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samples, OPN levels were significantly influenced by diet with DHA exhibiting 62% and 80% that of SAF and CRN, respectively. Thus, DHA suppression of OPN is a potential critical early event in the downregulation of aberrant humoral autoimmunity in murine lupus nephritis. 1785 MODULATION OF BODY FAT MASS AND LEAN WEIGHT IN DEOXYNIVALENOL-INDUCED BODY WEIGHT REDUCTION IN THE OBESE MOUSE. K. Hattori 1, 2 , B. Flannery 1 , C. Amuzie 1 and J. J. Pestka 1 . 1 Food Science and Human Nutrition, Michigan State University, East Lansing, MI and 2 Nutritional Science, Tokyo University of Agriculture, Setagaya-ku, Tokyo, Japan. Our laboratory has observed that deoxynivalenol (DON) can both prevent and ameliorate weight gain in the diet-induced obese (DIO) mouse model. Here we related DON’s therapeutic effects in DIO mice to food intake, body fat mass and lean weight. B6C3F1 mice (female, 11-week-old) were divided into 3 groups and fed each diet (10 kcal%, 45 kcal% and 60 kcal% from fat, Research Diets, Inc.) for 94 days. After inducing obesity, the mice were divided into 5 groups (n=8) and fed control diet (10 kcal%) or high-fat diets (45 kcal% or 60 kcal%) with or without DON (10 ppm) from Day 94 to 147. Body weights of the 45 kcal% + DON and 60 kcal% + DON groups rapidly decreased after DON intake and reached that of the 10 kcal% control by Day 105. As compared to the 45 and 60 kcal% groups, food intake by DON-fed groups significantly decreased at Day 98 and 101, which corresponded to the period in which DON-fed groups exhibited robust body weight decreases. As determined with MRI (EchoMRI-100), body fat mass and body fat percentages of the 45 and 60 kcal% with DON-fed mice gradually reduced to those of control. Lean weights of the DON-fed groups were significantly lower than those of the 45 and 60 kcal% groups after Day 122. We conclude that DON-induced reduction in body weight in the DIO mice results from decreased food intake, and this corresponds to decreases in both body fat mass and lean weight. 1786 NORMAL RANGE AND FORMS OF DIETARY SELENIUM PREVENTS METHYLMERCURY TOXICITY IN LONG EVANS RATS. N. V. Ralston. Energy & Environmental Research Center, University of North Dakota, Grand Forks, ND. Sponsor: M. Aschner. Methylmercury (MeHg) is a highly specific irreversible inhibitor of selenium (Se)- dependent enzymes (Se-enzymes). Over 30 genetically unique Se-enzymes are expressed in mammals, many with roles in preventing and reversing oxidative damage in the brain. The Se-enzymes employ selenocysteine (Sec) at their active sites and MeHg intoxication inhibits Se-enzyme activities in brain and neuroendocrine tissues. Supplemental Se has been known to counteract Hg toxicity since 1967, but mechanisms have only recently become clear. Since dietary Se must be reduced to inorganic forms before it can be incorporated into Sec, it was not known whether dietary Se from ocean fish would be as effective as inorganic Se provided in the diet. In the current study, 120 weanling male Long Evans rats were fed diets containing either low or high MeHg (0.5 or 50 nmol MeHg/g) with Se as inorganic Se (sodium selenite) at low, normal, or rich (0.1, 1.0, or 10 nmol Se/g) in diets prepared with torula yeast protein (as~30% of nutritionally complete AIN-93G diet). or Se from delipidated protein isolated from bigeye tuna, swordfish, or mako shark added as 10% of the total diet in place of an equivalent amount of torula yeast protein; (2 Hg levels x 6 Se diets = 12 dietary treatments). Contributions of additional MeHg in the fish supplemented diets were between 1.6 and 3.6 nmol MeHg/g, and Se ranged between 2.1 and 3.5 nmol Se/g. Rats were randomly assigned to each of the 12 diets (10 rats per group). After 5 weeks on low Se diets (without added MeHg) to deplete their Se reserves, all rats were switched to their assigned dietary treatments. Rats maintained on high MeHg, low Se diets showed growth inhibition after 4 weeks, and hind limb crossing after 9 weeks on the dietary treatment, but all other dietary treatment groups grew normally and were protected against neurofunctional defects. The MeHg from fish did not contribute to worsening MeHg toxicity, but the Se from fish was absorbed and utilized as readily as inorganic Se, and was equally effective in preventing MeHg toxicity. 1787 PRECLINCAL SAFETY EVALUATION OF U.S. FDA- APPROVED ONCOLOGY DRUGS: RECENT TRENDS IN CONCURRENCE WITH DRAFT ICH S9 GUIDELINE. M. Z. Dieter, S. L. Ralston, L. A. Gallenberg and J. E. Burkhardt. Abbott Laboratories, Abbott Park, IL. The approval packages of oncology compounds recently approved by the United States Food and Drug Administration (FDA) were evaluated in order to gauge trends in preclinical toxicology studies performed to support development of anticancer compounds, as outlined in the draft International Conference on Harmonisation (ICH) S9 guideline on Nonclinical Evaluation for Anticancer Pharmaceuticals. Analysis was limited to original applications approved from July 1999 through July 2009. Data was collected from Summary Basis of Approval (SBA) documents via the PharmaPendium database current as of July 2009. SBA’s for 28 oncology-indicated small molecule or biotherapeutic compounds were evaluated for the scope of toxicology studies conducted. ICH S7A “core battery” safety pharmacology studies were conducted for 12 compounds; however, 6 compounds were approved with no safety pharmacology studies performed. Acute single dose and repeat dose range-finding studies were conducted in at least one species for the majority of compounds. Pivotal repeat-dose studies were variable in length from 1 month to 1 year, but generally conducted for at least 6 months in two species. ICH S2 “standard battery” genotoxicity assays were performed for 17 compounds, including 5 with expected mechanism-based genotoxity. Genotoxicity assays were not conducted for two monoclonal antibodies. Carcinogenicity studies were conducted for 5 compounds. Embryofetal toxicity (Seg II) studies were conducted in both rodent and non-rodent species for 18 of the compounds; for each of the 8 compounds evaluated in only one species, the compound was considered a selective developmental toxicant. Fertility (Seg I) studies were conducted for the majority of compounds, whereas neonatal and postnatal development (Seg III) studies were conducted for only 4 compounds. The results signify that many recommendations contained in the draft ICH S9 guideline are already being adopted, and that this guideline, once finalized, should expedite development of oncology agents for advanced cancer patients. 1788 IMPACT OF DATA AVAILABILITY ON THE CALCULATION OF REACH DNELS FOR WORKER AND CONSUMER POPULATIONS. R. Roy, N. Pechacek, L. Milchak and R. Skoglund. 3M Company, St. Paul, MN. Under the European Union’s Registration, Evaluation, Authorization, and restriction of CHemicals (REACH) regulation, the Derived No-Effect Level (DNEL) represents a level of exposure above which humans should not be exposed. Chemical-specific DNELs for worker (W-DNEL) and consumer (C-DNEL) populations are often derived as part of the chemical safety assessment. The European Chemicals Agency (ECHA) has developed guidance for the calculation of DNELs for both workers and consumers. Steps in DNEL calculation include establishing study “dose descriptor(s)” such as NOAEL, LOAEL, etc. and their modification for bioavailability, route-to-route extrapolation and exposure conditions; and, lastly, application of Assessment Factors (AFs) for intra-and inter-species differences, duration of exposure, etc. While it is preferable to use chemical-specific modifiers/factors in DNEL calculations, many are not [readily] available and, thus, ECHA provides default factors for use in these calculations. The impact of both chemical- and use-specific data (vs. defaults) is illustrated by calculating W-DNEL and C-DNEL for: (1) long-term inhalation exposure based on rat inhalation data and (2) long-term dermal exposure based on oral rat data. Significant differences in W-DNEL and C-DNEL values can be observed depending on the use of chemical-specific data (e.g. dermal and oral absorption data for route-to-route extrapolation) and consumer use data (e.g. number of hours/day of exposure). For example, if both dermal and oral % absorption of a chemical is known, the use of these data can provide a significantly different DNEL vs. the DNEL calculated using ECHA defaults. As an example of case (2), above, the DNEL for a chemical with 100% and 10% absorption via oral and dermal routes, respectively, will be 10-fold greater than that calculated using the ECHA defaults. This exercise shows the importance of using reliable, available, chemical-specific data for calculation of DNELs for use in REACH compliance. 1789 ICCVAM RECOMMENDATIONS FOR USE OF THE LLNA FOR EVALUATING THE ALLERGIC CONTACT DERMATITIS POTENTIAL OF PESTICIDE FORMULATIONS. J. Matheson 1 , A. Jacobs 2 , M. Wind 1 , J. Chen 3 , M. Hashim 3 , M. Lewis 3 , E. Margosches 3 , D. McCall 3 , T. McMahon 3 , J. Redden 3 , R. Ward 3 and W. Stokes 4 . 1 CPSC, Bethesda, MD, 2 U.S. FDA, Silver Spring, MD, 3 U.S. EPA, Washington, DC and 4 NICEATM, NIEHS, Research Triangle Park, NC. ICCVAM has updated its 1999 validation report on the LLNA based on a recent evaluation of the usefulness and limitations of the LLNA for assessing the skin sensitizing potential of pesticide formulations. This review was initiated because the original report did not include an analysis of the LLNA for these types of substances, and there were growing regulatory concerns that the LLNA might not identify sensitizing pesticide formulations. LLNA data from 104 formulations were 380 SOT 2010 ANNUAL MEETING
included in the evaluation, most of which are water soluble and therefore were tested in an aqueous vehicle (1% Pluronic L92). Of the pesticide formulations for which LLNA and guinea pig data were available (n=23), the LLNA classified 52% (12/23) as sensitizers, while GP tests classified only 13% (3/23) as sensitizers. All three of the pesticide formulations identified as sensitizers in the GP test were also identified as sensitizers in the LLNA; there were no instances of underprediction by the LLNA. Thus, there is a greater likelihood of obtaining a positive result in the LLNA than in a GP test. These studies also provide data for aqueous solutions that emphasize the need for careful selection of an appropriate vehicle that maintains test substance contact with the skin (e.g., 1% Pluronic L92) to achieve adequate exposure when testing such substances. Based on these data, ICCVAM agreed with an international peer review panel that the LLNA could be used for testing pesticide formulations, and any other products, unless there are unique physicochemical properties that may interfere with the ability of the LLNA to detect sensitizing substances. ICCVAM recommendations are being forwarded to Federal agencies for their consideration for future regulatory acceptance. These recommendations should expand the use of the LLNA for skin sensitization testing, thereby reducing and refining animal use for this purpose. 1790 CURRENT DRUG SCHEDULING REVIEWS REPORTED BY THE DRUG ENFORCEMENT ADMINISTRATION. J. Vodela, S. Ghozland, C. Prioleau, S. Tella, S. Carr and C. Sannerud. Drug Enforcement Administration, U.S. Department of Justice, Arlington, VA. As mandated by the Controlled Substances Act (CSA), DEA collects and reviews scientific, medical and other data for substances with abuse potential to determine their appropriate control status for placement into one of five schedules. Administrative process for scheduling is currently ongoing for carisoprodol, dextromethorphan, Salvinorin A and hallucinogens such as 5-methoxy-N,N-dimethyltryptamine (5-MeO-DMT), 5-methoxy-alphamethyltryptamine (5-MeO-AMT), 5-methoxy-N,N-diethyltryptamine (5-MeO-DET), 5-methoxy-N-methyl-N-isopropyltryptamine (5-MeO-MIPT), N,N-diisopropyltryptamine (DIPT), and 4- hydroxy-N,N-diisopropyltryptamine (4-OH-DIPT). Administrative process for several petitions requesting control of tramadol and propofol, decontrol of sibutramine and 6-beta-naltrexol and amendment to CFR so as to allow generic products of dronabinol in sesame oil into schedule III. DEA is currently reviewing the data for cyclobenzaprine, nalbuphine and hallucinogens such as 4-iodo-2,5- dimethoxy-phenethylamine (2C-I), 2,5-dimethoxy-4-ethylthiophenethylamine (2C-T-2), and 2,5-dimethoxy-4-iodoamphetamine for possible control under the CSA. Chemical synthesis/pharmacological studies for 2,5-Dimethoxy-4-chloroamphetamine, 2,5-Dimethoxy-4-chlorophenethylamine, 2,5-Dimethoxy-4- methylphenethylamine, and 2,5-Dimethoxy-4-ethylphenethylamine are currently ongoing to determine if these substances meet the requirements for possible control under the CSA. In order to comply with the 1971 Convention on Psychotropic Substances, administrative process for scheduling is currently ongoing for zipeprol, amineptine, mesocarb, 4-methylthioamphetamine and brotizolam 1791 USE OF LINEAR EXTRAPOLATION OF CANCER POTENCY FOR REGULATING CHEMICALS: COLLISION OF SCIENCE AND POLICY. M. E. Stelljes 1 and A. Bailey 2 . 1 SLR International Corporation, Martinez, CA and 2 SLR International Corporation, Bothell, WA. Regulatory agencies extrapolate animal cancer dose-response data from high doses used in toxicity studies to environmentally relevant concentrations to which humans may be exposed. This is needed in order to develop concentrations considered acceptable in the environment, typically based on a target cancer risk of 1 in 1,000,000. The linearized multi-stage model is almost exclusively used for this extrapolation. For many chemicals, this is appropriate as there is either (1) evidence for low-dose linearity based on mechanistic data or epidemiological data or (2) no data suggesting a linear extrapolation is inappropriate. While this is a conservative and appropriate approach in these situations, it is not appropriate for situations where both mechanistic data and epidemiological evidence suggests less-than-linear extrapolations are warranted. Chloroform is a classic example where a threshold model for cancer was mechanistically supported; this model has since been incorporated into the U.S. EPA cancer potency for this chemical. A similar approach is now being implemented for dioxins. However, other chemicals with similar weightof-evidence for non-linearity are so far being regulated using the linearized dose model. Data will be presented for naphthalene neuroblastomas and arsenic skin cancers that strongly imply either threshold-based or sublinear-based models should be used to regulate these chemicals for environmental exposure by humans. 1792 TOXICOLOGICAL PRINCIPLES FOR AN IMPROVED HAZARD NOTATION SYSTEM TO PROTECT WORKERS FROM DERMAL EXPOSURES. A. Maier 1 , B. Gadagbui 1 and G. Dotson 2 . 1 Toxicology Excellence for Risk Assessment (TERA), Cincinnati, OH and 2 CDC/NIOSH, Cincinnati, OH. To alert workers and employers of potential health hazards arising from skin contact with chemicals the traditional practice has been to assign qualitative hazard designations called skin notations to indicate that a substance has the potential to be percutaneously absorbed, and thus affect the interpretation of inhalation-based occupational exposure limits. The National Institute for Occupational Safety and Health (NIOSH) has developed a new strategy for assigning skin notations capable of providing a warning beyond percutaneous absorption and to address the limitations associated with the historical approach used for assigning skin notations. The new strategy provides guidance for the systematic application of a weight-of-evidence approach. This includes critically evaluating available data (i.e., human, animal, in vivo, in vitro, and mathematical predictions) to assign multiple hazard-specific skin notations (SK) capable of clearly distinguishing between systemic effects, direct effects, and immune-mediated responses. This presentation will provide an overview of the new NIOSH strategy with emphasis on issues encountered during the evaluation of 140+ chemicals including 1) assigning a systemic effects notation where data or model predictions indicate absorption, but no or only limited dermal toxicity data are available; 2) differentiating among irritant severity levels when relying on qualitative studies that used different material dilutions and test systems; and 3) developing notations for sensitization when limited human studies and standard animal assays provide conflicting results. The lessons learned in evaluating such problematic data sets provide the basis for refining weight-of-evidence evaluation approaches for hazard notations. 1793 APPLYING THE MODERN PRINCIPLES OF RISK ASSESSMENT TO PROTECT WORKERS: UPDATE OF THE DERIVATION METHODS FOR IMMEDIATELY DANGEROUS TO LIFE AND HEALTH (IDLH) VALUES. G. Dotson 1 , A. Parker 2 , A. Maier 2 and L. Haber 2 . 1 CDC/NIOSH, Cincinnati, OH and 2 Toxicology Excellence for Risk Assessment (TERA), Cincinnati, OH. The ability of airborne contaminants to quickly overwhelm victims has been well demonstrated within occupational settings resulting in acute and chronic irreversible health effects, and even death. Since the 1970s, the National Institute for Occupational Safety and Health (NIOSH) has been tasked with establishing acute exposure guidelines called Immediately Dangerous to Life and Health (IDLH) values to aid in protecting workers from such high risk environments. IDLH values are defined as, “atmospheric concentrations of toxic, corrosive, or asphyxiant substances that, via inhalation exposure, pose an immediate threat to life or would cause immediate or delayed irreversible adverse health effects or would interfere with an individual’s ability to escape from a dangerous atmosphere in the event of a respirator failure.” NIOSH is in the process of revising the derivation process for IDLH values to ensure that they are sufficiently health protective. The objective of this presentation is to discuss the impact of a refined weight of evidence approach based on the modern principles of risk assessment for the derivation of new and revised IDLH values. The refined approach was applied to 20 case study chemicals; lessons learned from these case studies were used to hone the revised derivation method for IDLH values. 1794 ISSUES RELATED TO THE APPLICATION OF THE GHS STOT CRITERIA TO INHALED POORLY SOLUBLE PARTICULATES (PSP) OF LOW TOXICITY. T. Petry 1 , V. Verougstraete 2 , B. Davies 3 , S. A. Hubbard 4 , H. Waeterschoot 5 , N. R. Ranggasami 1 and A. R. Oller 6 . 1 ToxMinds BVBA, Brussels, Belgium, 2 EuroMetaux, Brussels, Belgium, 3 International Council on Mining and Metals (ICMM), London, United Kingdom, 4 Rio Tinto, London, United Kingdom, 5 Nickel Institute, Brussels, Belgium and 6 NIPERA, Durham, NC. The UN Globally Harmonized System of Classification and Labelling of Chemicals (GHS) include hazard classifications addressing specific target organ toxicity (STOT) after acute or repeated exposure to chemical substances. Specifically, GHS provides the criteria as well as guideline values for the classification of particulates that are considered to produce specific target organ toxicity following repeated inhalatory exposure as Category 1 (‘produces significant toxicity in humans’) or 2 (‘harmful to human health’). To date, much of the data on the respiratory effects of inhaled particles comes from rat inhalation studies. The rat has, however, been shown to be more sensitive than humans or other rodent species to SOT 2010 ANNUAL MEETING 381
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The Toxicologist Supplement to Toxi
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The Toxicologist Supplement to Toxi
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1 BIOLOGICAL PATHWAY ANALYSIS: AN I
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11 ICH INITIATIVES FOR CONDUCTING P
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models. Experimental approaches and
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30 SILICA AND ASBESTOS IMMUNOTOXICI
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40 NONCANCER TOXICITY POTENTIAL AT
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ased products for patient administr
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nase regulates Hsp27-induced reorga
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exposure resulted in splenomegaly.
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We investigated the effect of imati
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well plate prevented free cell move
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98 DERIVING SIGNATURES OF IN VIVO T
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sulfate, cinnamic aldehyde, 2,4-din
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The final product will be a system
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mercially available STP brands by m
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for six weeks, with 10 mg/kg azoxym
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eceived RES post-TCDD exposure when
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morigenesis. Knocking down of JARID
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163 MICROPET IMAGING OF [18F]-DFNSH
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These results are comparable to tha
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activity as assessed by lever press
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for measured physico-chemical param
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199 DEVELOPMENT OF A MULTIPARAMETER
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To cause PLD, a drug needs to enter
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In contrast to the parent PBDEs and
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transiently transfected HEK 293 cel
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TCDD exposure, 24 h prior to a 20 %
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244 NON-ADDITIVE EFFECTS OF PCB153
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253 COMPARISON OF MIXTURE TOXICITY
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two cerium oxide nanoparticles of v
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271 SIZE-DEPENDENT EFFECTS OF TUNGS
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adigms such as Tox 21 and Toxcast,
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QDs with emission maximum at 800nm
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Cleveland, while others were found
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without the need of animal testing.
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Conclusions: These results are cons
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ing oxime reactivation and organoph
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335 A NON-OXIME IMPROVES SURVIVAL I
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alties suffer from permanent lung i
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ies have established inflammatory b
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363 GENETIC VARIATION IN ISOGENIC M
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372 EVALUATING THE BIOLOGICAL INTER
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dose of 1/20 LD50 (400 mg/kg.bwt) f
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median CR-adjusted isoflavone conce
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data indicate that AhR deletion pro
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February 2006). The rabbit is one o
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tal neurotoxicity (DNT) test (OECD
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of selected microorganisms that are
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BVI. Histopathological analysis was
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446 MOLECULAR CLONING AND CHARACTER
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portant in predicting risk. CYPs 1A
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ats, which involves metabolic activ
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473 BOVINE CORNEAL OPACITY AND PERM
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482 TYPE III DEIODINASE (D3) IS PRO
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tancy evaluation and ranking of bat
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501 CHARACTERIZATION OF ESTERASE, G
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510 REDOX CYCLING BY ENDOGENOUS 2-
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prostate cancer cells. All 8 BEL de
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metallic nickel nanoparticles. Acti
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variety of more or less reactive ch
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550 QUALIFICATION STRATEGIES-GENOTO
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ferentiation, and 3) how mixtures o
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572 LOW-CHRONIC ARSENIC EXPOSURE: E
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582 IDENTIFICATION OF SENSITIVE URI
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duced by the genetic outcross of fe
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fects of new compounds are equally
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acterize the current state of the s
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620 CHARACTERIZATION OF POTENTIAL I
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ways. Moreover, both MAP kinase and
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641 POPS IN THE U.S. POPULATION AND
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studies such as the NCS, consider h
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the beginning of the academic caree
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trophil infiltration, a significant
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tactic response and optokinetic res
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usually high spontaneous PIG-A MFs.
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699 PROMUTAGEN ACTIVATION AND P450
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oxodG in bone marrow, spleen, kidne
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718 GENOTOXICITY OF ORGANIC EXTRACT
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ment were 18.0 and 4.5 nM for BEAS-
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strongest activation of nuclear fac
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746 MACROPHAGE INHIBITORY CYTOKINE-
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screening of cell migration. High-c
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dase inhibition). In contrast, inhi
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mice; the decrease was more pronoun
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Markers of oxidative damage reached
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793 PULMONARY RESPONSE, OXIDATIVE S
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cilitate clinical and industrial ap
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sion of p-p38, p-p53, p21 and cycli
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821 KIDNEY INJURY MOLECULE-2 GENE D
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commercial applications, and have b
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developmental effects. The residual
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strand breaks in an in vitro model
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etate (immunotoxicity). 2,4-D was t
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867 MELATONIN AMELIORATES CYCLOPHOS
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pharmacokinetic (PBPK) models. Ten
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of radiolabeled Mn (carrier-free 54
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893 UNVEILING ASSOCIATIONS BETWEEN
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using area under the concentration
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912 COMMERCIAL FISH DIETS INDUCE VI
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922 A STUDY OF PHOTOTOXICITY FOLLOW
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from 0.1 to 2.9 g/L (saturated vapo
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vasive method for assessing several
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950 ARSENITE DOWN-REGULATES THE CAR
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inflammatory signaling is altered b
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treated wood. Seventy-five of 132 w
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ergy homeostasis and raising levels
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treated with mercury and then with
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997 IN VIVO CORRELATES OF THE MANGA
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of the panel. The panel was compris
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sponse, location, and severity scor
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tant source of n-3 fatty acids such
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old for serious, irreversible or es
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1045 SUBCHRONIC TOXICITY EVALUATION
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sites collected 3 days after inject
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1063 MOLECULAR MECHANISM OF OLANZAP
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esponses, and can be available for
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hence more physiologically relevant
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thesized apoproteins, so we tested
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vate CYP3A5 but could be released b
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1108 STYRENE-INDUCED TOXIC EFFECTS
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1118 THE PRESENCE OF DIETHYL FUMARA
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zebrafish cells were first exposed
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utene-1,4-dial, which has been show
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groups, largely due to lower non-HD
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Exposure to gluten in individuals w
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contrast to VGSC activators such as
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1175 70% HYDROFLUORIC ACID (HF) CUT
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axis. An increase in hyaline drople
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1194 esiRNA AND siRNA HIGH-THROUGHP
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1203 ARYL HYDROCARBON RECEPTOR-DNA
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permeability (calcein), mitochondri
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olytic caspase activation, caspase-
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teristics of a human T-type voltage
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80% of the activity from the yellow
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1251 DEVELOPMENTAL EXPOSURE TO DELT
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1260 MANEB ENHANCES MPP + -INDUCED
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demonstrated by knockdown of beclin
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1278 PINK1 AND MITOCHONDRIAL DYNAMI
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treatment for number of live worms.
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1297 INVESTIGATION OF THE NEUROTOXI
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1306 DEVELOPMENT OF AN IN VITRO ASS
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1315 EVALUATION OF 3- AND 1-METHYLH
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prior to kainic acid-induced seizur
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1334 AFFECT OF GENETIC VARIATION ON
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1346 THE OTHER WORLD OF THE TRANSCR
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strate, leading to excess microvesi
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1368 OVERVIEW OF THERAPEUTIC VACCIN
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to a bovine adrenal cortical epithe
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DOTC had no effects. These results
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1398 PULMONARY TOXICITY OF CERIUM D
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PPARα, LXR, ER, AR and AhR activit
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1417 MECHANISM OF GENDER-DIVERGENT
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els, they disrupt homeostatic contr
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were to characterize exposure of th
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1448 ADVERSE OUTCOME PATHWAYS AND E
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the level in urine was 25% of the m
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1;akt-2 double mutant and pdk-1 mut
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jury effects when compared to contr
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tude than equivalent oral doses. Af
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cells; and increased iNOS and MCP-1
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B6.Cg-Kit W-sh mice. These findings
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1511 STATIN-TREATMENT EFFECTIVELY R
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1520 EFFECT OF INHALATION EXPOSURE
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numbers of IFN-γ producing cells w
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These data indicate that TCDD treat
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Page 375 and 376: 1740 PROFILING COMPOUNDS WITH CARDI
Page 377 and 378: dothelial cells confirmed caveolin-
Page 379 and 380: 1758 GINKGO BILOBA EXTRACT INDUCES
Page 381 and 382: arin-induced suppression of MDR1 ex
Page 383: 1780 ANTIANDROGENIC AND ANTIPROLIFE
Page 387 and 388: 1799 GUIDANCE ON THE APPLICATION OF
Page 389 and 390: However, substances with EC3 values
Page 391 and 392: 1816 CD-INDUCED EGFR TRANSACTIVATIO
Page 393 and 394: 1826 KERATIN 7 EXPRESSION IN INDEPE
Page 395 and 396: centa were collected at the time of
Page 397 and 398: 1845 SYSTEMATIC SCREENING OF YEAST
Page 399 and 400: underlying the development of co-mo
Page 401 and 402: eing measured in experimental roden
Page 403 and 404: ufactured in the US for more than 3
Page 405 and 406: nine (N7-THB-Gua) and N7-hydroxyphe
Page 407 and 408: 1892 EFFECT OF LAMBDA-CYHALOTHRIN O
Page 409 and 410: 22 in Phase I. Antimicrobial pestic
Page 411 and 412: kinetic and dynamic differences, an
Page 413 and 414: iphenyl, saccharin and melamine was
Page 415 and 416: 1930 DEVELOPMENT OF A RELATIVE SOUR
Page 417 and 418: 1939 MODE OF ACTION FOR THE CANCER
Page 419 and 420: 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
Page 425 and 426: 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
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vide many contributions: with its g
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to-metal joint replacement. For exa
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to be addressed or negotiated. Deci
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especially with anti-TNF therapies.
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genic line Tg(are:eGFP) was created
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2074 COMPUTATIONAL ASSESSMENT OF TH
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2084 INHIBITION OF 11β-HSD1 DECREA
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(T) and express several enzymes inv
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2101 GENISTEIN MODULATION OF BLOOD
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males per group were dosed orally o
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ate the feasibility of assessing re
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changed. Hepatic protein carbonyl l
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sought to examine alterations in he
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2147 A SINGLE AMINO ACID CONTROLS T
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Gstm7) was independent of both CAR
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ility of tungsten trioxide (WO3), t
Page 467 and 468:
ured by real-time PCR array and rel
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glucose, and creatinine levels, and
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Several studies have reported suppr
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exposure between TCDD-exposed labor
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Furthermore, with increasing number
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Society of Toxicology 2010 Author I
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Society of Toxicology 2010 Abstract
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49 th Annual Meeting and ToxExpo A
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The Official Journal of the Society
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