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chorioallontoic membrane (CAM) and in the mouse matrigel models. Equimolar concentrations (40 nM) of test compounds were combined with the basement membrane matrix matrigel seeded with 10 6 pancreatic tumor cells (PANC-1), incubated with CAM and harvested after 7 days to determine tumor mass and hemoglobin (Hb) concentrations (mg/ml) as indices of AG. PANC-1 cells are an established source of numerous angiogenic factors, including vascular-endothelium growth factor and fibroblast growth factor (FGF-2). All Hg compounds significantly (p
1394 COMPARATIVE EFFECTS OF METHYLMERCURY AND 1-METHYL-4-PHENYLPYRIDINIUM ON THE DOPAMINERGIC SYSTEM IN MN9D CELLS. Y. Shao and H. Chan. Community Health Science Program, University of Northern British Columbia, Prince George, BC, Canada. Recent studies have implicated a positive correlation between the prevalence of Parkinson’s Disease (PD) and environmental factors such as exposure to pesticides and heavy metals. The objective of this study was to investigate the toxic effects of methylmercury (MeHg) on the dopaminergic system, and to gain a better insight into the mechanism of dopamine regulation linked to PD. The hypothesis is that MeHg would decrease dopamine release in a similar mechanism to that of 1- Methyl-4-Phenylpyridinium (MPP + ), a known agent commonly used to induce pathogenesis of PD, in a dopaminergic neuronal cell line, MN9D. MN9D cells were exposed to MeHg (1–15μM) and MPP + (10-800μM) for 24h or 48h. Both MeHg and MPP + decreased cell viability measured by MTT assay at both time points and dose dependently. Exposure to both MeHg and MPP + decreased dopamine (DA) and its metabolites dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) released by the cells. The DOPAC+HVA/DA ratio also increased with dose. MeHg and MPP + down-regulated the expression of DA markers, tyrosine hydroxylase (TH), and dopamine transporter (DAT) at both gene and protein levels. Expression of the α-Synuclein (α-Syn) gene, a hallmark neuropathological indicator of PD, was up-regulated after either treatment. However, protein levels were down-regulated as analyzed by Immunoblot. These findings suggested MeHg can induce pathogenesis of PD similar to that of MPP + and the mechanism involves the disruption of DA synthesis, re-uptake, and metabolism processes as well as α-Syn alteration. 1395 CA 2+ CHANNEL α 1 SUBUNITS DIFFERENTIALLY MODULATE METHYLMERCURY (MEHG)-INDUCED CA 2+ DYSREGULATION IN HEK-293 CELLS. H. Hannon, E. M. Sparkenbaugh, K. Krcmarik and W. D. Atchison. Pharmacology/Toxicology, Michigan State University, East Lansing, MI. MeHg causes a biphasic increase of neuronal [Ca 2+ ] i consisting of Ca 2+ release from intracellular stores (Phase1- P1) and extracellular Ca 2+ influx (Phase 2-P2). The [Ca 2+ ] i increase in P2 is slowed, in part, by nifedipine, ω-conotoxin GVIA, and Ni 2+ , illustrating the contribution of individual voltage-gated Ca 2+ channel (VGCC) isoforms in the cellular response to MeHg. Heterologous expression was used in this study to probe discrete effects of low μM concentrations of MeHg on individual VGCC isoforms. HEK 293 cells were transfected with a 1:1:1 M mixture of α 1 , α 2 δ, and β 3 subunits of human neuronal VGCC cDNA. The α 1 subunit was varied to produce L-, P/Q, and N-type VGCCs (Ca v 1.2, 2.1, and 2.2, respectively), corresponding to α 1C , α 1A , and α 1B subunits. Fura-2AM, a ratiometric Ca 2+ fluorophore, was used to measure [Ca 2+ ] i in transfected cells exposed to 5 μM MeHg. P1 and P2 time-to-onset was fastest in cells expressing Ca v 2.2 (77±30 and 339±71 s, mean ± SEM) compared to those expressing either Ca v 1.2 (155±60 and 548±107 s) or Ca v 2.1 (155±54 and 452±71 s). Exposure to 2.5 μM MeHg/0 [Ca 2+ ] e delayed P1 time-to onset in cells expressing Ca v 2.1 (278±37 s); the P2 response was eliminated for all isoforms. P1 onset was not affected in either Ca v 1.2 or Ca v 2.2-expressing cells. The consequences of differential susceptibility of VGCCs to MeHg were also examined using cytotoxicity assays. Transfected cells were exposed to 2 μM MeHg for 3 h and stained in a commercial live/dead assay 24 h later. Cytotoxicity was highest in Ca v 2.1-expressing cells (19.0±2.9% dead); Ca v 2.2-expressing cells were least affected (6.1±0.4% dead). Together, these results suggest MeHg differentially affects VGCC isoforms to disturb Ca 2+ homeostasis and induce Ca 2+ -mediated cell death. Understanding differences in VGCC susceptibility and response will allow a better understanding of selective neuronal vulnerability to MeHg toxicity. 1396 IDENTIFICATION AND CHARACTERIZATION OF MOLECULAR MODULATORS OF METHYLMERCURY- INDUCED DOPAMINE NEURON PATHOLOGY IN C. ELEGANS. N. VanDuyn, R. Settivari, G. Sinclair and R. Nass. Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN. Methylmercury (MeHg) exposure from occupational, environmental, and food sources is a significant threat to public health. MeHg poisonings in adults may result in severe psychological and neurological deficits, and in utero exposures can confer embryonic defects and developmental delays. Recent epidemiological and vertebrate studies suggest that MeHg exposure may also contribute to dopamine (DA) neuron vulnerability and the propensity to develop Parkinson’s disease (PD). We have developed a novel Caenorhabditis elegans (C. elegans) model of MeHg toxicity that shows that low, chronic exposure confers embryonic defects, developmental delays, decreases in brood size and animal viability, and DA neuron degeneration. Toxicant exposure results in the robust induction of the glutathione-S-transferases (GSTs) gst-4, gst-5, gst-12, gst-21, and gst-38, with some GSTs largely dependent on the PD-associated phase II antioxidant transcription factor SKN-1/Nrf2. We also demonstrate that the expression of SKN-1, a protein previously localized to a small subset of chemosensory neurons and intestinal cells in the nematode, is also expressed in the DA neurons, and a reduction in SKN-1 gene expression increases MeHg-induced animal vulnerability and DA neuron degeneration. We will also present our initial studies from 2 genome-wide reverse genetic screens to identify mediators and suppressors of MeHg-induced DA neuron degeneration, as well as our investigations utilizing DA-associated mutants to elucidate the role that the neurotransmitter may play in the toxicity. 1397 ION CHANNEL GENE TRANSCRIPTION IS AFFECTED DIFFERENTIALLY IN RAT CEREBELLUM AFTER POSTNATAL METHYLMERCURY EXPOSURE. A. Colón-Rodriguez, R. K. Hajela, Y. Yuan and W. D. Atchison. Pharmacology/Toxicology, Michigan State University, East Lansing, MI. Two sets of membrane ion channels are especially sensitive to methylmercury (MeHg): GABAA receptors and several types of voltage gated Ca2+ channels (VGCC), resulting in effects on synaptic transmission and [Ca2+ ]i homeostasis. We compared the effects of MeHg on gene expression of α1, α6, and δ subunits of the GABAA receptors, and the pore forming subunits (α1), of the L, N, P/Q and Rtype VGCC. Two proteins associated with intracellular Ca2+ buffering- Calbindin D28K and the IP3 receptor (IP3R) were also examined. Comparing the expression of the proteins can reveal whether MeHg exposure results in lasting changes in gene expression of nerve membrane proteins for which functional effects of MeHg occur in cerebellum. Rats were treated with 0.75 and 1.5mg/kg/day MeHg sc starting at PND5. Treatment was maintained for 15 or, 30 days, then stopped for a clearing period of 30 days(PND65). Quantitative real time PCR on reverse transcript (cDNA) of RNA isolated from 10 mg of cerebellum was used to assay the transcription of the target protein genes. MeHg did not affect expression of CalbindinD28K or IP3R. All four VGCC subunits were upregulated after 15 days of MeHg, but not at 30 days when compared to the control. Conversely all 3 of the GABAA receptor subunits showed a downregulation that increased with the treatment and the days of exposure. This appears consistent with our previous observations that MeHg gradually decreases GABA A receptor-mediated inhibitory postsynaptic potential and inhibitory synaptic transmission to complete block. The upregulation of some VGCC subunits may appear consistent with the fact that MeHg causes increase in [Ca 2+ ] i . The approximately 5-10% increase in the VGCCs and a similar decrease in the GABA A receptor transcription appeared to be more pronounced in the initial phases of treatment and appeared to stabilize at somewhat less pronounced levels by 60 days. Supported by NIH grants R01ES03299 and R25NS065777. 1398 MOLECULAR MECHANISMS OF IRREVERSIBLE INHIBITION OF SELENOENZYMES BY HIGH METHYLMERCURY EXPOSURES. N. V. Ralston and L. J. Raymond. Energy & Environmental Research Center, University of North Dakota, Grand Forks, ND. Since the molecular mechanism of methylmercury (MeHg) toxicity has now been identified, it is necessary to refine toxicological understanding of exposure related issues. This study examined the thermodynamic binding affinities and stoichiometries of MeHg and its binding partners in relation to their tissue abundance based on their known physiological abundance in relation to low vs. high MeHg exposures. Methylmercury is a highly specific, irreversible inhibitor of selenium (Se)-dependent enzymes, and its toxic effects appear to be the direct result of interruption of these enzyme activities. The binding affinity between MeHg and the selenium that is the functional component of physiologically essential enzymes is a million times greater than MeHg’s affinity for thiomolecules analogues. The high binding affinities and relatively low intracellular abundance of Se make these enzymes extremely vulnerable to high MeHg exposures. The relative binding affinity between MeHg and selenocysteine (Sec) is much greater than for cysteine. (Cys). Because the Se of Sec is the foremost intracellular soft nucleophile, it selectively binds with high affinities to soft electrophiles such as the Hg of MeHg. Instead of being kinetically driven, binding interactions between soft nucleophiles and electrophiles are under thermodynamic control. At equilibrium, the distribution of absorbed MeHg bound with available intracellular Se vs. sulfur is predictable based on thermodynamic affinities and relative intracellular mass abundance. Since ocean fish are among the richest dietary sources of Se, the abundance of Se present in seafoods SOT 2011 ANNUAL MEETING 299
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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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Page 255 and 256: have now compared the IC50 values b
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Page 263 and 264: weight (P=0.016) and small for gest
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Page 267 and 268: posure groups. However, the differe
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Page 275 and 276: modating a reliable data evaluation
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Page 283 and 284: mation was decreased to the same le
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Page 287 and 288: luted OFR and CRL. Culture media ex
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Page 293 and 294: mice, each with 4 dose groups. One
Page 295 and 296: exposure to both ATR and DACT has a
Page 297 and 298: third tetratricopeptide repeats (TP
Page 299 and 300: 7d. 28d after TMT injury there was
Page 301: subunits. Each cell type was treate
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Page 307 and 308: vated only in high-dose-treated ani
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Page 311 and 312: cisplatin; 1.2-, 1.9- and 2.9-fold
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Page 325 and 326: throughput in vitro approach was us
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Page 329 and 330: (CIA) and the Streptococcal cell wa
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Page 333 and 334: 1530 MINIMAL RISK LEVELS FOR STYREN
Page 335 and 336: ical groups in the field of regulat
Page 337 and 338: vitro with this potentially insect-
Page 339 and 340: their performance on toxicological
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Page 345 and 346: gene expression post-transcriptiona
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its nuclear translocation was reduc
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were collected from TK animals at d
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egulated targets were selected for
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U/L after tetracycline. Minocycline
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peri-pubertal FasL-/- mice show a d
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showed similar levels of apoptosis
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1676 TWO BIOMARKERS FOR EVALUATION
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motifs selected. This system was ap
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1693 VOC SERUM LEVELS IN THE GENERA
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1702 DOES THE CLOCK MAKE THE POISON
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those with high nickel content are
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isk assessment. However, unique cha
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model of APAP metabolism and glutat
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logically & morphologically similar
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posure, blood chemistry was analyze
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elated to oxidative stress by measu
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ostasis), but work is needed to tra
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tokine products during carcinogenes
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ways as chemical stressors and, the
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toxicity of nanomaterials relates s
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1815 MEASURING COMPOUND SELECTIVITY
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1825 EFFECTS OF METABOLISM BY INTES
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cyanoacetic acid increased 2-3 fold
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1845 IS THE PROMISCUITY OF THE ARYL
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crorarray analysis. RT-PCR results
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are a family of phase-II biotransfo
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ous labs. As a result of positive s
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down the doses may produce more tox
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spectively. Below 100 mg/l of gemfi
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1900 GENERATION OF PRECISION CUT LI
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iomarkers or observation of lesions
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creased reticulocytes and lymphocyt
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statistically significant interacti
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monize sample preparation and analy
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NPC and sinonasal cancer in neighbo
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showed incidences of lung and nasal
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utylbenzenes, exhibited most simila
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1975 DIFFERENTIAL MODULATION OF CYP
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organic As to MMA(V) and a lower ca
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ole in invasion and metastasis of c
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3T3-L1 cells to low-levels of arsen
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2011 IDENTIFICATION OF A NOVEL VX M
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This work was supported by Cooperat
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2029 EFFICACY OF ENDOTRACHEAL ADMIN
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Diazepam injections and its combina
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2047 ESTERASE ACTIVITIES AND HEMOST
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nanoparticle-induced toxicity progr
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house, were iv infused into rats ov
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een explored. This study investigat
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croscopic analysis revealed that on
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egg yolk collected from turtles inh
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consistency of results in both expe
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2111 CYTOCHROME P450 3A5 GENOTYPE I
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esidues of organophosphates or thei
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manganism. Recent work from our lab
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Aβ1-40 in CSF and hippocampus in P
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2147 CATALASE MANIPULATIONS MODIFY
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ation based on real-world exposure
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NPs. Aggregation of citrate-stabili
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2175 THE ROLE OF SURFACE CHEMISTRY
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seen rapid uptake in biological ima
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effect on uterine weight or vaginal
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dicating widespread exposure. While
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components into the liver parenchym
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2223 ISOLATION AND DETECTION OF RIC
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stored (-20 celsius degree). The co
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2241 DDA, A BIOMARKER FOR ENVIRONME
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2249 INTERACTION BETWEEN DIETARY SE
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2258 PHARMACOKINETICS, EXCRETION BA
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2267 SENSITIVE AND SPECIFIC FLUORES
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2276 METABOLISM AND DISPOSITION OF
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ment of hypertension in companion a
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for the propyl series can be used f
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2304 IN VITRO EXPOSURE AND EVALUATI
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2313 THE SYNERGISTIC EFFECT OF SODI
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genes that play a crucial role in M
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2330 THE ROLE OF TRANSFORMING GROWT
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ined following up to 96 h continuou
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effect doses obtained with the rat
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diated transcriptional response of
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docrine disruptor activities of EDC
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individuals. Week 6 results were qu
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functionality of photosystem II and
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wild mice (Mus musculus) from areas
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2406 TOXICITY AND BIOACCUMULATION O
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Isocitric acid is the acid in the h
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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
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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
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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
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(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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The Toxicologist - Society of Toxicology

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