<?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%">Norman D Forsberg</style></author><author><style face="normal" font="default" size="100%">Rodriguez-Proteau, R</style></author><author><style face="normal" font="default" size="100%">Ma, L</style></author><author><style face="normal" font="default" size="100%">Morré, J</style></author><author><style face="normal" font="default" size="100%">Christensen, J M</style></author><author><style face="normal" font="default" size="100%">Maier, C S</style></author><author><style face="normal" font="default" size="100%">Jeffrey J Jenkins</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%">Organophosphorus pesticide degradation product in vitro metabolic stability and time-course uptake and elimination in rats following oral and intravenous dosing.</style></title><secondary-title><style face="normal" font="default" size="100%">Xenobiotica</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Xenobiotica</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Administration, Oral</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Environmental Monitoring</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Injections, Intravenous</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Mass Spectrometry</style></keyword><keyword><style  face="normal" font="default" size="100%">Organophosphorus Compounds</style></keyword><keyword><style  face="normal" font="default" size="100%">Pesticides</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%">Time Factors</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">05/2011</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">41</style></volume><pages><style face="normal" font="default" size="100%">422-9</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Levels of urinary dialkylphosphates (DAPs) are currently used as a biomarker of human exposure to organophosphorus insecticides (OPs). It is known that OPs degrade on food commodities to DAPs at levels that approach or exceed those of the parent OP. However, little has been reported on the extent of DAP absorption, distribution, metabolism and excretion. The metabolic stability of O,O-dimethylphosphate (DMP) was assessed using pooled human and rat hepatic microsomes. Time-course samples were collected over 2 h and analyzed by LC-MS/MS. It was found that DMP was not metabolized by rat or pooled human hepatic microsomes. Male Sprague-Dawley rats were administered DMP at 20 mg kg(-1) via oral gavage and i.v. injection. Time-course plasma and urine samples were collected and analyzed by LC-MS/MS. DMP oral bioavailability was found to be 107 ± 39% and the amount of orally administered dose recovered in the urine was 30 ± 9.9% by 48 h. The in vitro metabolic stability, high bioavailability and extent of DMP urinary excretion following oral exposure in a rat model suggests that measurement of DMP as a biomarker of OP exposure may lead to overestimation of human exposure.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">5</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/21446834?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%">Crowell, Susan Ritger</style></author><author><style face="normal" font="default" size="100%">Amin, Shantu G</style></author><author><style face="normal" font="default" size="100%">Kim A Anderson</style></author><author><style face="normal" font="default" size="100%">Krishnegowda, Gowdahalli</style></author><author><style face="normal" font="default" size="100%">Sharma, Arun K</style></author><author><style face="normal" font="default" size="100%">Soelberg, Jolen J</style></author><author><style face="normal" font="default" size="100%">Williams, David E</style></author><author><style face="normal" font="default" size="100%">Corley, Richard A</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Preliminary physiologically based pharmacokinetic models for benzo[a]pyrene and dibenzo[def,p]chrysene in rodents.</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%">Administration, Oral</style></keyword><keyword><style  face="normal" font="default" size="100%">Algorithms</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Benzo(a)pyrene</style></keyword><keyword><style  face="normal" font="default" size="100%">Benzopyrenes</style></keyword><keyword><style  face="normal" font="default" size="100%">Environmental Pollutants</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Injections, Intravenous</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">Models, Biological</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%">Tissue Distribution</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">12/2011</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">257</style></volume><pages><style face="normal" font="default" size="100%">365-76</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 environmental contaminants generated as byproducts of natural and anthropogenic combustion processes. Despite significant public health concern, physiologically based pharmacokinetic (PBPK) modeling efforts for PAHs have so far been limited to naphthalene, plus simpler PK models for pyrene, nitropyrene, and benzo[a]pyrene (B[a]P). The dearth of published models is due in part to the high lipophilicity, low volatility, and myriad metabolic pathways for PAHs, all of which present analytical and experimental challenges. Our research efforts have focused upon experimental approaches and initial development of PBPK models for the prototypic PAH, B[a]P, and the more potent, albeit less studied transplacental carcinogen, dibenzo[def,p]chrysene (DBC). For both compounds, model compartments included arterial and venous blood, flow limited lung, liver, richly perfused and poorly perfused tissues, diffusion limited fat, and a two compartment theoretical gut (for oral exposures). Hepatic and pulmonary metabolism was described for both compounds, as were fractional binding in blood and fecal clearance. Partition coefficients for parent PAH along with their diol and tetraol metabolites were estimated using published algorithms and verified experimentally for the hydroxylated metabolites. The preliminary PBPK models were able to describe many, but not all, of the available data sets, comprising multiple routes of exposure (oral, intravenous) and nominal doses spanning several orders of magnitude.&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/22001385?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><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%">Jones, B A</style></author><author><style face="normal" font="default" size="100%">Tinsley, I J</style></author><author><style face="normal" font="default" size="100%">Lowry, R R</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Toxicology of brominated fatty acids: metabolite concentration and heart and liver changes.</style></title><secondary-title><style face="normal" font="default" size="100%">Lipids</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Lipids</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adipose Tissue</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Bromine</style></keyword><keyword><style  face="normal" font="default" size="100%">Dietary Fats</style></keyword><keyword><style  face="normal" font="default" size="100%">Fatty Acids</style></keyword><keyword><style  face="normal" font="default" size="100%">Heart</style></keyword><keyword><style  face="normal" font="default" size="100%">Liver</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Myocardium</style></keyword><keyword><style  face="normal" font="default" size="100%">Rats</style></keyword><keyword><style  face="normal" font="default" size="100%">Rats, Inbred Strains</style></keyword><keyword><style  face="normal" font="default" size="100%">Tissue Distribution</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1983</style></year><pub-dates><date><style  face="normal" font="default" size="100%">1983 Apr</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">18</style></volume><pages><style face="normal" font="default" size="100%">327-34</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Rats were fed for 35 days diets containing 2% of either brominated corn oil (BCO), monoglyceride of dibromostearate (DBS), monoglyceride of tetrabromostearate (TBS) or a mixture of the two monoglycerides (BMG) which provided proportions of brominated acids comparable to that of the BCO. Hearts from all animals fed BCO were yellow colored and firm in texture. Myocardial cellular degeneration, mild to moderate edema and occasional small necrotic foci were observed. Hearts from animals fed DBS showed moderate edema and some slight necrosis. All diets produced an increase in lipid content of heart. Animals fed the experimental diets developed enlarged livers and showed elevated liver lipid content. The tetrabromostearate appeared to be the more active in producing these changes, in particular a severe intracellular fatty degeneration. Shorter-chain (C-16, C-14) metabolites of di- and tetrabromostearate were identified and the concentration of brominated fatty acids in heart, liver and adipose tissue determined and found to account for 80% of the bromine detected in these tissues by neutron activation analysis. TBS accumulated in liver while the highest concentration of DBS was observed in heart lipids. Although the concentrations of brominated acids in heart and liver lipids were comparable in rats fed BCO or BMG, BCO produced the more pronounced effects. This differential could be due to additional active components in BCO or to a variation in response associated with changes in the location of the fatty acid on the glycerol molecule.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">4</style></issue></record></records></xml>