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exhibited DNA fragmentation following BPA treatment; cells over expressing the TRPV1 receptor exhibited increased levels of apoptosis. Activating the TRPV1 receptors with capsaicin (5 microM) further enhanced apoptosis. In addition, BPAinduced inhibition of TGFbeta expression was observed in wild type, but not HEK/TRPV1 cells. Levels of downstream mediators including the pro-inflammatory cytokine TNF-alpha following BPA administration in both cell types. Taken together, our results indicate that calcium and TGF beta signaling may be inversely regulated in BPA-induced responses. We speculate that these changes mediate, in part, the renal toxicity of BPA. 826 THE EFFECTS OF FLUORIDE ON RENAL FUNCTION OF ICR-DERIVED GLOMERULONEPHRITIS (ICGN) BY SUBACUTE ADMINISTRATION OF FLUORIDE IN DRINKING WATER. H. Mayuko 1 , A. Hideo 2 , K. Takaya 1 , S. Chiemi 2 , I. Yoko 2 , T. Masashi 2 , I. Kazuyoshi 3 , K. Yukio 4 , S. Yoshiko 4 and A. Yoshiharu 2 . 1 Kitasato University Graduate School of Medical Sciences, Sagamihara, Kanagawa, Japan, 2 Preventive Medicine and Public Health, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan, 3 School of Medicine Iwate Medical University, Morioka, Iwate, Japan and 4 National Institute of Science, Setagaya, Tokyo, Japan. Many inhabitants who drink water with high concentrations of fluoride (F) are suffering from endemic fluorosis. To clarify the effects of F on individuals with impaired kidney function, F was administrated to ICR-derived glomerulonephritis (ICGN) mice at 0, 25, 50, 100, and 150 ppm in drinking water for 4 wk. F was also administered to ICR mice with normal kidney function at 0 and 150 ppm in the drinking water. Blood was sampled from the tail artery of each mouse twice a week and the blood urea nitrogen (BUN) in the serum was determined. The creatine (CRE) or F concentrations in serum was also determined under the same protocol. The mean values on the body weight, relative organ weights, BUN, and CRE on the last day of the observation period was calculated. When a mouse was died during the observation period, the date from the day closest to the death was assigned. All ICGN mice in the 150-ppm group were died during the observation period. In contrast, no ICR mice were died even in the 150-ppm group. Mean body weight value of the ICGN mouse exposed to 150 ppm was significantly lower than those in the other groups. Mean value of BUN in the 150-ppm administered ICGN mice was significantly higher than those in the other groups. The mean CRE in the 150-ppm ICGN mice was also significantly higher than those in other groups. The mean relative liver weight of the 150-ppm group was significantly lower compared with the control group. There were no significant differences in there indexes between the 0 and 150 ppm for ICR mice. The serum F in ICGN mice exposed to 100 ppm that remained alive was significantly higher than those in the other groups. Kidney insufficiency enhances F toxicity and, in turn, F deteriorates renal function even more. 827 INDUCTION OF APOPTOSIS IN PRIMARY MESANGIAL CELL BY DEOXYNIVALENOL. J. Seo 1, 2 , J. Kim 1 and J. J. Pestka 1 . 1 Food Science and Human Nutrition, Michigan State University, East Lansing, MI and 2 Korea Food and Drug Administration, Seoul, Republic of Korea. Deoxynivalenol (DON) is trichothecene mycotoxin produced by Fusarium fungi in cereals and processed grain products. Dietary exposure to DON in the mouse induces IgA overproduction with resultant immune complex formation and kidney mesangial deposition in a manner that mimics the common human glomerulonephritis IgA nephropathy. Here, we evaluated whether DON could induce proinflammatory cytokines directly or have cytotoxic effects in primary mesangial cell cultures isolated from mouse kidney. We found that mesangial cells treated with LPS as a positive control induced IL-6 and TNF, but cytokine induction was not observed in DON-treated cultures. However, DON was found to reduce mesangial cell viability in concentration- and time-dependent manner. Mesangial cells treated with high DON concentrations (0.5 – 50 μg/ml) exhibited the characteristics of apopotosis including increased of cytoplasmic histone-complexed DNA fragments (mono- and oligonucleosomes) as revealed cell death detection ELISA as well as increased binding of annexin V as determined by flow cytometry. Moreover, DON induced phosphorylation of c-Jun N- terminal kinase (JNK) and p38 in mesangial cells. DON-induced apoptosis in mesangial cells was suppressed by the JNK inhibitor SP600125, whereas the p38 inhibitor SB203580 did not enhance survival. Taken together, our data DON did not upregulate proinflammatory cytokines in murine mesangial cells but induced to JNK-dependent apoptosis. 828 HIERARCHY AMONG EXECUTIONERS: CYTOTOXIC ENDONUCLEASES REGULATE ONE ANOTHER IN VITRO AND IN MOUSE MODELS OF TOXIC KIDNEY INJURY. A. G. Basnakian 1, 2 , E. O. Apostolov 1 , X. Wang 1 and S. V. Shah 1, 2 . 1 University of Arkansas for Medical Sciences, Little Rock, AR and 2 Central Arkansas Veterans Healthcare System, Little Rock, AR. DNA fragmentation that is considered an endpoint of cell death pathways occurs both before and after the point-of-no-return. It is produced by nine cytotoxic (apoptotic) DNA endonucleases, which, despite some differences in molecular and enzymatic characteristics, catalyze the same reaction of DNA destruction. The relationships between the endonucleases are unknown. Our new findings indicate that at least one apoptotic endonuclease, DNase I, regulates the expression of another apoptotic endonuclease, EndoG, in various in vitro and in vivo models of toxic kidney tubular epithelial cell injury. We tested three models of kidney injury using DNase I knockout and wild-type mice: (1) ischemia-reperfusion by clamping of renal pedicles for 50 min followed by reflow for up to 96 hours; (2) cisplatin (20 mg/kg) nephrotoxicity, and (3) rhabdomyolysis kidney injury induced by intramuscular glycerol injection (50% glycerol, 8 ml/kg). In all these models, in wildtype mice, EndoG was induced and translocated to nuclei, inducing DNA fragmentation and cell death by both apoptosis and necrosis. At the same time, the EndoG induction was significantly restricted in DNase I knockout mice, which were protected against the injuries. Two other apoptotic endonucleases, DNase II and CAD, remained unaffected by DNase I inactivation. Overexpression of DNase I-CFP fusion protein in cultured mouse tubular epithelial TKPTS cells was cytotoxic and caused the induction of EndoG after treatment with cisplatin or hemin (in vitro model of rhabdomyolysis), while overexpression of CFP alone did not result in any induction of EndoG. Overexpression of EndoG-CFP in TKPTS cells was also cytotoxic but did not cause induction of DNase I. These observations indicate that there is a hierarchy among cytotoxic endonucleases: DNase I serves as an upstream regulator of EndoG, and suggest a possibility that endonucleases, similar to other apoptotic enzymes, may act as a network. 829 THE IN VITRO SCREENING OF TERATOGENICITY USING GENE EXPRESSION PROFILING IN CULTURED EMBRYOS IN RATS. R. Fukushima, K. Nishimura, C. Kondo, A. Hishikawa, T. Uehara, M. Kaneto and M. Torii. Drug Safety Evaluation, Shionogi & Co., Ltd., Toyonaka, Osaka, Japan. Sponsor: K. Nakamura. The prediction about the teratogenicity is a great help for the risk aversion in the drug development. Whole embryo culture (WEC) is a validated alternative developmental toxicity test which allows the in vitro assessment of effects of chemicals on organogenesis. Toxicogenomics approaches in WEC system may provide the more sensitive method of prediction about teratogenicity. In this study, we used following compounds to search the marker genes for teratogenicity using toxicogenomics analysis in WEC system, which were positive control (three compounds, four groups) [100 μg/mL A77 1726 (A77: active metabolite of leflunomide), 0.1 or 1.0 μg/mL all-trans retinoic acid (RA-low or -high, respectively), 0.5 μg/mL 5-fluorouracil (5FU)], negative control (three compounds, four groups) [0.1 μg/mL valproic acid (VPA), 0.1 μg/mL saccharine sodium salt (SCN), 0.1 or 100 μg/mL penicillin G (PCG-low or -high, respectively)] and 0.1% DMSO (vehicle, as the control group). At first, rat embryos on day 10.5 were exposed for 48 hours to these compounds for evaluating their external morphology. The morphological change was observed in A77, RA-high and 5FU groups. For gene expression analysis, rat embryos on day 10.5 were exposed for 24 hours and total RNA was isolated from whole cultured embryos. The gene expression analysis was conducted using Affymetrix GeneChip Rat Genome 230 2.0 Array. Discriminant analysis of gene expression profile showed expression change in 52 genes in response to the morphological change in cultured embryos. Furthermore, twelve genes were selected from 52 genes based on their signal levels and gene annotations, as the candidate of marker genes for teratogenicity. This study suggests the feasibility of prediction about teratogenicity using toxicogenomics approach in WEC system. 830 DEVELOPMENTAL TOXICITY OF PERFLUOROALKYL ACID MIXTURES IN CD-1 MICE. K. R. Tatum-Gibbs 1 , C. Lau 2 , K. P. Das 2 and B. Abbott 2 . 1 Curriculum in Toxicology, University of North Carolina, Chapel Hill, NC and 2 Developmental Biology Branch, U.S. EPA, Research Triangle Park, NC. Perfluorooctanoic acid (PFOA), perfluorooctane sulfonate (PFOS) and perfluorononanoic acid (PFNA) belong to a family of fluoro-organic compounds known as perfluoroalkyl acids (PFAAs). PFAAs have been widely used in industrial and 176 SOT 2010 ANNUAL MEETING
commercial applications, and have been found to be both ubiquitous and highly persistent in the environment. Previous studies have indicated robust developmental toxicity associated with exposure to PFOS, PFOA, and PFNA individually in laboratory rodent models. However, multiple PFAAs are present in the environment and detectable to varying extent in humans. Hence, effects of these chemicals in mixtures must be taken into consideration for their health risk assessment. The current study examines the developmental effects of various mixtures of PFAAs and makes comparisons to exposures to individual compounds. Timed-pregnant CD-1 mice were given PFAAs either alone (8 mg PFOA/kg, 12 mg PFOS/kg, 4 mg PFNA/kg) or in mixtures (4 mg PFOA/kg + 2 mg PFNA/kg; 4 mg PFOA/kg + 6 mg PFOS/kg; or 6 mg PFOS/kg + 2 mg PFNA/kg) by oral gavage daily from gestation day 1-17; controls received 0.5 % Tween vehicle. PFOS, PFOA and PFNA singly produced developmental effects as previously reported. In mixtures, PFAAs appeared to have a dose additive effect on maternal weight gain, pup body weight, as well as maternal and neonatal liver weights. In contrast, PFAAs in mixtures induced a less-than- dose additive effect on neonatal mortality. In particular, the PFOS + PFOA group responded less than PFOS or PFOA alone, where as PFOS + PFNA had no response at all. These data suggest that prenatal exposure to a mixture scheme of PFAAs with higher carbon-chain length (C-8 and C-9) containing either a carboxylic or sulfonic functional group produce additive effects on some endpoints and less-than-additive effects on neonatal mortality in CD-1 mice. This abstract does not necessarily reflect U.S. EPA policy. 831 MAMMARY GLAND DEVELOPMENT AND RESPONSE TO PRENATAL ATRAZINE EXPOSURE IN THE SPRAGUE-DAWLEY AND LONG-EVANS RAT. C. J. Wolf, J. P. Stanko and S. E. Fenton. Toxicity Assessment Division, U.S. EPA, ORD, NHEERL, Research Triangle Park, NC. Mammary gland (MG) tumor development in Sprague-Dawley (SD) rats is increased by long-term dietary exposure to the chlorotriazine herbicide atrazine (ATR). ATR is proposed to cause these changes in the adult SD rat by altering hormonally-regulated estrous cyclicity. In Long-Evans (LE) rats, both puberty and MG development are delayed by brief prenatal ATR exposure. Prenatal exposure has not been tested in SD rats. We have observed that dimethylbenz[a]anthracene (DMBA) treatment results in a greater incidence of MG tumors in LE compared to SD rats and we hypothesize that this increased susceptibility is due to strain differences in the rate of MG differentiation, and that these differences are compounded by exposure to ATR. The purpose of this study was to assess the differences in MG development of female offspring of vehicle and ATR-exposed LE and SD rats. Timedpregnant LE and SD rats (n=9/treatment group) were orally gavaged with 0, 12.5, 25, or 50 mg ATR/kg body weight 2x/day on gestational days 15-19. Mammary glands were collected from female offspring on PNDs 4, 25, 33, and 45 and MG whole mounts were scored according to previously established developmental criteria. MG development was delayed by ATR on PND4 and PND25 in the SD rat at 50 mg/kg, and on PND33 in both strains at 25 and 50 mg/kg (p< 0.05). At PND45, MG differentiation was delayed in both strains at all doses (12.5 mg/kg, p< 0.01 in LE, p< 0.05 in SD; 25 mg/kg, p< 0.01 in LE, p< 0.001 in SD; 50 mg/kg, p< 0.001 in LE and SD). Additionally, MG of SD offspring were much more developed than that of LE offspring at respective ages, although age at VO was not different between strains. In summary, ATR delayed MG development in both LE and SD with a LOAEL of 25 mg/kg/day (12.5 mg/kg/dose), despite the difference in MG maturity between the strains. These data suggest less developed MG in the LE may render this strain more susceptible to DMBA-induced tumor promotion. This abstract does not necessarily reflect EPA policy. 832 DEVELOPMENTAL TOXICITY EVALUATION IN THE CYNOMOLGUS MONKEY: VARIABILITY OF PREGNANCY LOSS AND STATISTICAL GROUP SIZE CONSIDERATIONS. G. F. Weinbauer 1 , P. Jarvis 2 , S. Srivastav 1 , E. Vogelwedde 1 , J. Stewart 2 and T. Mitchard 2 . 1 Covance Laboratories GmbH, Muenster, Germany and 2 AstraZeneca Pharmaceuticals, Macclesfield, United Kingdom. The cynomolgus monkey (Macaca fascicularis) provides the established primate model for preclinical assessment of developmental toxicity. Group sizes are generally smaller than those used in rodent and rabbit studies. We explored in the monkey model the pregnancy outcome in control animals from 78 embryofetal development (EFD) studies terminated either on gestational day 100 or 150 and 14 pre-/postnatal development (PPND) studies until day 7 postpartum, comprising 1069 pregnancies during 1981-2000. Neither study type nor route/duration of dosing affected pregnancy outcome. Hazard rate was higher pre-1989 (0.3, 104/347) compared to post-1989 (0.13, 94/722). Hazard was greatest in early gestation (< gestational day 50) and at parturition. Monte-Carlo simulation experiment results closely correlated to the actual losses indicating that losses within and between studies were independent. Reference data for the variability and likelihood of pregnancy success could be derived. Systematic data were generated for predicting pregnancy outcome and hazard detection relative to group size at study initiation. For example, EFD studies with an initial vehicle group size of 16 and 20 will have 13 and 16 ongoing pregnancies, respectively, at gestational day 100 with 80% probability. For PPND studies with initial vehicle group sizes of 16, 20 and 28, life infant number at day 7 postpartum will be 9, 11 and 16, respectively, with 80% likelihood. With regard to statistical power, a PPND study initiated with a group size of 20 could detect a trebling of the hazard to live infant outcome. Moreover, the simulation data provide an objective tool facilitating decisions in ongoing studies whether supplementation with additional pregnant animals is indicated or not. 833 NEUROPATHY TARGET ESTERASE (NTE) MIGHT BE PLAYING A RELEVANT ROLE DURING CELL DIFFERENTIATION. M. A. Sogorb, D. Pamies, C. Estevan, A. C. Romero and E. Vilanova. Unidad de Toxicología y Seguridad Química, Instituto de Bioingeniería, Universdad Miguel Hernández de Elche, Elche, Alicante, Spain. Neuropathy Target Esterase (NTE) is a protein known because is the target of a delayed polyneuropathy caused by exposure to certain organophosphorus compounds. However, certain in vivo studies suggest that NTE might be relevant during the embryonic development because mice deficient in both NTE alleles are not viable. We have discriminated, using organophosphorus inhibitors, NTE activity among the pool of carboxylesterases found in embryonic stem cells (ESC) from mouse belonging to D3 line. These cells express an NTE activity of 23 nmol phenol/min/mg of protein (0.99 mg phenol/min/106 cells). The expression of Pnpla 6 (the gen codifying for NTE) increased in D3 ESC immediately after initiated the differentiation, reaching a maximum of expression around 5 or 30 hours after triggered the differentiation when cells were cultured in monolayer or forming embryonic bodies, respectively. This maximum of Pnpla6 expression also correlated with a maximum of enzymatic activity in monolayer cultures. The NTE activity and the Pnpla6 expression returned to basal levels after 48 hours (in monolayer cultures) and 10 days (in EBS) of differentiation, respectively. The changes in the Pnpla6 expression in D3 embryonic bodies did not correlate with changes noted in the expression of intermediate neurofilament (gene marker of neuroectoderm development), alpha-fetoprotein and Amnionless (both gene markers of endoderm development) and myosin heavy chain and Flk1 (both gene markers for mesoderm development). These results suggest that NTE may play an important role in the initial stages of cell differentiation and that mouse ESC might be a model for studying this role. Acknowledgment: This study was supported by Ministry of the Environment of the Government of Spain (Grant A051/2007/3-14.4). 834 SPECIES DIFFERENCES IN CATALASE AND ALCOHOL DEHYDROGENASE ACTIVITY IN MICE AND RABBITS. J. Sweeting 1 and P. G. Wells 1, 2 . 1 Pharmaceutical Sciences, The University of Toronto, Toronto, ON, Canada and 2 Pharmacology and Toxicology, The University of Toronto, Toronto, ON, Canada. Predictions of human risk for methanol (MeOH) developmental toxicity are based largely on rodent studies. Unlike humans, rodents use catalase rather than alcohol dehydrogenase (ADH) to metabolize MeOH, and use catalase and a non-saturable folate pathway for metabolizing the toxic formic acid (FA) metabolite, thereby preventing its accumulation and the subsequent acute toxicity observed in humans. However, catalase in both rodents and humans also detoxifies reactive oxygen species (ROS), which are implicated in the developmental toxicity of MeOH in rodents. Due to this potentially confounding dual role of catalase for MeOH in rodents but not humans, rodents may not constitute a reliable animal model for accurately assessing the human potential for MeOH teratogenesis. We previously showed that New Zealand white (NZW) rabbits more closely than mice reflect primate MeOH and FA disposition, exemplified by slower MeOH clearance and greater FA accumulation. Herein we report preliminary data for the enzymes responsible for MeOH and FA metabolism in rabbits. Catalase activity in hepatic tissue from male NZW rabbits and CD-1 mice was assessed using the Ferrous Oxidation in Xylenol Orange (FOX) assay. The mean catalase activity in mice was about 3-fold higher than that in rabbits (p < 0.0001), indicating a substantial species difference. Compared to mice, the hepatic catalase activity of rabbits more closely approximated that reported in primates, providing biochemical evidence that rabbits may be a more appropriate animal model for assessing the potential teratological risk of MeOH in humans. Studies examining the activity of ADH and other relevant enzymes in adult and fetal mice and rabbits are ongoing, the results of which will permit a more comprehensive assessment of these models. (Support: Methanol Fdn., CIHR) SOT 2010 ANNUAL MEETING 177
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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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Page 137 and 138: 620 CHARACTERIZATION OF POTENTIAL I
Page 139 and 140: ways. Moreover, both MAP kinase and
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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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22 in Phase I. Antimicrobial pestic
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kinetic and dynamic differences, an
Page 413 and 414:
iphenyl, saccharin and melamine was
Page 415 and 416:
1930 DEVELOPMENT OF A RELATIVE SOUR
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1939 MODE OF ACTION FOR THE CANCER
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human was about 1.5-fold lower (60
Page 421 and 422:
Disruption of BDEC integrity in alp
Page 423 and 424:
1968 A HUMAN HEPG2 LUCIFERASE ASSAY
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in the offspring during tumor devel
Page 427 and 428:
een developed to investigate perfus
Page 429 and 430:
to 131.73 μg/mL for KLH-specific I
Page 431 and 432:
cell lines (ATCC) were cultured in
Page 433 and 434:
flammation and xenobiotic metabolis
Page 435 and 436:
vide many contributions: with its g
Page 437 and 438:
to-metal joint replacement. For exa
Page 439 and 440:
to be addressed or negotiated. Deci
Page 441 and 442:
especially with anti-TNF therapies.
Page 443 and 444:
genic line Tg(are:eGFP) was created
Page 445 and 446:
2074 COMPUTATIONAL ASSESSMENT OF TH
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2084 INHIBITION OF 11β-HSD1 DECREA
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(T) and express several enzymes inv
Page 451 and 452:
2101 GENISTEIN MODULATION OF BLOOD
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males per group were dosed orally o
Page 455 and 456:
ate the feasibility of assessing re
Page 457 and 458:
changed. Hepatic protein carbonyl l
Page 459 and 460:
sought to examine alterations in he
Page 461 and 462:
2147 A SINGLE AMINO ACID CONTROLS T
Page 463 and 464:
Gstm7) was independent of both CAR
Page 465 and 466:
ility of tungsten trioxide (WO3), t
Page 467 and 468:
ured by real-time PCR array and rel
Page 469 and 470:
glucose, and creatinine levels, and
Page 471 and 472:
Several studies have reported suppr
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exposure between TCDD-exposed labor
Page 475 and 476:
Furthermore, with increasing number
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Society of Toxicology 2010 Author I
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Society of Toxicology 2010 Abstract
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49 th Annual Meeting and ToxExpo A
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The Official Journal of the Society
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