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process of hepatocarcinogenesis, 6-week-old male CARKO mice (C3H strain origin) and wild C3H mice were treated with 5,000 ppm PBO, 50,000 ppm DBDE or 500 ppm PB in diet for 27 weeks after the initiation with diethylnitrosamine (DEN). Control animals were fed basal diet alone after DEN initiation. As a result, in wild mice the PBO and PB treatments increased incidences and multiplicities of altered foci and adenomas in the liver, of which phenotypes were mainly eosinophilic. In CARKO mice, PBO and PB drastically reduced such eosinophilic lesions compared with the relevant treated wild mice, and no tumor was induced by PB. In contrast, DBDE mainly induced basophilic lesions in wild mice. Interestingly, multiplicity of basophilic lesions was greater in CARKO mice given DBDE compared with control CARKO mice, and comparable to those in DBDEtreated wild mice. These results indicate that CAR might play an important role in the mechanism of hepatocarcinogenesis induced by PBO or PB, while other mechanisms might exsist as a main pathway of DBDE-induced hepatocarcinogenesis. Taken together with short-term and two-stage carcinogenicity studies using CARKO mice, our results suggest a novel possibility that CAR-mediated hepatocarcinogenesis might follow different process from CAR-mediated liver hypertophy in mice. 2658 DNA DAMAGE MODULATION IN XPA(-/-)P53(+/-) AND WILD TYPE C57BL/6 MICE FED BENZO[A]PYRENE WITHOUT OR WITH CHLOROPHYLLIN (CHL) FOR 28 DAYS. K. John 1 , M. I. Churchwell 2 , F. A. Beland 2 , M. M. Pratt 3 , G. McMullen 1 and M. C. Poirier 1 . 1 Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD, 2 Division of Biochemical Toxicology, National Center for Toxicological Research, U.S. FDA, Jefferson, AR and 3 National Center for Environmental Assessment, Office of Research and Development, U.S. EPA, Washington, DC. Chlorophyllin (CHL), a chemopreventive agent, was previously shown to reduce formation of DNA damage in normal human mammary epithelial cells exposed to BP (John et al., Cancer Letters, 2010). Here we examined the effects of CHL on DNA adduct formation in nucleotide excision repair (NER)-deficient [Xpa(-/-)] and tumor suppressor haploinsufficient [p53(+/-)] mice, and their wild type (WT) counterparts, fed either control diet, or diet containing 100 ppm BP, or 100 ppm BP + 0.3% CHL for 28 days. DNA damage (expressed as adducts per 10 8 nucleotides ± SE, n=6-10 mice/group) was measured in liver, lung and esophagus by chemiluminescence immunoassay (CIA) using antiserum elicited against DNA modified with r7,t8-dihydroxy-t-9,10-oxy-7,8,9,10-tetrahydrobenzo[a]pyrene (BPDE). As expected, there was more DNA damage in Xpa(-/-)p53(+/-) mice compared to WT mice, confirming the absence of normal NER capacity in the transgenics. In Xpa(-/-)p53(+/-) mice fed BP + CHL there was no change in DNA adduct levels in esophagi and lungs, compared to mice fed BP alone. However, in liver the addition of CHL caused a significant reduction [104.9 ± 13.3 for BP vs. 36.7 ± 10.6 for BP + CHL]. In WT mice fed BP + CHL the adduct levels were unchanged in the lungs and significantly increased in esophagi [15.4 ± 1.5 for BP vs. 65.1 ± 8.7 for BP + CHL] and liver [54.5 ± 10.5 for BP vs. 261 ± 20.3 for BP + CHL], compared to mice fed BP alone. Analysis of BPdG adducts by HPLC- MS/MS in Xpa(-/-)p53(+/-)and WT mice is currently in progress. The increase in DNA damage in esophagi and livers of WT mice suggest that chronic human use of CHL for chemoprevention of PAH-mediated carcinogenesis should be viewed with caution as the burden of DNA damage may not be lowered in all organs. 2659 EXPOSURE TO URBAN PARTICULATE MATTER INDUCES A DECREASE IN E-CADHERIN EXPRESSION IN MULTICELLULAR TUMOR SPHEROIDS. F. M. Bernal-Herrera 1 , C. M. García-Cuéllar 2 , R. Morales-Barcenas 2 , Y. Sánchez-Pérez 2 and Y. I. Chirino 1 . 1 Unidad de Biomedicina, Universidad Nacional Autonoma de Mexico, Edo. Mex, Mexico and 2 Subdirección de Investigación Básica, Instituto Nacional de Cancerologia, Mexico, Mexico. Sponsor: H. Glauert. Epidemiological studies have demonstrated that exposure to particulate matter (PM) with an aerodynamic diameter smaller than 10 μm (PM10) is associated an augment the risk of lung cancer. To investigate the effects of PM10, several monolayer cell culture models have been studied, however, the PM10 effects on tumor cell models has not been completely explored. The loss of E-cadherin is associated with the invasiveness of tumors, metastatic dissemination and a poor prognosis. We hypothesized that PM10 exposure could induce a decrease in E-cadherin expression in an established tumor. To test this hypothesis, multicellular tumor spheroids (MTS) of lung adenocarcinoma cells were grown in 96-plates (40,000 cell per well in non-adherent conditions) for 4 days. On day 5, spheroids were exposed to PM10 (5 μg/mL, 10 μg/mL and 20 μg/mL) for 24 h. Then, spheroids were collected to 570 SOT 2011 ANNUAL MEETING western blot analysisis. The expression of E-cadherin, actin and GAPDH were performed. We compared the effect of PM10 exposure on the expression of above mentioned proteins in monolayer cell culture of the same cells. Our results show that PM10 induces a 20% decrease in E-cadherin expression in the higher concentration in MTS but monolayer cell culture remains without changes. We also found that PM10 induces a 10% increase in actin expression in MTS (10 μg/mL and 20 μg/mL) and using phalloidin, a dynamic actin polymerization to filamentous actin was observed by confocal microscopy in monolayer cell culture. The expression of GAPDH was used as loading control. Based on these results, we conclude that PM10 induced a decrease in E-cadherin expression in MTS and PM10 also induced an increase in actin expression that could be related to changes to filamentous actin. 2660 STUDIES ON METABOLISM OF 1, 4-DIOXANE. W. Eck 1 , J. Fishbein 2 , B. Ginevan 2 , N. Koissi 2 and N. Shah 2 . 1 Directorate of Toxicology, U.S. Army Public Health Command, Aberdeen Proving Ground, MD and 2 Department of Chemistry and Biochemistry, University of Maryland—Baltimore County, Linthicum, MD. 1,4-Dioxane is a water-miscible, semi-volatile organic compound that is found in ground water at many military installations as a consequence of being used as a stabilizer for the degreasing solvent 1,1,1-trichloroethane. Dioxane use continues for production of small arms ammunition and as a component of various other formulations. The U.S. Army is facing a significant environmental restoration liability because of dioxane contamination. The carcinogenic potential of dioxane is dependent upon its mode of action and the role of dioxane metabolites. Two possible metabolites have previously been identified—1,4-dioxan-2-one (dioxanone) and 2hydroxyethoxyacetic acid (HEAA); the former with electrophilic properties capable of genotoxicity. Questions have remained about the potential role and relationship between the two metabolites, which can exist in a simple equilibrium with one another. To better understand the thermodynamic and kinetic parameters of the equilibrium between dioxanone and HEAA, an analysis of the excreted metabolites without chemical derivatization was conducted. The equilibrium constant for the reaction between dioxanone and HEAA was found to greatly favor HEAA. Kinetic analysis found that the reaction was rapid, with the half-life of the hydrolysis reaction being approximately 0.4 hours. Further in vivo metabolism was studied in Sprague-Dawley rats. Analysis of blood and urine samples for up to 8 hours after oral gavage failed to detect the presence of any dioxanone in either medium, an observation that is consistent with the physico-chemical parameters of the reaction. These data suggest that there is a low probability that the dioxanone electrophillic metabolite is created and responsible for genotoxic induction of cancer. 2661 THE IN VIVO ROLE OF ADIPOCYTE-SPECIFIC PPARγ IN ENVIRONMENTAL RISK FACTOR-MEDIATED BREAST TUMOURIGENESIS. G. Skelhorne-Gross 1 , N. Peterson 1 , R. Rubino 1 , S. SenGupta 1 and C. Nicol 1, 2 . 1 Pathology and Molecular Medicine, Queen’s University, Kingston, ON, Canada and 2 Division of Cancer Biology and Genetics, Queen’s University, Kingston, ON, Canada. One in 28 women will die from the growth and spread of breast cancer. The interactions between genetic and environmental (chemical and western-style high fat diet (HF)) risk factors in this process remain unclear. HF consumption also correlates with increased secretion of adipocyte signaling factors linked to breast tumourigenesis. Peroxisome proliferator-activated receptor (PPAR)γ plays a role in many cancers and controls the expression of genes essential for normal fat and sugar metabolism. We have shown using PPARγ heterozygous (+/-) mice that PPARγ normally stops the in vivo progression of 7,12-dimethylbenz[a]anthracene (DMBA)-mediated breast tumours. Since many breast cell types express PPARγ, each with unique signal patterns, we aim to define which are required for these PPARγ-dependent effects. Here we examine the hypothesis that adipocyte-specific PPARγ signaling stops the progression of multi-risk factor (DMBA+HF)-mediated breast tumourigenesis. To do this, we generated PPARγ(+/-) and adipocyte-specific PPARγ knockout (PPARγ-A KO) mice and their wild-type (WT) controls. Eight week old female mice (n=10, n=12, n=25, respectively) were treated p.o. with 1mg DMBA once/week and given HF for the duration of the study (25 weeks). Our data show that DMBA+HF treated PPARγ-WT mice have significantly decreased overall survival and tumour latency (13 vs 25 weeks), and increased mammary (43% vs 18%) and skin (86% vs 64%) tumour multiplicity compared to DMBA+normal diet treated controls (p
(p 9 weeks) and CSC phenotype acquired. This phenotype appears to be associated with aberrant expression of at least some imprinted genes. This indicates that arsenic, a ubiquitous environmental contaminant and known human carcinogen, directly transforms stem cells into pluripotent CSCs. Thus, stem cells appear to be a primary target for arsenic-induced transplacental carcinogenic initiation. 2666 ACTIVATION OF THE ARYL HYDROCARBON RECEPTOR REPROGRAMS THE DEVELOPING IMMUNE SYSTEM. B. Winans, S. R. Marr and B. Lawrence. Department of Environmental Medicine, University of Rochester Medical Center, Rochester, NY. It is becoming increasingly recognized that early life exposure to environmental agents can lead to persistent alterations in immune function, but the mechanism by which this occurs is not yet known. To investigate the susceptibility of the developing immune system to reprogramming, our laboratory uses 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) as a model developmental immunotoxicant and influenza A virus as a prototypical human pathogen. TCDD is a ubiquitous pollutant, and represents a category of agents that activate the aryl hydrocarbon receptor (AhR), which recent studies suggest plays a role in developmental regulation. Our laboratory has demonstrated that developmental activation of AhR leads to persistent alterations in the immune response to influenza A virus in adult mice; specifically, there is a reduced clonal expansion and differentiation of CD8 + T cells. Further, this alteration results from a direct effect on hematopoietic cells. These findings show that sustained AhR activation reprograms the developing immune system, leading to persistent functional deregulation. Given that this change in SOT 2011 ANNUAL MEETING 571
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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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third tetratricopeptide repeats (TP
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7d. 28d after TMT injury there was
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subunits. Each cell type was treate
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1394 COMPARATIVE EFFECTS OF METHYLM
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1403 GENOTOXICITY AND PRE-NEOPLASTI
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vated only in high-dose-treated ani
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1421 DOSE-RESPONSE OF NAPHTHALENE-I
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cisplatin; 1.2-, 1.9- and 2.9-fold
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Day 11 and started to recover on Da
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1448 DEVELOPMENT OF A METHOD FOR QU
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1457 GLOBAL GENE PROFILING REVEALS
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cluding mouse and human macrophage,
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model of lung inflammation and host
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1484 NANOTOXICOLOGY AND NANOHEALTH
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throughput in vitro approach was us
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1502 IMMUNOLOGICAL ASPECTS OF AN AN
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(CIA) and the Streptococcal cell wa
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sitizers were 100% concordant among
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1530 MINIMAL RISK LEVELS FOR STYREN
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ical groups in the field of regulat
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vitro with this potentially insect-
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their performance on toxicological
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need for a better understanding of
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1577 AN IN VITRO MODEL SYSTEM FOR A
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gene expression post-transcriptiona
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1595 GENE EXPRESSION PROFILE OF RAT
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to confirm a hepatotoxic property o
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1613 AN INVESTIGATION OF THE CLEARA
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its nuclear translocation was reduc
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were collected from TK animals at d
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egulated targets were selected for
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U/L after tetracycline. Minocycline
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peri-pubertal FasL-/- mice show a d
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showed similar levels of apoptosis
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1676 TWO BIOMARKERS FOR EVALUATION
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motifs selected. This system was ap
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1693 VOC SERUM LEVELS IN THE GENERA
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1702 DOES THE CLOCK MAKE THE POISON
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those with high nickel content are
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isk assessment. However, unique cha
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model of APAP metabolism and glutat
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logically & morphologically similar
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posure, blood chemistry was analyze
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elated to oxidative stress by measu
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ostasis), but work is needed to tra
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tokine products during carcinogenes
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ways as chemical stressors and, the
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toxicity of nanomaterials relates s
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1815 MEASURING COMPOUND SELECTIVITY
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1825 EFFECTS OF METABOLISM BY INTES
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cyanoacetic acid increased 2-3 fold
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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
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2258 PHARMACOKINETICS, EXCRETION BA
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2267 SENSITIVE AND SPECIFIC FLUORES
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2276 METABOLISM AND DISPOSITION OF
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ment of hypertension in companion a
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for the propyl series can be used f
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2304 IN VITRO EXPOSURE AND EVALUATI
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2313 THE SYNERGISTIC EFFECT OF SODI
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genes that play a crucial role in M
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2330 THE ROLE OF TRANSFORMING GROWT
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ined following up to 96 h continuou
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effect doses obtained with the rat
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diated transcriptional response of
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docrine disruptor activities of EDC
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individuals. Week 6 results were qu
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functionality of photosystem II and
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wild mice (Mus musculus) from areas
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2406 TOXICITY AND BIOACCUMULATION O
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Page 525 and 526: 2425 EFFECTS OF FUMONISINS IN ETHAN
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Page 533 and 534: 2466 CRITICAL EVALUATION OF ANIMAL
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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
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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
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Page 559 and 560: tuna, swordfish, or mako shark (3.5
Page 561 and 562: nificantly reduce circulating thyro
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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 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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