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gene are associated with diseases such as cancer. Very little is known about the in vivo regulation of mEH. The purpose of this study was to determine the tissue distribution, ontogeny, and chemical induction of mEH in mice. For tissue distribution, thirteen tissues were collected from 8-week-old wild-type mice. For ontogeny, livers were collected from two days before birth through various postnatal ages. For chemical induction, male mice were administered microsomal enzyme inducers that activate critical transcription factors regulating xenobiotic metabolism, including AhR (TCDD), CAR (TCPOBOP), PXR (PCN), PPARα (clofibrate), and Nrf2 (oltipraz). Total RNA was isolated, and mEH mRNA expression was determined by the bDNA assay. The mEH mRNA was highest in in liver and testis in wild-type mice. The mRNA expression of mEH was low in prenatal livers, but increased with age in both males and females. The mEH mRNA was not readily induced by activators for AhR, PXR, or PPARα. In contrast, both CAR and Nrf2 activators induced mEH mRNA in liver. The induction was blocked in CAR- and Nrf2-null mice, indicating the induction was CAR- and Nrf2-dependent. In silico analysis identified putative binding sites for CAR and Nrf2 in and around the mEH gene locus. In conclusion, the mEH mRNA was found to be enriched in liver and testis, its expression in liver gradually increased with age, and mEH expression in liver can be induced through CAR and Nrf2 activation. (Supported by NIH grants ES013714, ES009649, ES009716, ES013714, RR021940) 1104 TRANSCRIPTIONAL AND TISSUE SPECIFIC REGULATION OF HUMAN MICROSOMAL EPOXIDE HYDROLASE (EPHX1) EXPRESSION IS MODULATED BY DIETARY ISOTHIOCYANATE DERIVATIVES. S. Su 1, 2 , X. Yang 1, 2 and C. J. Omiecinski 2, 3 . 1 Huck Institute of Life Sciences, Pennsylvania State University, University Park, PA, 2 Center for Molecular Toxicology and Carcinogenesis, Pennsylvania State University, University Park, PA and 3 Department of Veterinary and Biomedical Sciences, Pennsylvania State University, University Park, PA. Microsomal epoxide hydrolase (EPHX1) is a critical metabolic enzyme that catalyzes the hydrolysis of eletrophilic epoxides to less reactive dihydrodiols, thereby playing an important role in the detoxification of ROS and xenobiotic epoxide intermediates. However, under some circumstances, the enzyme bioactivates substrates, in particular the carcinogenic polycyclic aromatic hydrocarbons present in cigarette smoke. Our studies have determined that there are two prominent EPHX1 transcriptional variants present in human tissues. The transcripts are generated from the use of alternative gene promoters that produce products containing different first exons, denoted E1 and E1b, respectively. The E1-containing transcript is expressed most exclusively in liver while the E1b transcript, driven by the use of a promoter residing 18.5 kb upstream from the coding region of the gene, is the predominant EPHX1 transcript generated in all tissues. The regulatory mechanisms directing the respective expression levels and tissue-specific patterning of the E1 and E1b transcripts remain largely unknown. In this study, we investigated the effects of dietary isothiocyanate derivatives as potential modulators of EPHX1 expression. These compounds are under intensive study as potential chemopreventive agents in human trials. We determined that sulforaphane as well as 3-phenylpropylthiocyanate can potently and differentially regulate EPHX1 transcription in liver and lung cells. The tissue-specific expression pattern for the E1 and E1b transcripts was confirmed with protein immunoblotting experiments. These data suggest that the molecular mechanism of human EPHX1 regulation includes antioxidant response signaling, likely mediated through the nuclear factor erythroid 2-related factor 2 (Nrf2) master regulator pathway. 1105 OXIDATION OF 4-CHLOROBIPHENYL METABOLITES TO THEIR FREE RADICAL SPECIES BY PROSTAGLANDIN H SYNTHASE-2. O. Wangpradit 1 , E. Moman 2 , K. B. Nolan 3 , G. R. Buettner 4 , L. W. Robertson 1 and G. Luthe 1, 5 . 1 Interdisciplinary Graduate Program in Human Toxicology, The University of Iowa, Iowa city, IA, 2 Department of Pharmaceutical and Medicinal Chemistry, Saarland University, Saarbruckken, Germany, 3 Department of Pharmaceutical and Medicinal Chemistry, Royal College of Surgeons Ireland, Dublin, Ireland, 4 Free Radical and Radiation Biology Program, The University of Iowa, Iowa city, IA and 5 Institute for Life Science and Technology, Saxion University, Enschede, Netherlands. Polychlorinated biphenyls (PCBs) are a class of environmental pollutants that have entered the environment through both their use and disposal. PCBs are mainly metabolized by hepatic cytochrome P450 (CYPs) to mono-, and dihydroxy metabolites, which can undergo redox interconversion to quinones (Q). In our previous study we found that prostaglandin H synthase-2 (PGHS-2), an inducible enzyme found basally in extra-hepatic tissues, catalyzes the oxidation of dihydroxy PCB metabolites to corresponding Q as identified by LC-MS. Here we show that PGHS-2 also plays an important role in catalyzing the oxidation of these PCB metabolites to semiquinones (SQd-). Using 4-chlorobiphenyl-2’,5’-hydroquinone (4-CB-H2Q) as a model compound, two SQd- species were detected by electron paramagnetic resonance (EPR) spectroscopy. These results indicate that PGHS-2 is capable of catalyzing the oxidation of lower chlorinated PCB hydroquinones to Q by two sequential one-electron oxidations generating SQd-as intermediates. This study demonstrates the formation of SQd- and Q from PCB-metabolites by PGHS-2, and underscores the potential role of PGHS-2 in the metabolic activation of PCBs in extra-hepatic tissues. (Supported by NIH P42 ES 013661 and ES 05605.) 1106 MICRONUCLEUS FREQUENCIES AND DNA DAMAGE IN MALE MICE ADMINISTERED HYDROXYUREA. C. A. Hobbs 1 , L. Recio 1 , K. Shepard 1 , C. Baldetti 1 , A. Green 1 , J. Winters 1 , M. Streicker 2 and K. L. Witt 3 . 1 Genetic and Molecular Toxicology, ILS, Inc., Research Triangle Park, NC, 2 Investigative Toxicology, ILS, Inc., Research Triangle Park, NC and 3 National Toxicology Program (NTP), NIEHS, Research Triangle Park, NC. Hydroxyurea (HU), a chemotherapeutic agent, is the only effective medication for treatment of sickle cell disease in adults. Insufficient information about its longterm toxicity in young children—a growing patient population—remains a major concern. To evaluate the subacute genotoxic potential of HU in a rodent model, the NTP conducted two studies in male B6C3F1 mice using a combined micronucleus (MN)/Comet assay. HU (32-500 mg/kg) was administered by gavage once daily for 4 consecutive days. The highest dose was determined on the basis of bone marrow toxicity (reduction in % reticulocytes (RET)) in a range finding study and the lowest doses were selected to bracket the human equivalent dose. Blood samples were collected 4 hr after the final dosing for measurement of MN-RET frequencies by flow cytometry and samples of liver, blood, stomach, and colon were collected and processed for assessment of DNA damage using the pH>13 Comet assay. A significant, dose-related increase in MN-RET (p < 0.0001) was observed in the mice administered HU; considerable bone marrow toxicity, assessed by a decrease in the %RET, was also seen in the mice receiving doses ≥ 125 mg/kg. An observed downward shift in the MN median channel fluorescence intensity suggests the likelihood of highly fragmented DNA within the MN. DNA damage measured in the Comet assay was evident in cells from the stomach and liver of HU-treated mice at all doses tested, but no damage was detected in blood or colon cells. The observed damage appeared to correlate with significant increases in low molecular weight DNA, an indicator of cytotoxicity (apoptosis or necrosis), detected even at the lowest doses of HU tested. Together, the data obtained from this combined MN/Comet assay demonstrate significant genetic damage and associated cytotoxicity in B6C3F1 mice resulting from HU treatment. Supported by NIEHS/NTP contract N01-ES-35514. 1107 EVALUATION OF PHOTOGENOTOXICITY IN THE IN VITRO MICRONUCLEUS ASSAY IN HUMAN PERIPHERAL BLOOD LYMPHOCYTES. C. S. Farabaugh, M. M. Chan, A. N. Valliere, L. F. Stankowski and B. R. Fisher. Covance Laboratories, Inc., Vienna, VA. Recent demonstration of pseudophotoclastogenicity has cast doubt on the specificity and utility of current test systems used for detecting photogenotoxicity. However, studies to date largely have been performed in transformed cell lines that are genetically unstable. Thus, we adapted the in vitro micronucleus (MN) assay in human peripheral blood lymphocytes (HPBL) to evaluate photogenotoxicity. Venous blood was collected and HPBL were isolated and stimulated to grow (t = 0) in mass culture. Individual 5 mL cultures were prepared in 60-mm dishes (t = 48 hr) and treated with 8-methoxypsoralen (8-MOP) or the concurrent vehicle and unirradiated positive controls. Cultures were pre-incubated with the test and control articles in the dark for ~10 minutes, and half of the cultures were irradiated with a Xenon arc solar simulator lamp with a UV filter (290 nm cut off). Cultures were re-incubated until the end of treatment (t = 51 hr), washed by centrifugation, and transferred to media containing cytochalasin B. Cultures were harvested (t = 72 hr) and slides were prepared and stained with Giemsa and May-Grunwald. For each culture, 200 cells were scored for cytotoxicity (cytochalasin B blocked proliferation index, CBPI), and 400 binucleated cells were scored for micronuclei (%MN- BN). Statistically significant, dose-dependent increases in %MN-BN were induced in the vehicle control cultures by extended UV exposure (as compared to unirradiated controls), as well as in cultures treated with 8-MOP that were irradiated for at least 50 seconds (as compared to the matched irradiated controls). In contrast, 8- MOP was uniformly negative in the absence of light exposure. These results demonstrate the feasibility of detecting micronuclei induced by photogenotoxic compounds in HPBL. Additional validation studies with lomefloxacin and nalidixic acid are ongoing. 236 SOT 2010 ANNUAL MEETING
1108 STYRENE-INDUCED TOXIC EFFECTS IN ALDH2 KNOCKOUT MICE. R. Wang 1 , K. Ohtani 1 , L. J. McGarrity 2 , Z. Weng 1 and N. Mei 2 . 1 Japan National Institute of Occupational Safety and Health, Kawasaki, Japan and 2 National Center for Toxicological Research/U.S. FDA, Jefferson, AR. Styrene is an important chemical widely used in manufacturing plastics and synthetic rubber. Styrene exposure has been reported to cause DNA damage as shown by the increased DNA adducts and chromosomal aberrations. This effect has been correlated with the genetic polymorphisms of metabolizing enzymes such as CYPs and GSTs, and DNA repair enzymes. Aldehyde dehydrogenase 2 (ALDH2) is also involved in the metabolism of styrene, but the enzyme activity is deficient in about 40 percent of East Asian population due to a mutant allele of the gene encoding the enzyme. In this study, we used ALDH2 gene knockout (KO) mice to detect any difference in styrene induced effects such as micronuclei and other endpoints compared with those in wild type (WT) mice. Male and female mice were administrated with styrene at 0, 100, 400 and 800 mg/kg, p.o., per day, 5 days per week, for 4 consecutive weeks. Peripheral blood was sampled 24 hr after the last treatment and the micronucleus in the reticulocytes was detected by a flow cytometric method using kit from Litron Laboratories. The background of the frequency of micronucleated reticulocytes (MN-RETs) was higher in KO mice than in the WT mice for both male and female. The percentage of the MN-RETs was significantly increased by approximately 40% in the male mice treated with the high dose of styrene and this effect was not observed in the male WT mice. No evident change in the groups of low and middle doses was detected. In female KO mice, the percentage of MN-RETs showed a dose-dependent induction with styrene treatment, with statistically significant increase in the middle and high dose groups as compared with the control. Again this toxic effect was only found in the KO, but not WT mice. These results suggest that ALDH2 polymorphisms is another genetic factor that may modify the toxic effects of styrene and may be used as a biomarker of susceptibility to styrene exposure. 1109 EVALUATION OF L-MENTHONE IN AN IN VIVO MOUSE MICRONUCLEUS TEST. J. Scognamiglio, V. T. Politano and A. Api. Research Institute for Fragrance Materials, Woodcliff Lake, NJ. A mouse micronucleus test was conducted on l-menthone (CAS # 14073-97-3), a widely used fragrance ingredient, to determine its potential to induce micronuclei in the polychromatic erythrocytes (PCEs) in the bone marrow of the mouse to evaluate clastogenic potential. In the dose range-finding phase, 2000 mg/kg bodyweight was determined suitable as it was the maximum guideline-recommended dose. In the definitive study, l-menthone was then administered orally at dose levels of 500, 1000 or 2000 mg/kg in corn oil to NMRI mice (5/sex/dose). The control groups were treated with the vehicle, corn oil, or cyclophosphamide (CPA) at 40 mg/kg as the positive control. The control and test article were both orally administered at a volume of 10 mL/kg body weight. Bone marrow cells were harvested 24 and 48 hours after treatment. At least 2000 PCEs per animal were scored for micronuclei. The number of PCEs showed no statistically significant increases when compared to that of the vehicle control. Therefore, l-menthone administered at doses up to 2000 mg/kg did not induce a statistically significant increase in micronuclei in either male or female mice and is not genotoxic. 1110 EVALUATION OF ISOAMYL ALCOHOL IN AN IN VIVO MOUSE MICRONUCLEUS TEST. D. McGinty, V. T. Politano and A. Api. Research Institute for Fragrance Materials, Inc., Woodcliff Lake, NJ. Isoamyl alcohol, a widely used fragrance ingredient, was tested in an in vivo mouse micronucleus assay to evaluate the clastogenic potential as measured by its ability to induce micronucleated polychromatic erythrocytes in mouse bone marrow. This test is a short-term in vivo cytogenetic assay for detecting agents that induce chromosomal breakage and spindle malfunction. In the dose range-finding phase, 2000 mg/kg bodyweight was determined suitable as it was the maximum guideline-recommended dose. The definitive micronucleus study consisted of several groups, each containing 5 male and 5 female NMRI mice. The control groups were treated with the vehicle, corn oil, or cyclophosphamide (CPA) at 40 mg/kg as the positive control. Isoamyl alcohol was tested at dosages of 500, 1000, or 2000 mg/kg. Both the test and control articles were administered via gavage at a dose volume of 10 ml/kg body weight. Bone marrow cells (polychromatic erythrocytes, PCEs) were collected 24 and 48h after the treatment and examined microscopically for the presence of micronuclei. At least 2000 PCEs per animal were scored for micronuclei. There was no statistically significant increase in the incidence of micronucleated polychromatic erythrocytes observed in test article treated groups relative to respective vehicle control groups. Therefore, isoamyl alcohol at doses up to and including 2000 mg/kg did not induce a significant increase in micronuclei in either male or female NMRI mice and may be concluded as negative in the mouse micronucleus assay. 1111 AN IN VIVO MOUSE MICRONUCLEUS TEST WITH GAMMA-NONALACTONE. C. Letizia, A. Api and V. Politano. RIFM, Woodcliff Lake, NJ. An in vivo mammalian erythrocyte micronucleus test was conducted to evaluate the potential of gamma-nonalactone (CAS No. 104-61-0), a widely used fragrance material, to induce micronuclei in polychromatic erythrocytes (PCEs) in the bone marrow of the mouse. The study was conducted in compliance with GLP and OECD Test Guideline 474 (Mammalian Erythrocyte Micronucleus Test). Male and female NMRI mice (5/sex/dose) were administered gamma-nonalactone orally at dose levels of 500, 1000 or 2000 mg/kg body weight in corn oil at a dose volume of 10 ml/kg body weight and sacrificed at 24 or 48 hours after dosing. Control groups received the vehicle alone or cyclophosphamide (40 mg/kg body weight) as a positive control. PCEs were collected at 24 and 48 hours after administration and examined microscopically for the presence of micronuclei. At least 2000 PCEs per animal were scored for micronuclei. The number of PCEs was not substantially decreased in gamma-nonalactone treated groups compared to the mean value of PCEs of the vehicle control group indicating that gamma-nonalactone did not produce any cytotoxic effects in the bone marrow. There was no significant increase in the incidence of micronucleated PCEs in gamma-nonalactone treated groups relative to their respective vehicle controls in either male or female mice, regardless of dose level or bone marrow collection time. The mean values of micronuclei observed in the gamma-nonalactone treated groups were below or near vehicle control values. Cyclophosphamide induced a statistically significant increase in micronucleated PCEs in both male and female mice. It was concluded that under the conditions of the test, gamma-nonalactone was not genotoxic. 1112 DOSE-RESPONSE CHARACTERIZATION OF VINYL ACETATE AND ACETALDEHYDE-INDUCED MICRONUCLEI IN HUMAN TK6 CELLS. R. Budinsky 1 , B. Gollapudi 1 , R. J. Albertini 2 , R. Valentine 3 , M. Stavanja 4 , J. Teeguarden 5 , R. J. Fensterheim 6 and L. Recio 7 . 1 The Dow Chemical Company, Midland, MI, 2 The University of Vermont, Burlington, VT, 3 DuPont Haskell Global Centers for Health and Environmental Sciences, Newark, DE, 4 Celanese International Corporation, Dallas, TX, 5 Battelle, Pacific Northwest Division, Richland, WA, 6 RegNet Environmental Services, Washington, DC and 7 ILS, Inc., Research Triangle Park, NC. Chronic vinyl acetate monomer (VAM) inhalation induces rat nasal tumors when concentrations exceed 200 ppm. VAM’s metabolite, acetaldehyde (AA), is hypothesized to be the genotoxic metabolite produced by tissue carboxylesterase. AA metabolism to acetic acid, via acetaldehyde dehydrogenase, leads to acetic acid accumulation, reduced intracellular pH, cytotoxicity, and regenerative cell proliferation. To shed more light on VAM-induced nasal tumors, an investigation was undertaken to obtain robust dose-response information on the induction of cytogenetic damage by VAM and AA in human TK6 cell cultures. A flow cytometry-based micronucleus assay was utilized to enhance the quantitative sensitivity of cytogenetic damage. Micronucleus induction was accompanied by significant cytotoxicity. Five different dose-response modeling methods provided threshold estimates of 0.01 to 0.75 mM and 0.05 to 0.14 mM for VAM and AA, respectively. Physiologicallybased toxicokinetic model estimates of VAM and AA concentrations in regions associated with rodent nasal tumors are substantially lower than the estimated in-vitro micronuclei thresholds. Additional investigation is needed to evaluate the relevance of the in-vitro to in-vivo concentration comparisons. These results support the threshold nature of VAM-induced rat nasal tumors that are hypothesized to result from exceeding otherwise efficient metabolism of AA and consequent accumulation in AA or decreases in cellular pH when proton production exceeds the cellular buffering capacity. 1113 AUTOMATED MICRONUCLEUS/DNA CONTENT ASSAY BY QUANTITATIVE IMAGING CYTOMETRY. E. Holden, M. Henriksen, E. Luther and S. Baldwin. CompuCyte Corporation, Westwood, MA. Sponsor: P. Narayanan. The in vitro micronucleus (MN) assay is a well established test of compound genotoxic effects. We describe the validation of multi parameter in-vitro micronucleus assay with simultaneous measurement of cell counts and DNA content. Methods: SOT 2010 ANNUAL MEETING 237
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The Toxicologist Supplement to Toxi
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The Toxicologist Supplement to Toxi
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1 BIOLOGICAL PATHWAY ANALYSIS: AN I
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11 ICH INITIATIVES FOR CONDUCTING P
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models. Experimental approaches and
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30 SILICA AND ASBESTOS IMMUNOTOXICI
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40 NONCANCER TOXICITY POTENTIAL AT
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ased products for patient administr
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nase regulates Hsp27-induced reorga
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exposure resulted in splenomegaly.
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We investigated the effect of imati
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well plate prevented free cell move
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98 DERIVING SIGNATURES OF IN VIVO T
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sulfate, cinnamic aldehyde, 2,4-din
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The final product will be a system
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mercially available STP brands by m
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for six weeks, with 10 mg/kg azoxym
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eceived RES post-TCDD exposure when
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morigenesis. Knocking down of JARID
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163 MICROPET IMAGING OF [18F]-DFNSH
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These results are comparable to tha
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activity as assessed by lever press
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for measured physico-chemical param
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199 DEVELOPMENT OF A MULTIPARAMETER
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To cause PLD, a drug needs to enter
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In contrast to the parent PBDEs and
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transiently transfected HEK 293 cel
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TCDD exposure, 24 h prior to a 20 %
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244 NON-ADDITIVE EFFECTS OF PCB153
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253 COMPARISON OF MIXTURE TOXICITY
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two cerium oxide nanoparticles of v
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271 SIZE-DEPENDENT EFFECTS OF TUNGS
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adigms such as Tox 21 and Toxcast,
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QDs with emission maximum at 800nm
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Cleveland, while others were found
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without the need of animal testing.
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Conclusions: These results are cons
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ing oxime reactivation and organoph
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335 A NON-OXIME IMPROVES SURVIVAL I
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alties suffer from permanent lung i
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ies have established inflammatory b
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363 GENETIC VARIATION IN ISOGENIC M
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372 EVALUATING THE BIOLOGICAL INTER
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dose of 1/20 LD50 (400 mg/kg.bwt) f
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median CR-adjusted isoflavone conce
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data indicate that AhR deletion pro
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February 2006). The rabbit is one o
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tal neurotoxicity (DNT) test (OECD
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of selected microorganisms that are
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BVI. Histopathological analysis was
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446 MOLECULAR CLONING AND CHARACTER
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portant in predicting risk. CYPs 1A
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ats, which involves metabolic activ
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473 BOVINE CORNEAL OPACITY AND PERM
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482 TYPE III DEIODINASE (D3) IS PRO
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tancy evaluation and ranking of bat
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501 CHARACTERIZATION OF ESTERASE, G
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510 REDOX CYCLING BY ENDOGENOUS 2-
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prostate cancer cells. All 8 BEL de
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metallic nickel nanoparticles. Acti
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variety of more or less reactive ch
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550 QUALIFICATION STRATEGIES-GENOTO
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ferentiation, and 3) how mixtures o
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572 LOW-CHRONIC ARSENIC EXPOSURE: E
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582 IDENTIFICATION OF SENSITIVE URI
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duced by the genetic outcross of fe
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fects of new compounds are equally
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acterize the current state of the s
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620 CHARACTERIZATION OF POTENTIAL I
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ways. Moreover, both MAP kinase and
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641 POPS IN THE U.S. POPULATION AND
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studies such as the NCS, consider h
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the beginning of the academic caree
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trophil infiltration, a significant
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tactic response and optokinetic res
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usually high spontaneous PIG-A MFs.
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699 PROMUTAGEN ACTIVATION AND P450
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oxodG in bone marrow, spleen, kidne
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718 GENOTOXICITY OF ORGANIC EXTRACT
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ment were 18.0 and 4.5 nM for BEAS-
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strongest activation of nuclear fac
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746 MACROPHAGE INHIBITORY CYTOKINE-
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screening of cell migration. High-c
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dase inhibition). In contrast, inhi
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mice; the decrease was more pronoun
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Markers of oxidative damage reached
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793 PULMONARY RESPONSE, OXIDATIVE S
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cilitate clinical and industrial ap
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sion of p-p38, p-p53, p21 and cycli
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821 KIDNEY INJURY MOLECULE-2 GENE D
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commercial applications, and have b
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developmental effects. The residual
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strand breaks in an in vitro model
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etate (immunotoxicity). 2,4-D was t
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1346 THE OTHER WORLD OF THE TRANSCR
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strate, leading to excess microvesi
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1368 OVERVIEW OF THERAPEUTIC VACCIN
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to a bovine adrenal cortical epithe
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DOTC had no effects. These results
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1398 PULMONARY TOXICITY OF CERIUM D
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PPARα, LXR, ER, AR and AhR activit
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1417 MECHANISM OF GENDER-DIVERGENT
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els, they disrupt homeostatic contr
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were to characterize exposure of th
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1448 ADVERSE OUTCOME PATHWAYS AND E
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the level in urine was 25% of the m
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1;akt-2 double mutant and pdk-1 mut
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jury effects when compared to contr
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tude than equivalent oral doses. Af
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cells; and increased iNOS and MCP-1
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B6.Cg-Kit W-sh mice. These findings
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1511 STATIN-TREATMENT EFFECTIVELY R
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1520 EFFECT OF INHALATION EXPOSURE
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numbers of IFN-γ producing cells w
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These data indicate that TCDD treat
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esponse to allogenic cells, where P
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larly suppressed LPS-induced TNF-α
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1565 INFLUENCE OF EXPOSURE ROUTE AN
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veloping animals to adverse effects
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the observed CL values were 0.07 L/
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which is most relevant for potentia
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tive impairment, suggesting that ox
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1611 AN IN VITRO METABOLOMICS APPRO
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Expression of the β6 integrin (Itg
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ats (10 μg/kg TCDD). Here we repor
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at liver slices and how the metabon
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with gender differences in AUC and
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oxetine (30 mg/kg reduced to 15 mg/
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eleased from necrotic cells where i
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plants, they are present in surface
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ferentiation (quantitative in-cell
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control for macrophage activation).
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to 0.5μg/ml. Minimal inhibitory co
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lines tested. Given that dex and AT
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tion in the absence of an immune re
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treated rats had lower calcium load
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1740 PROFILING COMPOUNDS WITH CARDI
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dothelial cells confirmed caveolin-
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1758 GINKGO BILOBA EXTRACT INDUCES
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arin-induced suppression of MDR1 ex
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1780 ANTIANDROGENIC AND ANTIPROLIFE
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included in the evaluation, most of
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1799 GUIDANCE ON THE APPLICATION OF
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However, substances with EC3 values
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1816 CD-INDUCED EGFR TRANSACTIVATIO
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1826 KERATIN 7 EXPRESSION IN INDEPE
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centa were collected at the time of
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1845 SYSTEMATIC SCREENING OF YEAST
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underlying the development of co-mo
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eing measured in experimental roden
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ufactured in the US for more than 3
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nine (N7-THB-Gua) and N7-hydroxyphe
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1892 EFFECT OF LAMBDA-CYHALOTHRIN O
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22 in Phase I. Antimicrobial pestic
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kinetic and dynamic differences, an
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iphenyl, saccharin and melamine was
Page 415 and 416:
1930 DEVELOPMENT OF A RELATIVE SOUR
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1939 MODE OF ACTION FOR THE CANCER
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human was about 1.5-fold lower (60
Page 421 and 422:
Disruption of BDEC integrity in alp
Page 423 and 424:
1968 A HUMAN HEPG2 LUCIFERASE ASSAY
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in the offspring during tumor devel
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een developed to investigate perfus
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to 131.73 μg/mL for KLH-specific I
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cell lines (ATCC) were cultured in
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flammation and xenobiotic metabolis
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vide many contributions: with its g
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to-metal joint replacement. For exa
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to be addressed or negotiated. Deci
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especially with anti-TNF therapies.
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genic line Tg(are:eGFP) was created
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2074 COMPUTATIONAL ASSESSMENT OF TH
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2084 INHIBITION OF 11β-HSD1 DECREA
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(T) and express several enzymes inv
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2101 GENISTEIN MODULATION OF BLOOD
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males per group were dosed orally o
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ate the feasibility of assessing re
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changed. Hepatic protein carbonyl l
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sought to examine alterations in he
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2147 A SINGLE AMINO ACID CONTROLS T
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Gstm7) was independent of both CAR
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ility of tungsten trioxide (WO3), t
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ured by real-time PCR array and rel
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glucose, and creatinine levels, and
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Several studies have reported suppr
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exposure between TCDD-exposed labor
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Furthermore, with increasing number
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Society of Toxicology 2010 Author I
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Society of Toxicology 2010 Abstract
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49 th Annual Meeting and ToxExpo A
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The Official Journal of the Society
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