<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Rude, Christian I</style></author><author><style face="normal" font="default" size="100%">Smith, Jordan N</style></author><author><style face="normal" font="default" size="100%">Scott, Ricky P</style></author><author><style face="normal" font="default" size="100%">Schultz, Katherine J</style></author><author><style face="normal" font="default" size="100%">Kim A Anderson</style></author><author><style face="normal" font="default" size="100%">Tanguay, Robyn L</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A mixture parameterized biologically based dosimetry model to predict body burdens of polycyclic aromatic hydrocarbons in developmental zebrafish toxicity assays.</style></title><secondary-title><style face="normal" font="default" size="100%">Toxicol Sci</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Toxicol Sci</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Body Burden</style></keyword><keyword><style  face="normal" font="default" size="100%">Dose-Response Relationship, Drug</style></keyword><keyword><style  face="normal" font="default" size="100%">Embryo, Nonmammalian</style></keyword><keyword><style  face="normal" font="default" size="100%">Models, Biological</style></keyword><keyword><style  face="normal" font="default" size="100%">Polycyclic Aromatic Hydrocarbons</style></keyword><keyword><style  face="normal" font="default" size="100%">Toxicity Tests</style></keyword><keyword><style  face="normal" font="default" size="100%">Toxicokinetics</style></keyword><keyword><style  face="normal" font="default" size="100%">Water Pollutants, Chemical</style></keyword><keyword><style  face="normal" font="default" size="100%">Zebrafish</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2025</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2025 Jun 01</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">205</style></volume><pages><style face="normal" font="default" size="100%">326-343</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Polycyclic aromatic hydrocarbons (PAHs) are a group of environmental toxicants found ubiquitously as complex mixtures in human-impacted environments. Developmental zebrafish exposures have been used widely to study PAH toxicity, but most studies report nominal exposure concentrations. Nominal exposure concentrations can be unreliable dose metrics due to differences in toxicant bioavailability resulting from disparate exposure methodologies and chemical properties. Toxicokinetic modeling can predict toxicant tissue doses to facilitate comparison between exposures of different chemicals, methodologies, and biological models. We parameterize a biologically based dosimetry model for developmental zebrafish toxicity assays for 9 PAHs. The model was optimized with measurements from media, tissue, and plastic plate walls throughout a static developmental exposure to a mixture of 10 PAHs of high abundance within the Portland Harbor Superfund Site. Plate binding, volatilization, zebrafish permeability, and tissue-media partitioning coefficients vary widely between PAHs. Model predictions accounted for 83% and 54% of 48 hpf body burdens within a factor of 2 resulting from exposures to mixtures and individual PAHs, respectively. Accounting for solubility significantly improves model performance. Competition for active sites in metabolizing enzymes may change biotransformation kinetics between individual PAH and mixture exposures. Area under the curve estimations of concentrations in zebrafish resulted in altered hazard rankings from nominal exposure concentrations. Future work will be oriented to generalizing the model to other PAHs. This PAH dosimetry model improves the interpretability of developmental zebrafish toxicity assays by providing time-resolved body burdens from nominal exposure concentrations.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">2</style></issue></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Mitra Geier</style></author><author><style face="normal" font="default" size="100%">Chlebowski, Anna C</style></author><author><style face="normal" font="default" size="100%">Truong, Lisa</style></author><author><style face="normal" font="default" size="100%">Staci M Simonich</style></author><author><style face="normal" font="default" size="100%">Kim A Anderson</style></author><author><style face="normal" font="default" size="100%">Robyn L Tanguay</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Comparative developmental toxicity of a comprehensive suite of polycyclic aromatic hydrocarbons.</style></title><secondary-title><style face="normal" font="default" size="100%">Arch Toxicol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Arch. Toxicol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Cytochrome P-450 CYP1A1</style></keyword><keyword><style  face="normal" font="default" size="100%">Embryo, Nonmammalian</style></keyword><keyword><style  face="normal" font="default" size="100%">Larva</style></keyword><keyword><style  face="normal" font="default" size="100%">Polycyclic Aromatic Hydrocarbons</style></keyword><keyword><style  face="normal" font="default" size="100%">Toxicity Tests</style></keyword><keyword><style  face="normal" font="default" size="100%">Zebrafish</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2018</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2018 Feb</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">92</style></volume><pages><style face="normal" font="default" size="100%">571-586</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Polycyclic aromatic hydrocarbons (PAHs) are widespread environmental contaminants that occur in complex mixtures. Several PAHs are known or suspected mutagens and/or carcinogens, but developmental toxicity data is lacking for PAHs, particularly their oxygenated and nitrated derivatives. Such data are necessary to understand and predict the toxicity of environmental mixtures. 123 PAHs were assessed for morphological and neurobehavioral effects for a range of concentrations between 0.1 and 50&amp;nbsp;µM, using a high throughput early-life stage zebrafish assay, including 33 parent, 22 nitrated, 17 oxygenated, 19 hydroxylated, 14 methylated, 16 heterocyclic, and 2 aminated PAHs. Additionally, each PAH was evaluated for AHR activation, by assessing CYP1A protein expression using whole animal immunohistochemistry (IHC). Responses to PAHs varied in a structurally dependent manner. High-molecular weight PAHs were significantly more developmentally toxic than the low-molecular weight PAHs, and CYP1A expression was detected in five distinct tissues, including vasculature, liver, skin, neuromasts and yolk.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">2</style></issue></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Knecht, Andrea L</style></author><author><style face="normal" font="default" size="100%">Goodale, Britton C</style></author><author><style face="normal" font="default" size="100%">Truong, Lisa</style></author><author><style face="normal" font="default" size="100%">Simonich, Michael T</style></author><author><style face="normal" font="default" size="100%">Swanson, Annika J</style></author><author><style face="normal" font="default" size="100%">Matzke, Melissa M</style></author><author><style face="normal" font="default" size="100%">Kim A Anderson</style></author><author><style face="normal" font="default" size="100%">Katrina M Waters</style></author><author><style face="normal" font="default" size="100%">Robyn L Tanguay</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Comparative developmental toxicity of environmentally relevant oxygenated PAHs.</style></title><secondary-title><style face="normal" font="default" size="100%">Toxicol Appl Pharmacol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Toxicol. Appl. Pharmacol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Abnormalities, Drug-Induced</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Biological Markers</style></keyword><keyword><style  face="normal" font="default" size="100%">Embryo, Nonmammalian</style></keyword><keyword><style  face="normal" font="default" size="100%">Environmental Pollutants</style></keyword><keyword><style  face="normal" font="default" size="100%">Extracellular Space</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Regulation, Developmental</style></keyword><keyword><style  face="normal" font="default" size="100%">Immunohistochemistry</style></keyword><keyword><style  face="normal" font="default" size="100%">Mitochondria</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxidation-Reduction</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxidative Stress</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxygen Consumption</style></keyword><keyword><style  face="normal" font="default" size="100%">Polycyclic Hydrocarbons, Aromatic</style></keyword><keyword><style  face="normal" font="default" size="100%">Real-Time Polymerase Chain Reaction</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA</style></keyword><keyword><style  face="normal" font="default" size="100%">Teratogens</style></keyword><keyword><style  face="normal" font="default" size="100%">Zebrafish</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2013</style></year><pub-dates><date><style  face="normal" font="default" size="100%">11/2013</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">271</style></volume><pages><style face="normal" font="default" size="100%">266-75</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Oxygenated polycyclic aromatic hydrocarbons (OPAHs) are byproducts of combustion and photo-oxidation of parent PAHs. OPAHs are widely present in the environment and pose an unknown hazard to human health. The developing zebrafish was used to evaluate a structurally diverse set of 38 OPAHs for malformation induction, gene expression changes and mitochondrial function. Zebrafish embryos were exposed from 6 to 120h post fertilization (hpf) to a dilution series of 38 different OPAHs and evaluated for 22 developmental endpoints. AHR activation was determined via CYP1A immunohistochemistry. Phenanthrenequinone (9,10-PHEQ), 1,9-benz-10-anthrone (BEZO), xanthone (XAN), benz(a)anthracene-7,12-dione (7,12-B[a]AQ), and 9,10-anthraquinone (9,10-ANTQ) were evaluated for transcriptional responses at 48hpf, prior to the onset of malformations. qRT-PCR was conducted for a number of oxidative stress genes, including the glutathione transferase(gst), glutathione peroxidase(gpx), and superoxide dismutase(sod) families. Bioenergetics was assayed to measure in vivo oxidative stress and mitochondrial function in 26hpf embryos exposed to OPAHs. Hierarchical clustering of the structure-activity outcomes indicated that the most toxic of the OPAHs contained adjacent diones on 6-carbon moieties or terminal, para-diones on multi-ring structures. 5-carbon moieties with adjacent diones were among the least toxic OPAHs while the toxicity of multi-ring structures with more centralized para-diones varied considerably. 9,10-PHEQ, BEZO, 7,12-B[a]AQ, and XAN exposures increased expression of several oxidative stress related genes and decreased oxygen consumption rate (OCR), a measurement of mitochondrial respiration. Comprehensive in vivo characterization of 38 structurally diverse OPAHs indicated differential AHR dependency and a prominent role for oxidative stress in the toxicity mechanisms.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">2</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/23684558?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Goodale, Britton C</style></author><author><style face="normal" font="default" size="100%">Susan C Tilton</style></author><author><style face="normal" font="default" size="100%">Corvi, Margaret M</style></author><author><style face="normal" font="default" size="100%">Glenn R Wilson</style></author><author><style face="normal" font="default" size="100%">Janszen, Derek B</style></author><author><style face="normal" font="default" size="100%">Kim A Anderson</style></author><author><style face="normal" font="default" size="100%">Katrina M Waters</style></author><author><style face="normal" font="default" size="100%">Robyn L Tanguay</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Structurally distinct polycyclic aromatic hydrocarbons induce differential transcriptional responses in developing zebrafish.</style></title><secondary-title><style face="normal" font="default" size="100%">Toxicol Appl Pharmacol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Toxicol. Appl. Pharmacol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Embryo, Nonmammalian</style></keyword><keyword><style  face="normal" font="default" size="100%">Polycyclic Hydrocarbons, Aromatic</style></keyword><keyword><style  face="normal" font="default" size="100%">Structure-Activity Relationship</style></keyword><keyword><style  face="normal" font="default" size="100%">Transcription, Genetic</style></keyword><keyword><style  face="normal" font="default" size="100%">Zebrafish</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2013</style></year><pub-dates><date><style  face="normal" font="default" size="100%">11/2013</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">272</style></volume><pages><style face="normal" font="default" size="100%">656-70</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous in the environment as components of fossil fuels and by-products of combustion. These multi-ring chemicals differentially activate the aryl hydrocarbon receptor (AHR) in a structurally dependent manner, and induce toxicity via both AHR-dependent and -independent mechanisms. PAH exposure is known to induce developmental malformations in zebrafish embryos, and recent studies have shown cardiac toxicity induced by compounds with low AHR affinity. Unraveling the potentially diverse molecular mechanisms of PAH toxicity is essential for understanding the hazard posed by complex PAH mixtures present in the environment. We analyzed transcriptional responses to PAH exposure in zebrafish embryos exposed to benz(a)anthracene (BAA), dibenzothiophene (DBT) and pyrene (PYR) at concentrations that induced developmental malformations by 120 h post-fertilization (hpf). Whole genome microarray analysis of mRNA expression at 24 and 48 hpf identified genes that were differentially regulated over time and in response to the three PAH structures. PAH body burdens were analyzed at both time points using GC-MS, and demonstrated differences in PAH uptake into the embryos. This was important for discerning dose-related differences from those that represented unique molecular mechanisms. While BAA misregulated the least number of transcripts, it caused strong induction of cyp1a and other genes known to be downstream of the AHR, which were not induced by the other two PAHs. Analysis of functional roles of misregulated genes and their predicted regulatory transcription factors also distinguished the BAA response from regulatory networks disrupted by DBT and PYR exposure. These results indicate that systems approaches can be used to classify the toxicity of PAHs based on the networks perturbed following exposure, and may provide a path for unraveling the toxicity of complex PAH mixtures.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">3</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/23656968?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Saili, Katerine S</style></author><author><style face="normal" font="default" size="100%">Corvi, Margaret M</style></author><author><style face="normal" font="default" size="100%">Weber, Daniel N</style></author><author><style face="normal" font="default" size="100%">Patel, Ami U</style></author><author><style face="normal" font="default" size="100%">Das, Siba R</style></author><author><style face="normal" font="default" size="100%">Przybyla, Jennifer</style></author><author><style face="normal" font="default" size="100%">Kim A Anderson</style></author><author><style face="normal" font="default" size="100%">Robyn L Tanguay</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Neurodevelopmental low-dose bisphenol A exposure leads to early life-stage hyperactivity and learning deficits in adult zebrafish.</style></title><secondary-title><style face="normal" font="default" size="100%">Toxicology</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Toxicology</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Behavior, Animal</style></keyword><keyword><style  face="normal" font="default" size="100%">Benzhydryl Compounds</style></keyword><keyword><style  face="normal" font="default" size="100%">Chromatography, High Pressure Liquid</style></keyword><keyword><style  face="normal" font="default" size="100%">Dose-Response Relationship, Drug</style></keyword><keyword><style  face="normal" font="default" size="100%">Embryo, Nonmammalian</style></keyword><keyword><style  face="normal" font="default" size="100%">Endocrine Disruptors</style></keyword><keyword><style  face="normal" font="default" size="100%">Environmental Pollutants</style></keyword><keyword><style  face="normal" font="default" size="100%">Estradiol</style></keyword><keyword><style  face="normal" font="default" size="100%">Hydrazines</style></keyword><keyword><style  face="normal" font="default" size="100%">Hyperkinesis</style></keyword><keyword><style  face="normal" font="default" size="100%">Larva</style></keyword><keyword><style  face="normal" font="default" size="100%">Learning Disorders</style></keyword><keyword><style  face="normal" font="default" size="100%">Maze Learning</style></keyword><keyword><style  face="normal" font="default" size="100%">Phenols</style></keyword><keyword><style  face="normal" font="default" size="100%">Receptors, Estrogen</style></keyword><keyword><style  face="normal" font="default" size="100%">Receptors, G-Protein-Coupled</style></keyword><keyword><style  face="normal" font="default" size="100%">Reversal Learning</style></keyword><keyword><style  face="normal" font="default" size="100%">Teratogens</style></keyword><keyword><style  face="normal" font="default" size="100%">Zebrafish</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">01/2012</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">291</style></volume><pages><style face="normal" font="default" size="100%">83-92</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Developmental bisphenol A (BPA) exposure has been implicated in adverse behavior and learning deficits. The mode of action underlying these effects is unclear. The objectives of this study were to identify whether low-dose, developmental BPA exposure affects larval zebrafish locomotor behavior and whether learning deficits occur in adults exposed during development. Two control compounds, 17β-estradiol (an estrogen receptor ligand) and GSK4716 (a synthetic estrogen-related receptor gamma ligand), were included. Larval toxicity assays were used to determine appropriate BPA, 17β-estradiol, and GSK4716 concentrations for behavior testing. BPA tissue uptake was analyzed using HPLC and lower doses were extrapolated using a linear regression analysis. Larval behavior tests were conducted using a ViewPoint Zebrabox. Adult learning tests were conducted using a custom-built T-maze. BPA exposure to &amp;lt;30μM was non-teratogenic. Neurodevelopmental BPA exposure to 0.01, 0.1, or 1μM led to larval hyperactivity or learning deficits in adult zebrafish. Exposure to 0.1μM 17β-estradiol or GSK4716 also led to larval hyperactivity. This study demonstrates the efficacy of using the zebrafish model for studying the neurobehavioral effects of low-dose developmental BPA exposure.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">1-3</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22108044?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Hillwalker, Wendy E</style></author><author><style face="normal" font="default" size="100%">Sarah E Allan</style></author><author><style face="normal" font="default" size="100%">Robyn L Tanguay</style></author><author><style face="normal" font="default" size="100%">Kim A Anderson</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Exploiting lipid-free tubing passive samplers and embryonic zebrafish to link site specific contaminant mixtures to biological responses.</style></title><secondary-title><style face="normal" font="default" size="100%">Chemosphere</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Chemosphere</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Embryo, Nonmammalian</style></keyword><keyword><style  face="normal" font="default" size="100%">Embryonic Development</style></keyword><keyword><style  face="normal" font="default" size="100%">Environmental Monitoring</style></keyword><keyword><style  face="normal" font="default" size="100%">Lipids</style></keyword><keyword><style  face="normal" font="default" size="100%">Rivers</style></keyword><keyword><style  face="normal" font="default" size="100%">Water Pollutants, Chemical</style></keyword><keyword><style  face="normal" font="default" size="100%">Zebrafish</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2010</style></year><pub-dates><date><style  face="normal" font="default" size="100%">03/2010</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">79</style></volume><pages><style face="normal" font="default" size="100%">1-7</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The Biological Response Indicator Devices Gauging Environmental Stressors (BRIDGES) bio-analytical tool was developed in response to the need for a quantitative technology for assessing the toxicity of environmentally relevant contaminant mixtures. This tool combines passive samplers with the embryonic zebrafish model. When applied in an urban river it effectively linked site specific, bioavailable contaminant mixtures to multiple biological responses. Embryonic zebrafish exposed to extracts from lipid-free passive samplers that were deployed at five locations, within and outside of the Portland Harbor Superfund Megasite, displayed different responses. Six of the eighteen biological responses observed in 941 exposed zebrafish were significantly different between sites. This demonstrates the sensitivity of the bio-analytical tool for detecting spatially distinct toxicity in aquatic systems; bridging environmental exposure to biological response.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/20172587?dopt=Abstract</style></custom1></record></records></xml>