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0-9) in the pesticide retailers compared to 2.75 (range 0-8) in the control group (p=0.18). There were no statistically significant differences in the frequency of NPBs, BUDs, necrotic cells, or apoptotic cells between the pesticide retailers and the control group. However, lymphocytes from pesticide retailers displayed a higher nuclear division index than those from controls (p
esidues of organophosphates or their metabolites. Between 2004 and 2008, fruit, vegetable, nuts and grains were routinely collected and analyzed for a variety of pesticide residues. Per capita availability data was also obtained from the USDA to determine how much Americans consume of each commodity. The results of this review indicate that wheat and corn are the commodities most likely contributing to organophosphate exposure in children. Percentage of wheat samples with detectable concentrations of chlorpyrifos were reported as 20.8, 23.1, and 16.7 during 2004, 2005, and 2006, respectively. Similarly, percentage of wheat samples with detectable concentrations of malathion were reported as 49.4, 66.9, and 63.0 during 2004, 2005, and 2006, respectively. Estimated per capita wheat consumption was and still is presumably approximately 95 pounds per year. Percentage of corn samples with detectable concentrations of chlorpyrifos were reported as 30.0 and 17.8 during 2007 and 2008, respectively. Percentage of corn samples with detectable concentrations of malathion were reported as 37.9 and 33.7 during 2007 and 2008, respectively. Estimated per capita corn consumption decreased from 52 to 49 pounds from 2007 to 2008. Corn is widely used for the production of sweeteners such as high fructose corn syrup. Children are at risk of exposure to multiple pesticide residues from consuming the very same commodity and cumulative exposures are likely to occur. More research needs to be conducted to determine the organophosphate residue content found in food products made from grain. Exposure to multiple organophosphate pesticides has been linked to the development of learning disabilities in children. 2121 HIGH-THROUGHPUT ASSESSMENT OF CELLULAR MANGANESE (MN) IDENTIFIES NOVEL MECHANISM UNDERLYING A MN DEFICIT OF HUNTINGTON’S DISEASE MODEL. G. Kwakye 1 , D. Li 1 , O. Kabobel 1 , M. Wegrzynowicz 1 , K. M. Erikson 2 , M. Aschner 1 and A. B. Bowman 1 . 1 Neuroscience, Vanderbilt University Medical Center, Nashville, TN and 2 Nutrition, University of North Carolina, Greensboro, NC. Expression of mutant Huntingtin (Htt) is associated with impaired manganese (Mn) accumulation in a striatal cell line and mouse models of Huntington’s disease (HD). To evaluate this mechanism, we have developed and validated a highthroughput fluorescence-quenching based assay (Cellular Fura-2 Manganese Extraction Assay - CFMEA) to measure Mn transport kinetics and storage properties in cultured striatal cells and rodent tissues. We have applied CFMEA to confirm the impaired Mn uptake observed in mutant striatal cells following 27 hours Mn exposure. Here, we demonstrate that the impaired Mn phenotype in mutant striatal cells is observed as early as 1 hour following 200 μM Mn exposure. In addition, this deficit is not dependent on other di-/trivalent metals, serum proteins, or known co-transporter ions in the culture media and exposure buffers. Moreover, mutant striatal cells’ Mn uptake deficit is independent of the divalent metal transporter 1 (DMT1) and 2-APB blockable channels. Importantly, mitochondrial function has been reported to be impaired in mutant striatal cells. Thus, we hypothesized that expression of mutant Htt would impair the mitochondrial regulatory functions of metal ion homeostasis via the PPARγ mediated pathway. To test this hypothesis, we utilized a PPARγ agonist and antagonist and failed to observe an influence of the PPARγ mediated pathway on the Mn deficit in mutant striatal cells. In spite of similar instantaneous Mn uptake and efflux rates between wildtype and mutant striatal cells, we demonstrate that there is a significant decrease in net Mn storage capacity in mutant compared to wildtype striatal cells. Finally, we have applied CFMEA in mouse brain tissues to assess temporal and spatial Mn accumulation. In conclusion, our data show that the Mn deficit in mutant striatal cell lines is likely due to impairment of Mn storage capabilities and not uptake. Support: ES016931, ES016931-02S1, ES016931-02S2 2122 CTR1, BUT LESS LIKELY DMT1, PLAYS A CRITICAL ROLE IN MANGANESE (MN)-INDUCED COPPER (CU) ACCUMULATION IN THE BLOOD-CSF BARRIER. G. Zheng and W. Zheng. School of Health Sciences, Purdue University, West Lafayette, IN. The blood-cerebrospinal fluid barrier (BCB) in the choroid plexus plays a key role in maintaining Cu homeostasis in the brain. Previous studies from this lab show that Mn exposure alters cerebral Cu homeostasis, which may underlie the development of neurodegenerative manganism. Cu transporter-1 (Ctr1) and divalent metal transporter-1 (DMT1) are known to transport metals; however, their roles in Cu transport in BCB under Mn exposure have not been defined. This study investigated the role of Ctr1 and DMT1 in Cu uptake in the choroidal Z310 cells. Mn exposure (100 μM) for 24 hr increased the 64Cu uptake by the cells, and up-regu- lated the protein levels of both Ctr1 and DMT1. Ctr1 knockdown using Ctr1 siRNA before Mn exposure diminished the Mn-induced increase of 64Cu uptake. Unexpectedly, however, knocking down DMT1 by DMT1 siRNA, followed by Mn exposure, resulted in an increase of the cellular [64Cu] uptake. To distinguish the exact role of these two transporters, we established Z310 cell-based tetracycline (Tet)-inducible Ctr1 or DMT1 expression cell lines that carry Tet repressor (TetR). When Tet is added to the culture medium and binds to the TetR, the transcription of Ctr1 or DMT1 gene proceeds, leading to the gene overexpression. The Ctr1- or DMT1- inducible cells were treated with 100 μM Mn for 24 hr and then incubated with Tet for another 6 hr, followed by 64Cu uptake assay. Results showed that Tetinduced expression of Ctr1 further increased 64Cu uptake in Ctr1-inducible cells; over-expression of DMT1, however, did not increased 64Cu uptake in DMT1-inducible cells. Taken together, these data indicate that Mn exposure results in an increased cellular Cu uptake and increased protein expression of both Ctr1 and DMT1 in choroidal Z310 cells. It is Mn-induced upregulation of Ctr1, but less likely DMT1, that prompts Cu uptake by the choroidal epithelial cells. Unlike the role of DMT1 in Mn-Fe interaction, Ctr1 appears to play a critical role in response to Mn exposure and to regulate cellular Cu uptake. (Supported by NIH/NIEHS RO1-ES008146) 2123 EXAMINING A POTENTIAL GENE-ENVIRONMENT INTERACTION BETWEEN THE PD-ASSOCIATED GENE PARKIN AND MANGANESE IN A C. ELEGANS MODEL. S. Chakraborty 1 and M. Aschner 2, 3 . 1 Neuroscience Graduate Program, Vanderbilt University, Nashville, TN, 2 Pediatrics, Vanderbilt University, Nashville, TN and 3 Vanderbilt Kennedy Center, Vanderbilt University, Nashville, TN. Manganese (Mn) is a trace element that serves as a vital micronutrient in human diet. However, overexposure from the environment can lead to a toxic condition known as Manganism. This disorder shares similar neuropathology with Parkinson’s disease (PD), implicating dopaminergic (DAergic) cell loss as the primary target. Both manganism and PD lead to neurological and motor deficits, along with increased mitochondrial dysfunction. The mechanisms behind these disorders are still not clearly understood. Of recent interest are methods to elucidate a potential gene-environment interaction, using C. elegans as a genetic model that contains the necessary DAergic machinery. Many genes associated with PD have been identified in the literature, including the parkin/PARK2 (pdr-1 in worms) gene that encodes for an E3-ubiquitin ligase protein that is also involved in inducing mitophagy. It has been previously shown that Mn toxicity exhibits specificity to DAergic cells, and that parkin confers protection to these cells from Mn exposure in vitro. We, therefore, hypothesized that a loss-of-function mutation in parkin increases the vulnerability of C. elegans to Mn toxicity. Synchronous L1 worms from wildtype N2 and pdr-1 mutant strains were acutely treated with a range of Mn doses (0-200 mM MnCl 2 ) for 30 minutes, followed by lethality scoring of approximately 200 worms 24 hours post-treatment. Using transgenic worms with a pdr-1 deletion, we show that a loss in parkin increases sensitivity to Mn toxicity (LD 50 =33.64 mM MnCl 2 ) compared to wild-type N2 worms (LD 50 =59.27 mM MnCl 2 ), as seen with a leftward shift in the dose-response curve. This data indicate that parkin is protective against Mn toxicity in vivo, with loss of parkin potentially producing increased oxidative stress from impaired mitophagy. 2124 HSPS ARE IMPORTANT MEDIATORS OF MN- INDUCED TOXICITY IN C. ELEGANS. D. Avila and M. Aschner. Pediatrics/Toxicology, Vanderbilt University, Nashville, TN. Heat shock proteins (HSPs) are essential for survival under conditions of acute stress. Particularly, HSPs are protective in Alzheimer’s and Huntingtons’ disease. Furthermore, it has been hypothesized that these chaperones act in association with DJ-1 and PINK-1, translocating these proteins to the mitochondria in order to exert their antioxidant response. Mutations in the genes that codify DJ-1 and PINK-1 are associated with early-onset Parkinson’s disease, a neurodegenerative disease that impairs the motor system because of degeneration of dopamine (DA)-producing neurons. Similarly, manganese (Mn) poisoning also causes degeneration of DAergic neurons by causing mitochondrial dysfunction, oxidative stress and motor defects. We have previously observed that DJ-1 and PINK -1 are highly expressed after Mn exposure in Caenorhabiditis elegans, probably in an attempt to protect the cells against the damaging mitochondrial effects of this metal. Considering the putative importance of HSP to DJ-1 and PINK-1 function, we hypothesized that loss-of-function of hsp would impair their translocation to mitochondria, increasing Mn toxicity in C. elegans. N2 wild type worms and hsp knockout worms (15 strains) were maintained as standardized conditions. Synchronous L1 worms were SOT 2011 ANNUAL MEETING 455
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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
Page 407 and 408: down the doses may produce more tox
Page 409 and 410: spectively. Below 100 mg/l of gemfi
Page 411 and 412: 1900 GENERATION OF PRECISION CUT LI
Page 413 and 414: iomarkers or observation of lesions
Page 415 and 416: creased reticulocytes and lymphocyt
Page 417 and 418: statistically significant interacti
Page 419 and 420: monize sample preparation and analy
Page 421 and 422: NPC and sinonasal cancer in neighbo
Page 423 and 424: showed incidences of lung and nasal
Page 425 and 426: utylbenzenes, exhibited most simila
Page 427 and 428: 1975 DIFFERENTIAL MODULATION OF CYP
Page 429 and 430: organic As to MMA(V) and a lower ca
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Page 433 and 434: 3T3-L1 cells to low-levels of arsen
Page 435 and 436: 2011 IDENTIFICATION OF A NOVEL VX M
Page 437 and 438: This work was supported by Cooperat
Page 439 and 440: 2029 EFFICACY OF ENDOTRACHEAL ADMIN
Page 441 and 442: Diazepam injections and its combina
Page 443 and 444: 2047 ESTERASE ACTIVITIES AND HEMOST
Page 445 and 446: nanoparticle-induced toxicity progr
Page 447 and 448: house, were iv infused into rats ov
Page 449 and 450: een explored. This study investigat
Page 451 and 452: croscopic analysis revealed that on
Page 453 and 454: egg yolk collected from turtles inh
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Page 457: 2111 CYTOCHROME P450 3A5 GENOTYPE I
Page 461 and 462: manganism. Recent work from our lab
Page 463 and 464: Aβ1-40 in CSF and hippocampus in P
Page 465 and 466: 2147 CATALASE MANIPULATIONS MODIFY
Page 467 and 468: ation based on real-world exposure
Page 469 and 470: NPs. Aggregation of citrate-stabili
Page 471 and 472: 2175 THE ROLE OF SURFACE CHEMISTRY
Page 473 and 474: seen rapid uptake in biological ima
Page 475 and 476: effect on uterine weight or vaginal
Page 477 and 478: dicating widespread exposure. While
Page 479 and 480: components into the liver parenchym
Page 481 and 482: 2223 ISOLATION AND DETECTION OF RIC
Page 483 and 484: stored (-20 celsius degree). The co
Page 485 and 486: 2241 DDA, A BIOMARKER FOR ENVIRONME
Page 487 and 488: 2249 INTERACTION BETWEEN DIETARY SE
Page 489 and 490: 2258 PHARMACOKINETICS, EXCRETION BA
Page 491 and 492: 2267 SENSITIVE AND SPECIFIC FLUORES
Page 493 and 494: 2276 METABOLISM AND DISPOSITION OF
Page 495 and 496: ment of hypertension in companion a
Page 497 and 498: for the propyl series can be used f
Page 499 and 500: 2304 IN VITRO EXPOSURE AND EVALUATI
Page 501 and 502: 2313 THE SYNERGISTIC EFFECT OF SODI
Page 503 and 504: genes that play a crucial role in M
Page 505 and 506: 2330 THE ROLE OF TRANSFORMING GROWT
Page 507 and 508: ined following up to 96 h continuou
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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
Page 521 and 522:
2406 TOXICITY AND BIOACCUMULATION O
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Isocitric acid is the acid in the h
Page 525 and 526:
2425 EFFECTS OF FUMONISINS IN ETHAN
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centration(μg/g) were: 5.1-95.3; 2
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2445 AUTOPHAGY IN DEVELOPMENT: A LI
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sures to inhaled Mn in dust. Nevert
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2466 CRITICAL EVALUATION OF ANIMAL
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elationships predict that resting r
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2489 COMPARATIVE TOXICITY OF BIODIE
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2497 TRANSCRIPTIONAL REGULATION OF
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2506 TOXICOLOGICAL CONSIDERATIONS O
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launched with the aim of developing
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forms mRNA expression levels were a
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2534 CUTANEOUS WOUND HEALING IN THE
Page 549 and 550:
wells (0, 1, 5, 10, 25, 50, 100, an
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2553 AN ORGANOTYPIC MICROLIVER PLAT
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serum-free media. At 24 hrs, the gr
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2572 INCREASED ARSENIC BIOACCESSIBI
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nology to develop improved methods.
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tuna, swordfish, or mako shark (3.5
Page 561 and 562:
nificantly reduce circulating thyro
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grouped into 9 observation periods
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histopathological or biochemical ev
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exhibited a hyperactive phenotype,
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the search of effective drugs for e
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2644 COVALENT BINDING OF 14 C 2-MET
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aries targeting all transcription f
Page 575 and 576:
(p 9 weeks) and CSC phenotype acqui
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2673 IMMUNE-MEDIATED VASCULAR INJUR
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for risk identification and charact
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to control toxicant delivery in tob
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Author Index (Continued) The numera
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Keyword Index (Continued) Arsenite
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Keyword Index (Continued) Covalent
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Keyword Index (Continued) flow cyto
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Keyword Index (Continued) innate im
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Keyword Index (Continued) nanoparti
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Keyword Index (Continued) preservat
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Keyword Index (Continued) Thrombocy
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Toxicological Sciences The Official
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