. Fay, K. Jensen, M. Kahl, D. Knapen, P. Kosian, S. Poole, E. Randolph, A. Schroeder, L. Vergauwen, and D. Villeneuve. Impaired swim bladder inflation in early-life stage fathead minnows exposed to a deiodinase inhibitor, iopanoic acid (article). ENVIRONMENTAL TOXICOLOGY AND CHEMISTRY. Society of Environmental Toxicology and Chemistry, Pensacola, FL, USA, 36(11): 2942-2952, (2017).

The present study investigated whether inhibition of deiodinase, the enzyme which converts thyroxine (T4) to the more biologically-active form, 3,5,3'-triiodothyronine (T3), would impact inflation of the posterior and/or anterior chamber of the swim bladder, processes previously demonstrated to be thyroid-hormone regulated. Two experiments were conducted using a model deiodinase inhibitor, iopanoic acid (IOP). In the first study, fathead minnow (Pimephales promelas) embryos were exposed to 0.6, 1.9, or 6.0 mg IOP/L or control water in a flow-through system until reaching 6 days post-fertilization (dpf) at which time posterior swim bladder inflation was assessed. To examine effects on anterior swim bladder inflation, a second study was conducted with 6 dpf larvae exposed to the same IOP concentrations until reaching 21 dpf. Fish from both studies were sampled for T4/T3 measurements, gene transcription analyses, and thyroid histopathology. In the embryo study, incidence and length of inflated posterior swim bladders were significantly reduced in the 6.0 mg/L treatment at 6 dpf. Incidence of inflation and length of anterior swim bladder in larval fish were significantly reduced in all IOP treatments at 14 dpf, but inflation recovered by 18 dpf. Throughout the larval study, whole body T4 concentrations were significantly increased and T3 concentrations were significantly decreased in all IOP treatments. Consistent with hypothesized compensatory responses, significant up-regulation of deiodinase-2 mRNA was observed in the larval study, and down-regulation of thyroperoxidase mRNA was observed in all IOP treatments in both studies. Taken together, these results support the hypothesized adverse outcome pathways linking inhibition of deiodinase activity to impaired swim bladder inflation. This dataset is associated with the following publication: Cavallin, J., G. Ankley, B. Blackwell, C. Blanksma, K. Fay, K. Jensen, M. Kahl, D. Knapen, P. Kosian, S. Poole, E. Randolph, A. Schroeder, L. Vergauwen, and D. Villeneuve. Impaired swim bladder inflation in early-life stage fathead minnows exposed to a deiodinase inhibitor, iopanoic acid (article). ENVIRONMENTAL TOXICOLOGY AND CHEMISTRY. Society of Environmental Toxicology and Chemistry, Pensacola, FL, USA, 36(11): 2942-2952, (2017).

The data set provides all data that were reported in results, tables, and figures associated with Stinckens et al., "The effect of thyroperoxidase and deiodinase inhibition on anterior swim bladder inflation in the zebrafish". The data set includes: 1) Effects of three test chemicals on thyroperoxidase enzyme activity 2) Effects of three test chemicals on deiodinase enzyme activity 3) Thyroid hormone (T3 and T4) concentrations measured in exposed larvae 4) Measures of posterior and anterior swimbladder chamber inflation and surface areas. 5) Data on swimming behavior (distance) of exposed fish. 6) Measured concentrations of the test chemicals in the test media and tissues. This dataset is associated with the following publication: Stinckens, E., L. Vergauwen, B. Blackwell, G. Ankley, D. Villeneuve, and D. Knapen. Effect of thyroperoxidase and deiodinase inhibition on anterior swim bladder inflation in the zebrafish. ENVIRONMENTAL SCIENCE & TECHNOLOGY. American Chemical Society, Washington, DC, USA, 54(10): 6213-6223, (2020).

The data set provides all data that were reported in results, tables, and figures associated with Stinckens et al., "The effect of thyroperoxidase and deiodinase inhibition on anterior swim bladder inflation in the zebrafish". The data set includes: 1) Effects of three test chemicals on thyroperoxidase enzyme activity 2) Effects of three test chemicals on deiodinase enzyme activity 3) Thyroid hormone (T3 and T4) concentrations measured in exposed larvae 4) Measures of posterior and anterior swimbladder chamber inflation and surface areas. 5) Data on swimming behavior (distance) of exposed fish. 6) Measured concentrations of the test chemicals in the test media and tissues. This dataset is associated with the following publication: Stinckens, E., L. Vergauwen, B. Blackwell, G. Ankley, D. Villeneuve, and D. Knapen. Effect of thyroperoxidase and deiodinase inhibition on anterior swim bladder inflation in the zebrafish. ENVIRONMENTAL SCIENCE & TECHNOLOGY. American Chemical Society, Washington, DC, USA, 54(10): 6213-6223, (2020).

Data associated with exposures of fathead minnows to varying concentrations of metformin and/or guanylurea. Includes three individual studies: ex vivo steroidogenesis assay, 96 h time course assay, 23 d reproduction assay. This dataset is associated with the following publication: Blackwell, B., G. Ankley, A. Biales, J. Cavallin, A. Cole, T. Collette, D. Ekman, R. Hofer, W. Huang, K. Jensen, M. Kahl, A. Kittelson, S. Romano, M. See, Q. Teng, C. Tilton, and D. Villeneuve. Effects of Metformin and its Metabolite Guanylurea on Fathead Minnow (Pimephales promelas) Reproduction (FY22 Manuscript). ENVIRONMENTAL TOXICOLOGY AND CHEMISTRY. Society of Environmental Toxicology and Chemistry, Pensacola, FL, USA, 41(11): 2708-2720, (2022).

Data associated with exposures of fathead minnows to varying concentrations of metformin and/or guanylurea. Includes three individual studies: ex vivo steroidogenesis assay, 96 h time course assay, 23 d reproduction assay. This dataset is associated with the following publication: Blackwell, B., G. Ankley, A. Biales, J. Cavallin, A. Cole, T. Collette, D. Ekman, R. Hofer, W. Huang, K. Jensen, M. Kahl, A. Kittelson, S. Romano, M. See, Q. Teng, C. Tilton, and D. Villeneuve. Effects of Metformin and its Metabolite Guanylurea on Fathead Minnow (Pimephales promelas) Reproduction (FY22 Manuscript). ENVIRONMENTAL TOXICOLOGY AND CHEMISTRY. Society of Environmental Toxicology and Chemistry, Pensacola, FL, USA, 41(11): 2708-2720, (2022).

Fathead minnows (Pimephales promelas) were exposed to 100 ug/L indomethacin, 200 ug/L ibuprofen, or 20 ug/L celecoxib for 96 h. Effects on cycloxygenase enzyme activity in ovary, prostaglandin F2alpha concentrations in plasma, 17beta-estradiol concentrations in plasma, and vitellogenin concentrations in plasma were measured. Gene expression in ovary samples was evaluated using a 15,000 probe oligonucleotide microarray. Transcriptomics data (raw data and normalized) are available through the National Center for Biotechnology Information, Gene Expression Omnibus (GEO), accession number GSE72976. Metabolite profiles in liver tissue were measured by proton nuclear magnetic resonance. In addition to these data, the data set also contains identification of differentially expressed genes, pathway enrichment and gene set enrichment analyes, ToxCast data for indomethacin and celecoxib, chemical-gene interaction data derived from the Comparative Toxicogenomics database, and results from Level 1, Level 2, and Level 3 SeqAPASS analyses that examine conservation of target proteins across species (https://seqapass.epa.gov/seqapass/). This dataset is associated with the following publication: Martinovic-Weigelt, D., A. Mehinto, G. Ankley , J. Berninger, T. Collette , J. Davis , N. Denslow, E. Durhan, E. Eid, D. Ekman , K. Jensen , M. Kahl , C. LaLone , Q. Teng , and D. Villeneuve. Derivation and evaluation of putative adverse outcome pathways for the effects of cyclooxygenase inhibitors on reproductive processes in female fish. TOXICOLOGICAL SCIENCES. Society of Toxicology, 156(2): 344-361, (2017).

This data set describes developmental and physiological effects observed in fathead minnow embryos that were exposed to sodium nitrate or conductivity-matched controls. Exposures were conducted in the laboratory from fertilization through 21 days post-fertilization (dpf). Nitrate doses were 0, 2, 5, 10, 25, or 100 milligrams per liter nitrate-nitrogen; conductivity controls were matched to the 10 and 100 milligrams per liter nitrate-nitrogen treatments. During the experiment, we assessed heart rate and percent arrhythmic heart beats at 3 dpf, timing of hatch and inflation of the posterior and anterior swim bladders, presence of pericardial edema or scoliosis, fish metrics at 21 dpf (fish length and weight; swim bladder length, width, and volume), and mortality. Water quality data during the exposure period are also presented, and include conductivity, pH, nitrate-nitrogen, total ammonia, unionized ammonia, and dissolved oxygen.

Adult fathead minnows were exposed to dilutions of a historically estrogenic wastewater treatment plant effluent in a 21-d reproduction study. This dataset is comprised of a variety of endpoints representing key events along adverse outcome pathways linking estrogen receptor activation and other molecular initiating events to reproductive impairment. This study demonstrates the value of using an integrative approach that encompasses analytical chemistry, in vitro bioassays, and in vivo apical and pathway-based approaches with endpoints spanning from molecular- (e.g., gene expression) to organismal- (e.g., reproduction) levels of biological organization to help infer causal relationships between chemistry and potential effects on reproduction. This dataset is associated with the following publication: Cavallin , J., K. Jensen , M. Kahl , D. Villeneuve , K. Lee, A. Schroeder , J. Mayasich, E. Eid, K. Nelson, R. Milsk, B. Blackwell, J. Berninger , C. LaLone, C. Blanksma, T. Jicha , C. Elonen , R. Johnson , and G. Ankley. Pathway-based approaches for assessment of real-time exposure to an estrogenic wastewater treatment plant effluent on fathead minnow reproduction. ENVIRONMENTAL TOXICOLOGY AND CHEMISTRY. Society of Environmental Toxicology and Chemistry, Pensacola, FL, USA, 35(3): 702-716, (2016).