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characterized mouse hepatoma cell line, Hepa1c1c7, was chosen as a cellular model. In a first step, two concentrations (50 nM and 5 μM) and four time points (2, 4, 12 and 24 h) were used for comprehensive transcriptome analysis. Thus, RNA was isolated and applied to Affymetrix exon arrays. Analysis showed a total of 2000 genes to be significantly regulated either by concentration or by time and concentration. About 89 regulated genes are transcription factors, raising the possibility of transcription factor cross-talk in BaP signalling. Genes related to transcription/translation, cell adhesion and DNA repair are among the regulated genes. Some of the robustly regulated genes are those encoding for cytochrome P450 enzymes and the TCDD-inducible poly(ADP-ribose) polymerase, Tiparp. These are known targets of the aryl hydrocarbon receptor (AhR), which is activated by BaP. To start to link these regulations in the transcriptome to the cellular phenotype, changes in cell number were explored over 48 hours of exposure to up to 5 μM BaP. Indeed, cell number increased over time with no apparent differences up to 500 nM BaP. At 5 μM BaP, however, cell number stayed constant over the entire exposure time, thereby indicating disruption of the cell cycle. Our next goal is to identify how cellular functions change if Tiparp is knocked down. 1600 TRANSCRIPTOMICS ANALYSIS OF NANOPARTICLE- CONTAINING HAIR DYES. D. A. Sarigiannis, G. Cimino Reale, E. Marafante, B. Casati, R. Brustio and A. Collotta. Institute for Health and Consumer Protection, European Commission - Joint Research Centre, Ispra, Varese, Italy. Sponsor: L. Birnbaum. The overall objective of this study was to explore the applicability of transcriptomics for risk assessment of mixtures of chemicals in consumer products such as cosmetics and in particular hair dyes so as to develop a systems toxicology framework for consumer product risk assessment. In particular, this approach is expected to identify genetic biomarkers of exposure and early effects related to chronic exposure to low doses of commercially relevant hair dye preparations. According to the study design these biomarkers would be identified through the use of whole genome gene expression micro-arrays and corroborated with quantitative PCR using micro-fluidic cards for specific gene families and biological processes. The study comprised in vivo analysis on urinary bladder and on skin from rat for the identification of gene expression patterns in target organs, and quantitative PCR using micro-fluidic cards for specific inflammation genes. Comparison was made with formulations including reactants usually applied in the products application (e.g. p-phenylendiamine and atninophenol). Three different formulations were tested: the active substance (p-phenylendiamine, PPD); a commercial hair dye formulation using PPD as its principal active ingredient (HD); a similar commercial hair dye using nanoparticle-bound PPD for better dyeing and duration effects (HD nano). The chemicals were applied both on the skin and on the hair of the treated rats. A number of biological processes that were significantly induced compared to the controls after treatment are characteristic of specific products. Blood circulation, clotting and vesicular transport were induced by HD nano only, suggesting that the overall chemical mixture in the HD nano preparation behaves differently than the conventional HD preparation. Blood circulation features should be tested when assessing the toxic potency of HD nano. Moreover, several metabolic processes were induced after treatment with HD nano, including fatty acid, cholesterol, amino acid and nitrogen metabolism. 1601 A TOXICOGENOMIC COMPARISON OF PRIMARY VERSUS PHOTOCHEMICALLY ALTERED AIR POLLUTANTS IN HUMAN LUNG CELLS. J. E. Rager 1 , K. G. Sexton 1 , L. Smeester 1 , I. Jaspers 2 and R. C. Fry 1 . 1 Environmental Sciences and Engineering, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC and 2 Center for Environmental Medicine, Asthma, and Lung Biology, School of Medicine, University of North Carolina, Chapel Hill, NC. Outdoor air pollution contributes significantly to global increases in mortality, particularly within urban environments. Studies have investigated lung responses caused by single pollutants, such as individual gases or particulate matter. There is, however, limited knowledge on the mechanisms underlying health effects resulting from exposure to pollutant mixtures. Toxicogenomic analyses can increase our mechanistic understanding through the study of gene expression alterations and associated molecular pathways. Here, we set out to compare and contrast responses of lung cells exposed to primary pollutants relative to photochemically altered (PCA) pollutant mixtures found in urban atmospheres. We hypothesized that lung cells exposed to PCA pollutants would show increased modulation of inflammatory-associated genes and pathways relative to primary air pollutants. Human lung epithelial cells were exposed to either primary or PCA air mixtures. mRNA expression changes were assessed using microarrays and confirmed using RT-PCR on a subset 344 SOT 2011 ANNUAL MEETING of genes. There was a massive difference in cell response with primary air pollutants altering the expression levels of 19 genes, while PCA pollutants altered 709 genes. Functional and molecular analyses of the altered genes showed that pollutant exposure modifies the signaling of pathways associated with cancer and inflammation. To confirm the altered inflammatory response, protein was collected and interleukin-8 was measured at significantly increased levels. Our study shows for the first time that photochemically produced secondary pollutants initiate significantly more robust changes in gene expression patterns in comparison to primary components of air pollution. This difference may, in part, explain the health effects related to air pollutant exposure. 1602 UNCOVERING TRANSCRIPTIONAL REGULATORS OF KIDNEY INJURY MOLECULE-1 IN CISPLATIN- INDUCED KIDNEY TOXICITY. M. P. Wagoner, J. Milano, D. Brott, D. Thurman, Y. Dragan, L. B. Kinter and B. Jeffy. Safety Assessment U.S., AstraZeneca, Wilmington, DE. Kidney Injury Molecule 1 (KIM-1) is emerging as an important biomarker for drug induced histologically defined renal tubular injury (DIKI), as it is a more sensitive and more accurate measure of DIKI than current clinically available tests. Nephrotoxic compounds such as cisplatin or gentamicin increase both tubular KIM-1 mRNA and urinary KIM-1 protein. While it is understood that urinary KIM-1 protein levels are driven by increased KIM-1 transcription, the transcription factors responsible are as of yet unknown. We used an acute dose model of cisplatin induced nephrotoxicity to identify putative KIM-1-inducing transcription factors, examining kidney transcriptional profiles from 54 rats from 3 different strains following varying doses of cisplatin. Genes induced by cisplatin in a manner resembling KIM-1 expression patterns were identified implying that these genes may have common transcriptional regulators (Pearson correlation p
to confirm a hepatotoxic property of the compound in question, which might otherwise be disregarded based on traditional safety biomarker and histopathology screening. 1604 MUSCLE IMPLANTED PELLETS OF TUNGSTEN/NICKEL/COBALT, NICKEL, OR TANTALUM: A 12 MONTH STUDY OF METAL MOBILIZATION AND MICROARRAY EXPRESSION. D. I. Bannon 1 , A. B. Rosencrance 2 , W. E. Dennis 2 , W. Bao 3 , C. Tsu-Ming 3 , R. D. Wolfinger 3 and E. J. Perkins 4 . 1 Directorate of Toxicology, U.S. Army Public Health Command, Aberdeen Proving Ground, Aberdeen, MD, 2 Department of Chemistry, U.S. Army Center for Environmental Health Research, Fort Detrick, MD, 3 SAS Institute, Inc., Cary, NC and 4 Environmental Laboratory, U.S. Army Engineer Research and Development Center, Vicksburg, MS. Alloys of metals can include nickel, a known cancer inducing agent. In a 12 month study, a single pellet of either a tungsten/nickel/cobalt alloy (WNiCo), pure nickel (Ni), or tantalum (Ta) control were implanted, under anesthesia, into the leg muscle of C3H mice. At 3 week intervals up to 53 weeks, mice (n=5) were euthanized and samples taken for serum, urine (pooled), or microarray analysis (muscle tissue around pellet). Results show metals were excreted in urine at high rates in the first months of the study, after which elimination dropped significantly. Serum samples also showed metal concentration increases in the first months of the study related to treatment (WNiCo, Ni) with lower concentrations in the later months. Little or no metal was mobilized from animals treated with Ta control pellets. Microarray analysis showed that there were patterns of gene expression related to treatment and/or time. These results indicate that there is significant metal mobilization from WNiCo and Ni pellets and that these metals cause perturbations in gene expression that is a function of the metal type. 1605 EXPOSURE TO HEAVY METALS CAUSES DISTINCT CHANGES IN THE GENE EXPRESSION PATTERN OF A RAT LIVER-DERIVED CELL LINE. M. Permenter 2 , J.A.Lewis 1 and D. A. Jackson 1 . 1 U.S. Army Center for Environmental Health Research, Fort Detrick, MD and 2 Excet, Inc., Fort Detrick, MD. Nickel (Ni), cadmium (Cd), cobalt (Co), and chromium (Cr) are toxic industrial chemicals with an exposure risk in both occupational and environmental settings. While these substances are known to have adverse health effects, the detailed mechanisms of toxicity remain unclear. DNA microarrays measure the abundance of thousands of gene transcripts simultaneously, providing a snapshot of what is occurring inside a cell at a given moment. To elucidate the mechanisms of toxicity of Ni, Cd, Co, and Cr, H4-II-E-C3 rat liver-derived cell lines were treated with several concentrations of each metal based on initial viability assays and gene expression patterns were determined with DNA microarrays. Probe sets with an FDR of ≤ 0.001 and changing by at least 1.8 fold in one treatment group compared to the control were considered differentially expressed. The modulated genes were involved in biological processes and pathways including oxidative stress response, apoptosis, cell cycle regulation, and hypoxic response. Comparative analysis identified both common and unique modulated transcripts and perturbed pathways. All the metals affected genes involved in oxidative stress, while chromium most strongly affected those involved in DNA damage and repair, nickel triggered a hypoxic response, and cadmium activated the unfolded protein response. Therefore, we identified novel targets within known toxicity mechanisms that have potential as possible intervention points for Ni, Cd, Co, and Cr toxicity. Opinions, interpretations, conclusions, and recommendations are those of the authors and are not necessarily endorsed by the U.S. Army. The research described herein was sponsored by the U.S. Army Medical Research and Materiel Command, Military Operational Medicine Research Program. 1606 TRANSCRIPTIONAL SIGNATURES FOR CHEMICALLY INDUCED HEPATOXICITY: IN VIVO PREDICTIVE POWER OF 3D LIVER CO-CULTURE OVER 2D HEPATOTOXICITY. B. A. Naughton 1 , R. S. Thomas 3 , L. New 1 , C. I. Pearson 1 , A. H. Roter 2 and D. R. Applegate 1 . 1 RegeneMed Inc., San Diego, CA, 2 Entelos, Inc., Foster City, CA and 3 Genomics, The Hamer Institutes for Health Sciences, Research Triangle Park, NC. The two year rodent bioassay is often used to assess chronic toxicity of compounds. Because of its high cost and lengthy time, many chemicals of concern have not been tested. To increase throughput primary hepatocyte cultures are often used but they have serious limitations including partial expression of xenobiotic metabolizing enzymes and short-term function. A three-dimensional (3D) organotypic liver co-culture (3DLC) provides a physiologically relevant model of intact liver by culturing all hepatic cells on a 3D scaffold. These co-cultures form a tissue that maintains liver functions including cytochrome P450 induction for months. Chemically induced transcriptional profiles have been derived from 2D hepatocytes and 3DLC from the same donor along with in vivo dosing of sibling rodents to evaluate the ability of the two in vitro models to predict in vivo function. Microarray data was generated from cultures exposed to 12 toxicants representing five different compound classes (receptors AhR, CAR/PXR, PPAR; inflammation and hypoxia). The 2D hepatocyte cultures lack the multicellular milieu and structural organization of 3DLC and thereby are not successful in predicting complex toxicity signatures. Differential regulation of pathways known to be regulated by these compounds was similar between 3D cultures and in vivo liver: PPARα agonists upregulated genes in the fatty acid beta oxidation pathway; CAR/PXR agonists upregulated Cyp3A and Cyp2B; and AhR agonists upregulated Cyp1A1 and other AhR-responsive genes. Inflammatory agents induced an acute phase response in 3D cultures similar to that induced in vivo; not possible with 2D hepatocytes that lack inflammatory liver cells. Comparison to DrugMatrix (Entelos, Inc) rodent transcriptional database, showed that the 3DLC treatments scored positive against their respective in vivo derived classifiers whereas 2D prediction was limited. 1607 COMPARISON OF BDE-47 AND ITS HYDROXYLATED ANALOGUES ON THE DEVELOPMENT OF EMBRYONIC ZEBRAFISH. C. Y. Usenko 1, 2 and E. D. Bruce 1, 3 . 1 Biology, Baylor University, Waco, TX, 2 Biomedical Studies, Baylor University, Waco, TX and 3 Department of Environmental Science, Baylor University, Waco, TX. Polybrominated diphenyl ethers (PBDEs) are a class of compounds that have been used as flame retardants for the last 30 years. Recently, there has been growing concern over the potential for PBDEs to disrupt development. Furthermore, hydroxylated analogues have been detected in environmental and human samples worldwide. Currently, there is little information regarding the toxicity of these hydroxylated PBDEs, although there is significant concern that they may pose a greater risk from exposure than the parent compound. In this study, BDE 47 and three hydroxylated BDE 47 congeners were evaluated for developmental effects in zebrafish. Embryos were dechorionated at 6 hours post fertilization (hpf) and exposed to a concentration gradient of each of the congeners. BDE 47 elicited remarkably different effects than the hydroxylated BDE 47 compounds (3-OH-BDE 47, 5-OH-BDE 47, 6-OH-BDE 47). Embryos exposed to BDE 47 had alterations in spontaneous movement at 24 hpf, a curved body axis starting around 120 hpf, and resulted in mortality at 168 hpf when exposed to 5 μg/L and higher concentrations. Conversely, hydroxylated BDE 47 exposures did not affect behavior at any concentration. All congeners investigted, however, delayed development in a concentration-dependent manner. At lower concentrations where the embryos did continue to develop at the normal rate, embryos developed pericardial edema and fin malformations. Furthermore, the concentration-responses varied significantly between the three hydroxylated congeners with embryos most sensitive to 6-OH- BDE 47 exposures and least sensitive to 3-OH-BDE 47 exposures. The addition of the hydroxyl group greatly increased the toxic potential of BDE 47. The location of the hydroxyl group on the PBDE structure also influenced its biological activity. The results of this study indicate that there is a specific interaction between hydroxylated PBDEs and biological systems that is significantly different than that which is observed for the parent compound. 1608 STUDY OF ANTI-DIABETICS AND LMA BY MMP CHANGES ON HEPG2 CELLS USING LASER SCANNING CYTOMETER AND HYPERCYT-CYAN FLOW CYTOMETER. A. Juan-Garcia 1 , J. Robinson 1, 2 , V. Davisson 3 , C. Juan 4 , M. Ruiz 4 and G. Font 4 . 1 Basic Medical Science-PUCL, Purdue University, West Lafayette, IN, 2 Biomedical Engineering-PUCL, Purdue University, West Lafayette, IN, 3 Medicinal Chemistry and Molecular Pharmacology, Purdue University, West Lafayette, IN and 4 Medicina Preventiva i Salut Publica, Ciencies de l’ Alimentació, Toxicologia I Medicina Legal, Valencia University, Burjassot, Valencia, Spain. Antidiabetics, thiazolidinediones (TZD) and biguanides (BD) are involved in the reduction of fast plasma glucose and insulin levels. On the other hand, LMA as fibrates (FB) and statins (ST) are used in the treatment of hyperlypidaemias. Mitochondrial impairment is increasingly implicated in the etiology of toxicity caused by either some antibiabetics or LMA. 5 hypoglucemic compounds, 3 TZD (Rosiglitazone, Troglitazone and Pioglitazone) and 2 BD (Metformin and Phenformin) and 6 lipid modifying agents, 3 ST (Simvastatin, Pravastatin and SOT 2011 ANNUAL MEETING 345
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The Toxicologist Supplement to Toxi
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The Toxicologist Supplement to Toxi
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1 BIODEGRADABLE MATERIALS FOR TISSU
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that genetic toxicology data are ge
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well-orchestrated lung inflammation
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scribed in the literature. We have
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years ago). We will illustrate how
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involved in the biodegradation proc
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stem cells but rather a treatment i
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additional compound showed agreemen
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82 COMPARISON OF 3H-THYMIDINE INCOR
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irritants. While in practice these
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alleles are especially vulnerable t
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109 CD4+ T CELL INTRINSIC TNF RECEP
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118 TO STUDY THE SIGNAL TRANSDUCTIO
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PAHs, such as dioxins, are prevalen
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containing substituents and/or hydr
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146 COMPUTATIONAL MODELING FOR QT P
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suggest that the combination of too
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164 TRANSLOCATOR PROTEIN (18 KDA) (
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function as a metal binding protein
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laboratory has demonstrated that NR
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known. The aim of this study was to
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from 5 to 28 days in duration) in e
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positive cells, caspase-3 activatio
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creased level in the 46 kDa preproe
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invasiveness at concentrations repr
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thracene (DMBA,50 μg in acetone, a
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247 CO-CARCINOGENESIS OF N, N- DIET
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sponds to the endosomal dsRNA that
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ODD in both WT (maximum 177% of con
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Lastly, using p53siRNA cells, p53 w
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its receptor Mpl to exert its funct
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294 LOW LEVEL OF LEAD CAN INDUCE PH
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lunar surface presented potential h
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lar about cellular export mechanism
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DNA in the kidney medulla, grandula
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5.00 and 7.50 mg/kg/day by oral gav
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events and carcinogenesis. Here we
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tinization of cells of the hair fol
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358 CHARACTERIZATION OF GENOME-WIDE
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RNAi were also performed to identif
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376 A FUNCTIONAL CROSSTALK BETWEEN
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UGT1A gene induction, while this re
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tivity, specifically peroxisome pro
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and cytotoxic effects; however, its
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histone deacetylase that is necessa
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ment. Paradoxically, buthionine sul
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drug leflunomide and its major (A77
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442 GENE EXPRESSION AND MORPHOLOGIC
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451 INHIBITION OF THE MITOCHONDRIAL
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460 SULFORAPHANE PREVENTS ACETAMINO
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drophilic/lipophilic balance. Other
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pharmacokinetic and toxicological p
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489 USE OF ‘OMICS DATA TO IMPROVE
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498 APPLICATION OF AGE-SPECIFIC ADJ
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507 A DOSE VOLUME TOLERABILITY STUD
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involved the use of an acute inflam
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sorption in the gastrointestinal (G
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(ABC) transporters actively transpo
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545 BEHAVIORAL EFFECTS OF REPIN IN
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a blood pressure phenotype that res
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and inhalation exposure system that
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and lethality associated with these
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position, on vascular reactivity an
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therefore more accurate and reprodu
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commercial chrysotile product that
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elative to their controls. ST-depre
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ats. The majority of the studies fo
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in the China Jintan Child Cohort St
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corneum thickness, cellular epiderm
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645 EVALUATION OF THE IN VITRO EPIS
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654 TCDD ADSORBED ONTO NATURAL AND
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tion revealed no test article-relat
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671 INFLAMMATION AND TISSUE DAMAGE
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model, ethanol was found to inhibit
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689 ENHANCED SUPPRESSIVE FUNCTION O
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NAC + LPS yielded different levels
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707 LIFE-STAGE PBPK MODELS FOR MULT
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downstream of the apical endpoint o
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726 UPDATED ALUMINUM PHARMACOKINETI
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global parameter sensitivity analys
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and renal inflammation induced by 2
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754 PLASMA, URINE, AND TISSUE CONCE
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cently characterized transporter OA
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exposure system was developed from
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lood cell mass and decrease in urin
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practical alternatives to MC in non
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imals dosed with 167 mg/kg THU alon
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and organ weights, clinical signs a
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yet is induced in most bladder and
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830 RISK ASSESSMENT OF THE SPILL: C
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knowledgebase creation. Results are
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852 UNDERSTANDING STRUCTURAL AND PH
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for integrating epidemiology and an
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motor activity, including age of th
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y partial purification of urine (fr
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pacity for self-renewal and may dif
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sue. The depth of our analysis led
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910 IMPLEMENTING CALIFORNIA’S GRE
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concentrations in six tissues and b
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934 THE FDA’S LIVER TOXICITY KNOW
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943 GENOME-WIDE DNA METHYLATION DIF
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membrane localization and subsequen
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trols, respectively. Subtoxic and t
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survival using both smoking regimes
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as non-, weak, moderate, or strong
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988 NNK-INDUCED CYTOKINE ALTERATION
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group (one-way ANOVA, p90 % viabili
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ered as an organ involved in xenobi
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Transport of CPZ across the Caco-2
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estrous cycle and sexual behavior d
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mRNA expression levels. Collectivel
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1043 THE EFFECTS OF ENDOCRINE DISRU
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1052 MONO-2-ETHYLHEXYL PHTHALATE IN
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Results: MC was variable within and
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UtSMCs. Phosphorylation of FoxO1 wa
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nonpregnant and pregnant diabetic m
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1089 PFOA-INDUCED LIVER EFFECTS IN
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events in the liver. AZD9056 was ev
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The peppermint oil caused a concent
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OA did not affect food consumption.
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1126 PERSISTENT DEVELOPMENTAL ARYLH
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1135 BACH2 BINDING TO Prdm1 AS A ME
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The purpose of this project was to
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one marrow. Since Chk1 is an attrac
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1163 THE MRNA AND MIRNA PROFILE OF
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have now compared the IC50 values b
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1181 ELUCIDATION OF FACTORS DETERMI
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enced by pre-exposure to cigarette
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if abnormal PF was associated with
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weight (P=0.016) and small for gest
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portant cause of death, compared to
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posure groups. However, the differe
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Naphthalene is routinely analyzed i
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1245 SEASONAL CHARACTERIZATION OF H
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1255 URINARY T, T MUCONIC ACID LEVE
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modating a reliable data evaluation
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enzoquinone generate ROS and arylat
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teins (e.g. C3, 4, and 5, APOB, VDB
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1293 TRANSFORMING GROWTH FACTOR BET
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mation was decreased to the same le
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1312 EVALUATION OF THE SENSITIVITY
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luted OFR and CRL. Culture media ex
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urinary TCPy levels, blood and brai
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activity. The dose-response curves
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mice, each with 4 dose groups. One
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exposure to both ATR and DACT has a
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Page 317 and 318: 1457 GLOBAL GENE PROFILING REVEALS
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Page 373 and 374: those with high nickel content are
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1845 IS THE PROMISCUITY OF THE ARYL
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crorarray analysis. RT-PCR results
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are a family of phase-II biotransfo
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ous labs. As a result of positive s
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down the doses may produce more tox
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spectively. Below 100 mg/l of gemfi
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1900 GENERATION OF PRECISION CUT LI
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iomarkers or observation of lesions
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creased reticulocytes and lymphocyt
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statistically significant interacti
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monize sample preparation and analy
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NPC and sinonasal cancer in neighbo
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showed incidences of lung and nasal
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utylbenzenes, exhibited most simila
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1975 DIFFERENTIAL MODULATION OF CYP
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organic As to MMA(V) and a lower ca
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ole in invasion and metastasis of c
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3T3-L1 cells to low-levels of arsen
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2011 IDENTIFICATION OF A NOVEL VX M
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This work was supported by Cooperat
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2029 EFFICACY OF ENDOTRACHEAL ADMIN
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Diazepam injections and its combina
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2047 ESTERASE ACTIVITIES AND HEMOST
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nanoparticle-induced toxicity progr
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house, were iv infused into rats ov
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een explored. This study investigat
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croscopic analysis revealed that on
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egg yolk collected from turtles inh
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consistency of results in both expe
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2111 CYTOCHROME P450 3A5 GENOTYPE I
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esidues of organophosphates or thei
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manganism. Recent work from our lab
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Aβ1-40 in CSF and hippocampus in P
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2147 CATALASE MANIPULATIONS MODIFY
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ation based on real-world exposure
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NPs. Aggregation of citrate-stabili
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2175 THE ROLE OF SURFACE CHEMISTRY
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seen rapid uptake in biological ima
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effect on uterine weight or vaginal
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dicating widespread exposure. While
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components into the liver parenchym
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2223 ISOLATION AND DETECTION OF RIC
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stored (-20 celsius degree). The co
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2241 DDA, A BIOMARKER FOR ENVIRONME
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2249 INTERACTION BETWEEN DIETARY SE
Page 489 and 490:
2258 PHARMACOKINETICS, EXCRETION BA
Page 491 and 492:
2267 SENSITIVE AND SPECIFIC FLUORES
Page 493 and 494:
2276 METABOLISM AND DISPOSITION OF
Page 495 and 496:
ment of hypertension in companion a
Page 497 and 498:
for the propyl series can be used f
Page 499 and 500:
2304 IN VITRO EXPOSURE AND EVALUATI
Page 501 and 502:
2313 THE SYNERGISTIC EFFECT OF SODI
Page 503 and 504:
genes that play a crucial role in M
Page 505 and 506:
2330 THE ROLE OF TRANSFORMING GROWT
Page 507 and 508:
ined following up to 96 h continuou
Page 509 and 510:
effect doses obtained with the rat
Page 511 and 512:
diated transcriptional response of
Page 513 and 514:
docrine disruptor activities of EDC
Page 515 and 516:
individuals. Week 6 results were qu
Page 517 and 518:
functionality of photosystem II and
Page 519 and 520:
wild mice (Mus musculus) from areas
Page 521 and 522:
2406 TOXICITY AND BIOACCUMULATION O
Page 523 and 524:
Isocitric acid is the acid in the h
Page 525 and 526:
2425 EFFECTS OF FUMONISINS IN ETHAN
Page 527 and 528:
centration(μg/g) were: 5.1-95.3; 2
Page 529 and 530:
2445 AUTOPHAGY IN DEVELOPMENT: A LI
Page 531 and 532:
sures to inhaled Mn in dust. Nevert
Page 533 and 534:
2466 CRITICAL EVALUATION OF ANIMAL
Page 535 and 536:
elationships predict that resting r
Page 537 and 538:
2489 COMPARATIVE TOXICITY OF BIODIE
Page 539 and 540:
2497 TRANSCRIPTIONAL REGULATION OF
Page 541 and 542:
2506 TOXICOLOGICAL CONSIDERATIONS O
Page 543 and 544:
launched with the aim of developing
Page 545 and 546:
forms mRNA expression levels were a
Page 547 and 548:
2534 CUTANEOUS WOUND HEALING IN THE
Page 549 and 550:
wells (0, 1, 5, 10, 25, 50, 100, an
Page 551 and 552:
2553 AN ORGANOTYPIC MICROLIVER PLAT
Page 553 and 554:
serum-free media. At 24 hrs, the gr
Page 555 and 556:
2572 INCREASED ARSENIC BIOACCESSIBI
Page 557 and 558:
nology to develop improved methods.
Page 559 and 560:
tuna, swordfish, or mako shark (3.5
Page 561 and 562:
nificantly reduce circulating thyro
Page 563 and 564:
grouped into 9 observation periods
Page 565 and 566:
histopathological or biochemical ev
Page 567 and 568:
exhibited a hyperactive phenotype,
Page 569 and 570:
the search of effective drugs for e
Page 571 and 572:
2644 COVALENT BINDING OF 14 C 2-MET
Page 573 and 574:
aries targeting all transcription f
Page 575 and 576:
(p 9 weeks) and CSC phenotype acqui
Page 577 and 578:
2673 IMMUNE-MEDIATED VASCULAR INJUR
Page 579 and 580:
for risk identification and charact
Page 581 and 582:
to control toxicant delivery in tob
Page 583 and 584:
Author Index (Continued) The numera
Page 585 and 586:
Page 587 and 588:
Page 589 and 590:
Page 591 and 592:
Page 593 and 594:
Page 595 and 596:
Page 597 and 598:
Page 599 and 600:
Page 601 and 602:
Page 603 and 604:
Page 605 and 606:
Page 607 and 608:
Page 609 and 610:
Page 611 and 612:
Keyword Index (Continued) Arsenite
Page 613 and 614:
Keyword Index (Continued) Covalent
Page 615 and 616:
Keyword Index (Continued) flow cyto
Page 617 and 618:
Keyword Index (Continued) innate im
Page 619 and 620:
Keyword Index (Continued) nanoparti
Page 621 and 622:
Keyword Index (Continued) preservat
Page 623 and 624:
Keyword Index (Continued) Thrombocy
Page 625 and 626:
Toxicological Sciences The Official
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The Toxicologist - Society of Toxicology

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