<?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%">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%">D Sethajintanin</style></author><author><style face="normal" font="default" size="100%">Johnson, Eugene R</style></author><author><style face="normal" font="default" size="100%">Loper, Bobby R</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%">Bioaccumulation profiles of chemical contaminants in fish from the lower Willamette River, Portland Harbor, Oregon.</style></title><secondary-title><style face="normal" font="default" size="100%">Arch Environ Contam Toxicol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Arch. Environ. Contam. 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%">Environmental Monitoring</style></keyword><keyword><style  face="normal" font="default" size="100%">Environmental Pollutants</style></keyword><keyword><style  face="normal" font="default" size="100%">Fishes</style></keyword><keyword><style  face="normal" font="default" size="100%">Hazardous Waste</style></keyword><keyword><style  face="normal" font="default" size="100%">Insecticides</style></keyword><keyword><style  face="normal" font="default" size="100%">Mercury</style></keyword><keyword><style  face="normal" font="default" size="100%">Oregon</style></keyword><keyword><style  face="normal" font="default" size="100%">Polychlorinated Biphenyls</style></keyword><keyword><style  face="normal" font="default" size="100%">Reference Values</style></keyword><keyword><style  face="normal" font="default" size="100%">Tissue Distribution</style></keyword><keyword><style  face="normal" font="default" size="100%">Water Pollutants, Chemical</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2004</style></year><pub-dates><date><style  face="normal" font="default" size="100%">01/2004</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">46</style></volume><pages><style face="normal" font="default" size="100%">114-23</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Twenty-five PCBs (polychlorinated biphenyls), 15 organochlorine (OC) pesticides, and mercury were determined in fish from the Willamette River in Oregon, including a Portland Harbor superfund site. Fish were collected during the summer of 2000 along a 20-mile stretch of the lower Willamette River. Concentrations of sumPCBs (sum of 25 individually determined PCB congeners) and sumDDTs (sum of p,p&#039;-DDT, p,p&#039;-DDE, and p,p&#039;-DDD) in fish ranged from 14 to 530 and from 18 to 510 ng/g-wet weight, respectively. SumPCBs concentrations at all sites exceeded US EPA fish advisory&#039;s screening values. Hexachlorobiphenyl congener 153 was the most abundant of the PCBs detected and p,p&#039;-DDE was the most abundant OC pesticide detected. Low levels of dieldrin were detected in fish at all sites with the highest concentration at the superfund site (4.6 ng/g-wet weight), while other OC pesticides tested were near or below detection limits (approximately 2 ng/g). In general, organic chemical contaminant concentrations were highest in fish from the superfund site and were lower further upriver. Smallmouth bass had the highest levels of OC compounds of three fish species examined. They also had the largest site-to-site variations whereas black crappie had little variation throughout the study area. Mercury levels in fish ranged from 13 to 520 ng/g. Historical fish residue data are limited from the Portland Harbor superfund site, what data is available is over a decade old, generally consisted of only a few fish (&amp;lt; or = 3) and analyses quantified only a few PCB congeners (&amp;lt; 3).&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/15025171?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>