<?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%">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%">Yang, Dongren</style></author><author><style face="normal" font="default" size="100%">Kim, Kyung Ho</style></author><author><style face="normal" font="default" size="100%">Phimister, Andrew</style></author><author><style face="normal" font="default" size="100%">Bachstetter, Adam D</style></author><author><style face="normal" font="default" size="100%">Ward, Thomas R</style></author><author><style face="normal" font="default" size="100%">Stackman, Robert W</style></author><author><style face="normal" font="default" size="100%">Mervis, Ronald F</style></author><author><style face="normal" font="default" size="100%">Wisniewski, Amy B</style></author><author><style face="normal" font="default" size="100%">Klein, Sabra L</style></author><author><style face="normal" font="default" size="100%">Kodavanti, Prasada Rao S</style></author><author><style face="normal" font="default" size="100%">Kim A Anderson</style></author><author><style face="normal" font="default" size="100%">Wayman, Gary</style></author><author><style face="normal" font="default" size="100%">Pessah, Isaac N</style></author><author><style face="normal" font="default" size="100%">Lein, Pamela J</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Developmental exposure to polychlorinated biphenyls interferes with experience-dependent dendritic plasticity and ryanodine receptor expression in weanling rats.</style></title><secondary-title><style face="normal" font="default" size="100%">Environ Health Perspect</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Environ. Health Perspect.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals, Newborn</style></keyword><keyword><style  face="normal" font="default" size="100%">Body Weight</style></keyword><keyword><style  face="normal" font="default" size="100%">Chlorodiphenyl (54% Chlorine)</style></keyword><keyword><style  face="normal" font="default" size="100%">Dendrites</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Regulation, Developmental</style></keyword><keyword><style  face="normal" font="default" size="100%">Green Fluorescent Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Litter Size</style></keyword><keyword><style  face="normal" font="default" size="100%">Maze Learning</style></keyword><keyword><style  face="normal" font="default" size="100%">Memory</style></keyword><keyword><style  face="normal" font="default" size="100%">Microtubule-Associated Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Neuronal Plasticity</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy</style></keyword><keyword><style  face="normal" font="default" size="100%">Prenatal Exposure Delayed Effects</style></keyword><keyword><style  face="normal" font="default" size="100%">Rats</style></keyword><keyword><style  face="normal" font="default" size="100%">Rats, Sprague-Dawley</style></keyword><keyword><style  face="normal" font="default" size="100%">Ryanodine Receptor Calcium Release Channel</style></keyword><keyword><style  face="normal" font="default" size="100%">Sex Ratio</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2009</style></year><pub-dates><date><style  face="normal" font="default" size="100%">03/2009</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">117</style></volume><pages><style face="normal" font="default" size="100%">426-35</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;strong&gt;BACKGROUND: &lt;/strong&gt;Neurodevelopmental disorders are associated with altered patterns of neuronal connectivity. A critical determinant of neuronal connectivity is the dendritic morphology of individual neurons, which is shaped by experience. The identification of environmental exposures that interfere with dendritic growth and plasticity may, therefore, provide insight into environmental risk factors for neurodevelopmental disorders.&lt;/p&gt;

&lt;p&gt;&lt;strong&gt;OBJECTIVE: &lt;/strong&gt;We tested the hypothesis that polychlorinated biphenyls (PCBs) alter dendritic growth and/or plasticity by promoting the activity of ryanodine receptors (RyRs).&lt;/p&gt;

&lt;p&gt;&lt;strong&gt;METHODS AND RESULTS: &lt;/strong&gt;The Morris water maze was used to induce experience-dependent neural plasticity in weanling rats exposed to either vehicle or Aroclor 1254 (A1254) in the maternal diet throughout gestation and lactation. Developmental A1254 exposure promoted dendritic growth in cerebellar Purkinje cells and neocortical pyramidal neurons among untrained animals but attenuated or reversed experience-dependent dendritic growth among maze-trained littermates. These structural changes coincided with subtle deficits in spatial learning and memory, increased [3H]-ryanodine binding sites and RyR expression in the cerebellum of untrained animals, and inhibition of training-induced RyR upregulation. A congener with potent RyR activity, PCB95, but not a congener with negligible RyR activity, PCB66, promoted dendritic growth in primary cortical neuron cultures and this effect was blocked by pharmacologic antagonism of RyR activity.&lt;/p&gt;

&lt;p&gt;&lt;strong&gt;CONCLUSIONS: &lt;/strong&gt;Developmental exposure to PCBs interferes with normal patterns of dendritic growth and plasticity, and these effects may be linked to changes in RyR expression and function. These findings identify PCBs as candidate environmental risk factors for neurodevelopmental disorders, especially in children with heritable deficits in calcium signaling.&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/19337518?dopt=Abstract</style></custom1></record></records></xml>