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showed an enhanced endoplasmic reticulum (ER) stress 5 days post v-Hras1 infection, characterized by enhanced vacuolation and higher levels of several ER stress markers. Surprisingly, this increased level of ER stress did not lead to an increase in oncogene-induced senescence in Pparβ/δ-null keratinocyte, but rather, Pparβ/δnull keratinocytes exhibited a lower level of cellular senescence compared to wildtype keratinocytes. Further, ligand activation of PPARβ/δ induced terminal differentiation in v-Hras1- infected wild-type keratinocytes and this effect was not observed in v-Hras1- infected Pparβ/δ-null keratinocytes. These results suggest that PPARβ/δ attenuates oncogenic-dependent neoplastic transformation by inhibiting Hras1 signaling in keratinocytes. (Supported by CA124533, CA126826) 2143 PPARβ/δ -DEPENDENT AND INDEPENDENT FUNCTIONS OF THE PPARβ/δ ANTAGONIST GSK3787. P. S. Palkar 1 , M. G. Borland 1 , C. Lee 1 , C. H. Ferry 1 , A. K. Sharma 2 , S. Amin 2 , A. N. Billin 3 , T. M. Wilson 3 , F. J. Gonzalez 4 and J. M. Peters 1 . 1 Department of Vet. and Biomed Sci, Penn State University, State College, PA, 2 Department of Pharmacology, Penn State Cancer Institute, Hershey, PA, 3 Nuclear Receptor Discovery Research, GlaxoSmithKline, Research Triangle Park, NC and 4 Laboratory of Metabolism, NCI, Bethesda, MD. The availability of high affinity agonists for peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) has led to significant advances in our understanding of the functional role of PPARβ/δ. The first PPARβ/δ antagonist (GSK0660) was recently described but this compound is not bioavailable precluding its application for in vivo analysis. In this study, the effect of a new PPARβ/δ antagonist, GSK3787, was examined using in vivo and in vitro models. Oral administration of GSK3787 effectively anatagonized GW0742-induced up-regulation of Angptl4 mRNA expression in wild-type mouse colon. This antagonism was due to reduced promoter occupancy based on chromatin immunoprecipitation (ChIP) analysis. GSK3787 effectively antagonized GW0742-induced expression of Angptl4 mRNA in wild-type mouse fibroblasts and keratinocytes, and this effect was not found in similarly treated PPARβ/δ-null cells. GW0742 did not significantly influence cell proliferation at concentrations up to 10 μM in wild-type or PPARβ/δ-null fibroblasts. Similar results were found in fibroblasts treated with GSK3787 as no changes in cell proliferation were observed at concentration up to 10 μM. GSK3787 did not inhibit proliferation of A549, MCF7, H1838 cells at concentrations that specifically antagonized gene expression. Results from these studies demonstrate that GSK3787 can antagonize PPARβ/δ in vivo and be highly specific in vitro at concentrations lower than 1 μM. However, results from these studies also show that inhibition of cell proliferation observed with higher concentrations (≥ 10 μM) affecting non-tumor cells and tumor cell lines are likely due to off-target mechanisms. (Supported by CA124533, CA126826) 2144 FUNCTIONAL EXAMINATION OF THE ROLE OF PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR-β/δ (PPARβ/δ) IN HUMAN COLON CANCER. J. E. Foreman 1 , J. L. Williams 2 , B. Rigas 2 , F. J. Gonzalez 3 and J. M. Peters 1 . 1 The Center for Mol. Toxicology & Carcinogenesis, Penn. State University, University Park, PA, 2 Division of Cancer Prevention, Stony Brook University, Stony Brook, NY and 3 Laboratory of Metabolism, NCI, Bethesda, MD. The role of peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) remains controversial. While some evidence suggests that activating PPARβ/δ promotes tumorigenesis, other reports suggest that activating PPARβ/δ has no effect or attenuates tumorigenesis. The latter observations are also supported by the well-established roles of PPARβ/δ in regulating glucose and lipid homeostasis and promoting cellular differentiation. Previous work has suggested that PPARβ/δ is up-regulated by the APC/β-catenin pathway in colon cancer and that the chemopreventive effects of non-steroidal anti-inflammatory drugs (NSAIDs) are mediated by repression of PPARβ/δ expression and function. However, more comprehensive analysis of human colon cancer cell lines with mutations in the APC/β-catenin pathway indicates that PPARβ/δ expression is not up-regulated by increased β-catenin-dependent activity. Further, increased expression of PPARβ/δ and function was also noted in human colon cancer cell lines treated with NSAIDs. Thus, there is a clear need for more quantitative analysis of PPARβ/δ function in colon cancer models. The present study examined expression of PPARβ/δ mRNA and protein in normal and cancerous human colon tissue. Colony formation assays using human colon cancer cell lines showed that activating PPARβ/δ either inhibited clonogenicity or had no effect on clonogencity in HT29, HCT116, DLD and RKO cells. Induction of apoptosis in human colon cancer cell lines with NSAIDs was associated with increased expression of PPARβ/δ and activating PPARβ/δ in the presence of NSAIDs either enhanced or had no effect on cleaved poly (ADP-ribose) polymerase (PARP). Collectively, results from these studies provide additional evidence demonstrating the ligand activation of PPARβ/δ either inhibits cell proliferation or has little effect in human colon cancer models. (Supported by CA124533, CA128826) 2145 DIELDRIN INDUCES THE RAT PARAOXONASE (PON1) PROMOTER VIA PXR, RXR. M. Dail, R. R. Pickin, J. A. Crow and J. E. Chambers. Center for Environmental Health, Mississippi State, Mississippi State, MS. Measurable levels of the legacy organochlorine insecticide, dieldrin, are still in soil and accumulation in exposed individuals is a possibility. Paraoxonase (PON1) is named for its ability to hydrolyze paraoxon, the active metabolite of the insecticide parathion, and is associated with HDL particles. In addition, PON1 has been inversely related to the prevalence of atherosclerotic cardiovascular disease. In vivo rat studies have shown that dieldrin can increase paraoxonase activity but the mechanism is unclear. Nuclear receptors can increase pesticide metabolism, and putative binding sites for PXR exist in the PON1 promoter. The present work examined the effect of dieldrin and nuclear receptors on PON1 promoter activity via the Dual-Glo TM Luciferase Assay System. Expression constructs were created containing rat liver PXR only, RXR only, and PXR-RXR combined on the same vector. A construct with the human PXR gene (SXR) was also obtained. The rat liver PON1 promoter was subcloned in front of the Renilla gene. Plasmids were transiently transfected, either alone or in combination, into the rat hepatoma cell line, McA- RH7777. Controls included the empty expression vector and a transfection control plasmid. Transfected cells were exposed to dieldrin concentrations from 100nM to 0.1mM for a 24 hour period. PON1 promoter activity was measured as a function of luminescence and compared to the level caused by vehicle (DMSO). Dieldrin concentrations from 10μM to 100μM significantly increased (P
2147 A SINGLE AMINO ACID CONTROLS THE FUNCTIONAL SWITCH OF HUMAN CAR1 TO THE XENOBIOTIC ACTIVATED SPLICING VARIANT CAR3. T. Chen 1, 2 , L. M. Tompkins 2 , G. Kim 2 , C. J. Omiecinski 1 and H. Wang 2 . 1 Center for Molecular Toxicology and Carcinogenesis, Pennsylvania State University, University Park, PA and 2 Pharmaceutical Sciences, University of Maryland School of Pharmacy, Batimore, MD. The constitutive androstane receptor (CAR) is constitutively activated in immortalized cell lines independent of xenobiotic stimuli. This feature of CAR has limited its use as a sensor for xenobiotic-induced expression of drug-metabolizing enzymes. Recent reports, however, revealed that a splicing variant of human CAR (hCAR3), which contains an insertion of 5 amino acids (APYLT), exhibits low basal but xenobiotic inducible activities in cell-based reporter assays. Nonetheless, the underlying mechanisms of this functional shift are not well understood. We have now generated chimeric constructs containing various residues of the 5 amino acids of hCAR3 and examined their response to typical hCAR activators. Our results showed that the retention of alanine (hCAR1+A) alone is sufficient to confer the constitutively activated hCAR1 to the xenobiotic sensitive hCAR3. Notably, hCAR1+A was significantly activated by a series of known hCAR activators, and displayed activation superior to that of hCAR3. Moreover, intracellular localization assays revealed that hCAR1+A exhibits nuclear accumulation upon CITCO treatment in COS1 cells, which differs from the spontaneous nuclear distribution of hCAR1. Mammalian two-hybrid and GST pull-down assays further demonstrated that hCAR1+A interacts with the co-activator SRC-1 and GRIP-1 at low level prior to activation, while at significantly enhanced level in the presence of CITCO. Thus, the alanine residue in the insertion of hCAR3 largely directs the xenobiotic response of hCAR3 through direct and indirect mechanisms. Activation of hCAR1+A may represent a sensitive methodology for the identification of hCAR activators. 2148 PXR STATUS IS ASSOCIATED WITH CYP INDUCTION, HISTOPATHOLOGICAL EFFECTS, AND REDUCED CLEARANCE OF NONYLPHENOL. L. C. Mota and W. Baldwin. Environmental Toxicology, Clemson University, Clemson, SC. Nonylphenol, a byproduct of alkylphenol ethoxylates, is a ubiquitous chemical that binds several nuclear receptors. Previous studies in our laboratory have demonstrated that nonylphenol also activates the pregnane X-receptor (PXR), a xenobiotic sensing nuclear receptor. Therefore, we are studying the role of PXR in protecting organisms from nonylphenol. Wild-type, PXR-null, and hPXR (PXR-null mice with the human PXR receptor) mice were treated with nonylphenol at 0, 50 and 75 mg/kg/day for one week, livers excised for histopathology and CYP induction, and serum collected to determine nonylphenol concentrations. Wild-type mice treated with nonylphenol show induction of Cyp2b (males and females), as well as Cyp2c and Cyp3a (only in males). Induction of CYPs in wild-type mice was PXR-dependent as determined by the lack of induction in PXR-null mice. Interestingly, hPXR mice only showed induction of Cyp2b. Liver histopathology indicated significant hepatocyte hypertrophy in nonylphenol-treated wild-type mice, indicating that wild-type mice had an acute response to compensate for nonylphenol exposure. PXR-null and hPXR mice did not show any significant liver histopathological changes; however, these mice show greater hepatocyte hypertrophy in untreated animals. Serum concentrations of nonylphenol were significantly higher in PXR-null mice compared to untreated mice. Taken together the histopathology, lack of CYP induction, and serum nonylphenol concentrations indicate that PXR-null mice are unable to respond to a nonylphenol challenge and eliminate the toxicant as observed by higher nonylphenol serum concentrations, and lack of CYP induction and liver hypertrophy. Overall this data suggest that PXR is important in eliminating nonylphenol and ultimately protecting individuals from its potential adverse effects. Funding for this research is provided by NIEHS. 2149 CRITICAL ROLE OF NRF2 CYSTEINE RESIDUES IN OXIDANT/ELETROPHILE-SENSING AND SIGNAL TRANSDUCTION. Q. Ma 1, 2 and X. He 1 . 1 Receptor Biology Lab/TMBB/HELD, National Institute for Occupational Safety and Health, Morgantown, WV and 2 Department of Biochemistry, West Virginia University School of Medicine, Morgantown, WV. Cells respond to oxidants and electrophiles by activating receptor/transcription factor Nrf2 to coordinate induction of cytoprotective genes critical for defense against oxidative and other stresses. Activation involves blocking the ubiquitination-proteasomal degradation of Nrf2. Modification of cysteine thiol groups by inducers in the linker region of Keap1, which congregates Nrf2 into the Keap1/Cul-3-based E3 complex for ubiquitination, is important but not sufficient for activation of Nrf2. Here we show that evolutionally conserved cysteine residues of Nrf2 are critical for Nrf2 regulation. FlAsH (an arsenic-based fluorophore) and phenylarsine oxide (PAO) potently induce Nrf2 target genes and bind to Nrf2 in vitro and in vivo. Binding is inhibited by prototypical inducers arsenic and tBHQ. PAO affinity pulldown and mutation of individual cysteine to alanine reveal that C235, C311, C316, C414 and C506 are critical for binding and binding is modulated by intra-molecular interactions. To corroborate the functions of cysteine residues, Nrf2 wild-type or mutants are expressed in Nrf2 knockout cells to reconstitute Nrf2 regulation. Nrf2 mutants have reduced t1/2 values that inversely correlate with increased binding to Keap1 and polyubiquitination of mutant proteins. Remarkably, the mutants fail to respond to arsenic for Nrf2 activation and gene induction. Furthermore, mutations at C119, C235, and C506 impede binding of Nrf2 to endogenous antioxidant response element and to coactivator CBP/p300. The findings demonstrate for the first time that Nrf2 cysteine residues critically regulate oxidant/eletrophile sensing, repress Keap1-dependent ubiquitination-proteasomal degradation, and promote recruitment of co-activators, such that chemical sensing, receptor activation, and transcription activation are integrated at the receptor molecule. 2150 SEARCHING FOR THE SPECIFIC INTRACELLULAR TARGET OF BORIC ACID THAT LEADS TO THE INHIBITION OF CALCIUM RELEASE IN PROSTATE CANCER CELL LINES. S. E. Kobylewski 1 , K. A. Henderson 1 and C. D. Eckhert 2 . 1 Molecular Toxicology, University of California Los Angeles, Los Angeles, CA and 2 Environmental Health Sciences, University of California Los Angeles, Los Angeles, CA. Boric acid (BA) is a dietary component found naturally in the environment. Low levels reduce the incidence and mortality of prostate cancer. Our current studies have shown that low doses of BA can inhibit calcium release from the ryanodine receptor (RyR) in the endoplasmic reticulum in response to RyR agonists in DU-145 prostate cancer cells. The dose of BA required to inhibit RyR-dependent release of stored calcium is 10 to 100 fold higher in non-tumor PWR-1E prostate cells than DU-145 cells, indicating that there may be differences in RyR isoform expression between cell lines. In this project our objective is to identify the specific RyR isoforms and/or accessory proteins that potentially interact with BA and cause the inhibition of calcium release. The identification of each cell line’s specific RyR isoforms was assessed with reverse-transcription PCR and restriction enzyme digestion. Both DU-145 and PWR-1E cells express RyR isoform 1 (RyR1) but LNCaP prostate cancer cells do not. All three cell lines express RyR2 and lack RyR3. Real-time PCR showed that RyR2 expression is lower in DU-145 cells than it is in the other two cell lines. Overall RyR mRNA expression in DU-145 cells treated with varying doses of BA was measured using real-time PCR. There was no significant change in mRNA expression indicating that BA exerts its effects at the receptor and not the transcription level. These results indicate that the BA-sensitivity between tumorgenic and non-tumorgenic cell lines is probably not due to a difference in RyR isoform expression. The cytoplasmic surface of all three RyR isoforms serves as a surface for binding of several accessory proteins that modulate opening and closing of the calcium channel. Future studies are needed to determine if differences in calcium release inhibition by BA can be explained by the interaction of BA with one or more of these accessory proteins or their RyR binding sites. 2151 TRPV1 MEDIATES LUNG TOXICITIES OF SPECIFIC PARTICULATE MATERIALS. C. A. Reilly, M. Johansen, K. Thomas, J. Veranth and G. Yost. Pharmacology and Toxicology, University of Utah, Salt Lake City, UT. Particulate materials (PM) are ubiquitous air contaminants with established effects on human respiratory and cardiovascular health. Multiple features of PM have been correlated with adverse outcomes. However, the molecular sensors that detect, differentiate, and initiate responses to PM as well as the contributions of PM:PM sensor interactions to PM toxicity have not been fully elucidated. We hypothesized that specific calcium channels expressed by lung cells can both differentially detect PM and initiate responses that ultimately manifest as lung damage. Transient Receptor Potential Vanilloid-1 (TRPV1) over-expressing lung cells engineered to express high levels of cell surface TRPV1, were treated with multiple prototype PM. Calcium flux initiated by 3 of the PM, coal fly ash medium (CFAm), crystalline silica (Xtal), and synthetic residual oil fly ash (ROFA) was inhibited by the TRPV1 SOT 2010 ANNUAL MEETING 457
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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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867 MELATONIN AMELIORATES CYCLOPHOS
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pharmacokinetic (PBPK) models. Ten
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of radiolabeled Mn (carrier-free 54
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893 UNVEILING ASSOCIATIONS BETWEEN
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using area under the concentration
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912 COMMERCIAL FISH DIETS INDUCE VI
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922 A STUDY OF PHOTOTOXICITY FOLLOW
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from 0.1 to 2.9 g/L (saturated vapo
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vasive method for assessing several
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950 ARSENITE DOWN-REGULATES THE CAR
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inflammatory signaling is altered b
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treated wood. Seventy-five of 132 w
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ergy homeostasis and raising levels
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treated with mercury and then with
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997 IN VIVO CORRELATES OF THE MANGA
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of the panel. The panel was compris
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sponse, location, and severity scor
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tant source of n-3 fatty acids such
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old for serious, irreversible or es
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1045 SUBCHRONIC TOXICITY EVALUATION
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sites collected 3 days after inject
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1063 MOLECULAR MECHANISM OF OLANZAP
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esponses, and can be available for
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hence more physiologically relevant
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thesized apoproteins, so we tested
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vate CYP3A5 but could be released b
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1108 STYRENE-INDUCED TOXIC EFFECTS
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1118 THE PRESENCE OF DIETHYL FUMARA
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zebrafish cells were first exposed
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utene-1,4-dial, which has been show
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groups, largely due to lower non-HD
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Exposure to gluten in individuals w
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contrast to VGSC activators such as
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1175 70% HYDROFLUORIC ACID (HF) CUT
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axis. An increase in hyaline drople
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1194 esiRNA AND siRNA HIGH-THROUGHP
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1203 ARYL HYDROCARBON RECEPTOR-DNA
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permeability (calcein), mitochondri
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olytic caspase activation, caspase-
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teristics of a human T-type voltage
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80% of the activity from the yellow
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1251 DEVELOPMENTAL EXPOSURE TO DELT
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1260 MANEB ENHANCES MPP + -INDUCED
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demonstrated by knockdown of beclin
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1278 PINK1 AND MITOCHONDRIAL DYNAMI
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treatment for number of live worms.
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1297 INVESTIGATION OF THE NEUROTOXI
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1306 DEVELOPMENT OF AN IN VITRO ASS
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1315 EVALUATION OF 3- AND 1-METHYLH
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prior to kainic acid-induced seizur
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1334 AFFECT OF GENETIC VARIATION ON
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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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Page 415 and 416: 1930 DEVELOPMENT OF A RELATIVE SOUR
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Page 447 and 448: 2084 INHIBITION OF 11β-HSD1 DECREA
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Page 451 and 452: 2101 GENISTEIN MODULATION OF BLOOD
Page 453 and 454: males per group were dosed orally o
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Page 465 and 466: ility of tungsten trioxide (WO3), t
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Page 469 and 470: glucose, and creatinine levels, and
Page 471 and 472: Several studies have reported suppr
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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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The Toxicologist - Society of Toxicology

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