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lower anxiety levels. We have previously reported induction of excessive cell death in various fetal brain areas with different sensitivity to BrdU exposure. However, at this stage, we could not clarify the effects of BrdU on the olfactory bulb (OB). Therefore, to examine the effects of BrdU on OB development, we conducted a histopathological examination of the OB on later brain stages, GD20 fetal brain and postnatal day (PD)11 neonatal brain in rat developmental disorder model. In the BrdU over control group, results revealed a thinner mitral cell layer and fewer distributions of tyrosine hydroxylase (TH) immunoreactive cells in glomerular layer of GD20 fetal brain. In PD11 neonatal group, disruption of the mitral cell layer structure was seen. Neurites of TH-positive cells in the glomerular layer showed abnormal spindle extension, suggesting induction of disturbances in synaptogenesis. Furthermore, fewer distributions of parbalbumin (PV), a Ca-binding protein coexisting with GABA neurons, and presence of underdeveloped neurites in external plexiform layer of TH-immunoreactive cells was also observed in the BrdU group. Using PD11 neonatal brains, we previously reported that BrdU affects GABAergic neurons in the cerebral and limbic cortex (the hippocampus, amygdale and entorhinal area). The present findings reinforce the idea that abnormal GABAergic neurons may contribute to BrdU-induced abnormal behaviors in rat. 2596 PHENCYCLIDINE-INDUCED APOPTOSIS AND CHANGES IN GENE EXPRESSION IN POSTNATAL RAT PUPS. N. V. Sadovova 1 , F. Liu 2 , X. Zhang 2 , L. Shi 3 , L. Guo 3 , F. Quan 4 , Z. Wen 4 , C. Wang 2 , T. A. Patterson 5 , J. P. Hanig 2 , M. G. Paule 2 and W. Slikker 2 . 1 Toxicologic Pathology Associates, Jefferson, AR, 2 Division of Neurotoxicology, NCTR/FDA, Jefferson, AR, 3 Division of System Toxicology, NCTR/FDA, Jefferson, AR, 4 Z-Tech, ICF International Company, Jefferson, AR and 5 CDER/FDA, Silver Spring, MD. Repeated administration of phencyclidine (PCP), an N-methyl-D-aspartate (NMDA) receptor antagonist, during development, may result in neuronal damage that leads to behavioral deficits in adulthood. The present study examined the potential neurotoxic effects of PCP exposure (10 mg/kg) in rats on postnatal days (PNDs) 7, 9 and 11 and the possible underlying mechanism(s) for neurotoxicity. Brain tissue was harvested for RNA extraction and morphological assessments. Elevated neuronal cell death was observed in layers II and III of the frontal cortex in PCP treated group, using Fluoro-Jade C staining. More active caspase-3 positive neurons in PCP treated group further confirmed the neurotoxic effects of PCP, indicating PCP induced rat neuron death is apoptosis in nature. RNA was collected from the frontal cortex for DNA microarray analysis and quantitative RT-PCR. Gene expression profiling was determined using Illumina Rat Ref-12 Expression BeadChips containing 22,226 probes. Based on criteria of a fold change greater than 1.4 and a P-value less than 0.05, 19 genes including NMDAR1 (N-methyl-Daspartate receptor) and four pro-apoptotic genes were up-regulated, and 25 genes including four anti-apoptotic genes were down-regulated, in the PCP-treated group. Quantitative RT-PCR confirmed the microarray results. These findings support the hypothesis that neurodegeneration caused by PCP occurs, at least in part, through the up-regulation of NMDA receptors, which makes neurons possessing these receptors more vulnerable to endogenous glutamate. Supported by NCTR/NTP IAG # 244-07-0007 (E-2155). 2597 GENE EXPRESSION IN KETAMINE-EXPOSED RAT BRAIN. C. Wang1 , Q. Shi2 , L. Guo3 , T. A. Patterson1 , S. Dial2 , Q. Li4 , N. Sadovova5 , X. Zhang1 and J. P. Hanig6 . 1Division of Neurotoxicology, National Center for Toxicological Research/FDA, Jefferson, AR, 2Division of Systems Toxicology, National Center for Toxicological Research/FDA, Jefferson, AR, 3Division of Biomedical Toxicology, National Center for Toxicological Research/FDA, Jefferson, AR, 4Microarray Core Facility, UTSW Medical Center, Dallas, TX, 5Toxicologic Pathology Associates, Jefferson, AR and 6Center for Drug Evaluation and Research/FDA, Silver Spring, MD. Ketamine, a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist, is associated with accelerated neuronal apoptosis in the developing rodent brain. Here, postnatal day (PND) 7 rats were treated with 20 mg/kg ketamine or saline in six successive doses (sc) at 2-h intervals. Brain frontal cortical areas were collected 6 h after the last dose and RNA isolated and hybridized to the Illumina Rat Ref-12 Expression BeadChip with 22,226 probes. Many of the differentially expressed genes were associated with cell death or differentiation and receptor activity. Ingenuity Pathway Analysis software identified perturbations in NMDA-type glutamate, GABA and dopamine receptor signaling. Q-PCR confirmed that NMDA receptor subunits were significantly up-regulated. Up-regulation of NMDA receptor mRNA signaling was further confirmed by in situ hybridization. These observations support our working hypothesis that prolonged ketamine exposure produces up-regulation of NMDA receptors and subsequent over-stimulation of the glutamatergic system by endogenous glutamate, triggering enhanced apoptosis in developing neurons. 556 SOT 2011 ANNUAL MEETING 2598 MIDAZOLAM-INDUCED CHANGES IN GENE EXPRESSION IN POSTNATAL RAT PUP BRAIN. F. Liu 1 , S. W. Rainosek 2 , J. Zhang 3 , L. Guo 4 , L. Shi 5 , N. Sadovova 6 , M. G. Paule 1 and W. Slikker 1 . 1 Division of Neurotoxicology, National Center for Toxicological Research, Jefferson, AR, 2 UAMS College of Medicine, Little Rock, AR, 3 Z-Tech, an ICF International Company at NCTR, Jefferson, AR, 4 Division of Biomedical Toxicology, NCTR/FDA, Jefferson, AR, 5 Division of System Toxicology, NCTR/FDA, Jefferson, AR and 6 Toxicologic Pathology Associates, Jefferson, AR. Midazolam is a short-acting drug in the benzodiazapine class, often used for induction and maintenance of anesthesia in combination with either N-methyl-D-aspartate (NMDA) receptor antagonists or other γ-Aminobutyric acid (GABA) receptor agonists in pediatric anesthesia. Little is known regarding its effects on the developing brain. In the present study, postnatal day (PND) 7 rats were treated subcutaneously with 9 mg/kg midazolam or saline at 2-h intervals for 3 times. Brain frontal cortical areas were collected 6 h after the last dose and RNA was isolated for gene expression analysis. Gene expression profiling was determined using a whole genome-wide expression array, Illumina Rat Ref-12 Expression BeadChip with 22,523 probes. The differentially expressed genes (DEGs) were selected using the criteria of a fold change greater than 1.4 and a P-value less than 0.05 comparing the treatment group to the control group. Based on these criteria, 93 genes were up-regulated, and 121 genes were down-regulated in midazolam-treated animals. These DEGs were then searched in the Kyoto Encyclopedia of Genes and Genomes (KEGG) for pathway identification. Twelve pathways were significantly altered by treatment with midazolam. Functionally, these signaling pathways belong to the following 4 categories: 1) metabolism, 2) transcription/genetic information processing, 3) cell death and growth/cellular processes, and 4) neurodegenerative diseases/human diseases. This gene expression analysis provides novel molecular insights into the effects of midazolam in the developing brain. 2599 DIFFERENT APOPTOTIC RESPONSE IN MOUSE BRAIN AFTER NEONATAL EXPOSURE TO DIFFERENT FLAME RETARDANTS. H. Viberg. Department Environmental Toxicology, Uppsala University, Uppsala, Sweden. Polybrominated diphenyl ethers (PBDEs) and tetrabromo bisphenol A (TBBPA) are used as flame retardants and are detected in environment, wildlife species and human tissues. Earlier studies have shown that exposure to PBDEs during the brain development in the neonatal period affects behavior, learning and memory in adult life, while exposure to TBBPA during the neonatal period did not affect behavioral variables in the adult mouse. PBDE 99, but not TBBPA, has also been shown to affect proteins important for normal brain development neonatally, for example CaMKII, GAP-43 and synaptophysin. There are indications that one of the neurotoxic mechanisms of PBDEs can be apoptosis and therefore we investigated apoptotic markers in neonatal mouse brain. Mouse pups, age 10 days, were exposed to PBDE 99 (12 mg/kg bw, po), TBBPA (11.5 mg/kg bw, po) or ketamine (50 mg/kg bw, sc) and sacrificed 24 or 48 hours after exposure. The brains were sliced and immunohistochemical analysis of caspase-3, caspase-9 and p53 were performed. After slicing the whole brain, a screening analysis were done for caspase-3 and 3 different levels were chosen for semi-quantitative analysis of caspase-3, caspase-9 and p53. So far these analysis have shown that the number of caspase-3 activated cells are significantly increased 24 h after PBDE 99 exposure (100%) and 24 h after ketamine exposure (600%) in two different structures in the neonatal mouse brain. 48 hours after exposure to PBDE 99 or ketamine, there were no significant differences seen. TBBPA did not increase the number of caspase-3 activated cells at any time. These results confirm that PBDE 99 and ketamine can act as neurotoxicants, possibly by inducing apoptosis and altering the levels of proteins important for normal brain development, which may be related to the behavioral and cognitive alterations earlier seen after neonatal exposure to PBDE 99 and ketamine. The lack of effect of TBBPA on caspase-3 activation further strengthen previous results, where TBBPA have been shown not to induce neurotoxic effects on behavior and protein levels after neonatal exposure. 2600 SEX SPECIFIC EFFECTS ON NEUROGLIAL DEVELOPMENT FOLLOWING DEVELOPMENTAL EXPOSURE TO PCBs: IMPLICATIONS FOR ADHD RISK IN MALES. R. F. Seegal 1, 2 , K. Andrews 1 , S. Sanchez-Morrissey 1 , K. O. Brosch 1 and V. M. Miller 1, 2 . 1 Wadsworth Center, New York State Department of Health, Albany, NY and 2 School of Public Health, University at Albany, Albany, NY. Developmental exposure to environmental toxicants, including polychlorinated biphenyls (PCBs), is associated with an increased risk of ADHD which is four-fold more likely in boys. Hypothyroidism is also a risk factor for ADHD and PCBs sig-
nificantly reduce circulating thyroid hormones. Imaging studies implicate the corpus callosum and the cerebellum in the pathophysiology of ADHD with the later structure contributing to the control of cognitive function. We asked whether gender and PCB exposure interact to alter the developmental trajectory of oligodendrocyte precursor cells (OPCs) in the cerebellum into either oligodendrocytes, by measuring myelin basic protein (MBP), or astrocytes, by measuring glial fibrillary acidic protein (GFAP). We exposed timed pregnant Long Evans dams to PCBs from gestational day 6 until weaning and obtained (i) sera for measurement of circulating thyroxine (T4) and IL-6 levels, the latter implicated in white matter development, and (ii) cerebellar tissue from both male and female offspring at 7, 14, 21 and 42 days of age. Although PCBs significantly reduced T4 levels, they did so equally in male and female offspring. Both IL-6 and cerebellar MBP levels were significantly elevated only in males. While cerebellar GFAP levels were lower in PCB exposed males and higher in females. These data demonstrate that PCBs alter IL-6 and differentiation of OPCs in a sex specific manner leading to greater expression of cerebellar MBP in males and GFAP in females. These findings may aid in understanding the role of environmental contaminants in the etiology of ADHD and elucidate potential mechanisms responsible for the greater incidence of ADHD in boys. Future studies will examine interactions between thyroidal and gonadal hormones and cytokines in the etiology of ADHD and related disorders. Supported in part by NIEHS grant ES015688-01 to RFS. 2601 PRE-PULSE INHIBITION AND THE STARTLE RESPONSE IN GENETICALLY DIFFERENT PCB- TREATED MICE. C. P. Curran, B. Hays, E. Altenhofen, R. Floyd and A. Mynhier. Biological Sciences, Northern Kentucky University, Highland Heights, KY. Polychlorinated biphenyls (PCBs) are ubiquitous industrial chemicals banned in the 1970s due to their wide-ranging toxicity. Children exposed in utero and lactationally have a higher risk of learning, memory, behavioral and auditory deficits. The goal of our research is to identify genes which affect susceptibility to these pervasive pollutants. The liver enzyme CYP1A2 can sequester toxicants such as dioxins and coplanar PCBs. The aryl hydrocarbon receptor (AHR) binds dioxins and coplanar PCBs, initiating transcription of several genes including CYP1A2. Rodent studies have demonstrated that Cyp1a2(+/+) and poor-affinity Ahr d mothers can protect their offspring from developmental dioxin and PCB exposure compared with Cyp1a2(-/-) knockout and high-affinity Ahr b1 mice. Our previous research found genetic differences in the Acoustic Startle Response in PCB-treated mice when comparing three mouse lines varying at the Ahr and Cyp1a2(-/-) loci. Our current work extends those findings by using a newly developed mouse line, Ahr d Cyp1a2 (- /-), and the background strain Ahr b1 Cyp1a2(+/+) as a comparison group. Pregnant dams were treated at gestational day 10.5 (GD10.5) and postnatal day 5 (PND 5) with an environmentally relevant mixture of PCBs or the corn oil vehicle. Offspring were tested at 60 days of age. We measured the baseline startle response to a 110db stimulus and examined pre-pulse inhibition (PPI) using pre-pulse tones of 74 and 76db. There was a trend toward significance for a genotype x treatment interaction (P=0.073) with PCB-treated Ahr d Cyp1a2 (-/-)mice showing an enhanced baseline startle response. All groups showed normal sensorimotor gating; however, PCBtreated Ahr d Cyp1a2 (-/-)mice had significantly reduced pre-pulse inhibition at the 74dB level compared with corn oil treated controls. The knockout mice also had significantly reduced pre-pulse inhibition compared with wild type mice under both the 74db (P
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The Toxicologist Supplement to Toxi
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The Toxicologist Supplement to Toxi
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1 BIODEGRADABLE MATERIALS FOR TISSU
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that genetic toxicology data are ge
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well-orchestrated lung inflammation
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scribed in the literature. We have
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years ago). We will illustrate how
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involved in the biodegradation proc
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stem cells but rather a treatment i
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additional compound showed agreemen
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82 COMPARISON OF 3H-THYMIDINE INCOR
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irritants. While in practice these
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alleles are especially vulnerable t
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109 CD4+ T CELL INTRINSIC TNF RECEP
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118 TO STUDY THE SIGNAL TRANSDUCTIO
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PAHs, such as dioxins, are prevalen
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containing substituents and/or hydr
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146 COMPUTATIONAL MODELING FOR QT P
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suggest that the combination of too
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164 TRANSLOCATOR PROTEIN (18 KDA) (
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function as a metal binding protein
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laboratory has demonstrated that NR
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known. The aim of this study was to
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from 5 to 28 days in duration) in e
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positive cells, caspase-3 activatio
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creased level in the 46 kDa preproe
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invasiveness at concentrations repr
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thracene (DMBA,50 μg in acetone, a
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247 CO-CARCINOGENESIS OF N, N- DIET
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sponds to the endosomal dsRNA that
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ODD in both WT (maximum 177% of con
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Lastly, using p53siRNA cells, p53 w
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its receptor Mpl to exert its funct
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294 LOW LEVEL OF LEAD CAN INDUCE PH
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lunar surface presented potential h
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lar about cellular export mechanism
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DNA in the kidney medulla, grandula
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5.00 and 7.50 mg/kg/day by oral gav
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events and carcinogenesis. Here we
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tinization of cells of the hair fol
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358 CHARACTERIZATION OF GENOME-WIDE
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RNAi were also performed to identif
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376 A FUNCTIONAL CROSSTALK BETWEEN
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UGT1A gene induction, while this re
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tivity, specifically peroxisome pro
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and cytotoxic effects; however, its
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histone deacetylase that is necessa
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ment. Paradoxically, buthionine sul
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drug leflunomide and its major (A77
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442 GENE EXPRESSION AND MORPHOLOGIC
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451 INHIBITION OF THE MITOCHONDRIAL
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460 SULFORAPHANE PREVENTS ACETAMINO
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drophilic/lipophilic balance. Other
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pharmacokinetic and toxicological p
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489 USE OF ‘OMICS DATA TO IMPROVE
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498 APPLICATION OF AGE-SPECIFIC ADJ
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507 A DOSE VOLUME TOLERABILITY STUD
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involved the use of an acute inflam
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sorption in the gastrointestinal (G
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(ABC) transporters actively transpo
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545 BEHAVIORAL EFFECTS OF REPIN IN
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a blood pressure phenotype that res
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and inhalation exposure system that
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and lethality associated with these
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position, on vascular reactivity an
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therefore more accurate and reprodu
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commercial chrysotile product that
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elative to their controls. ST-depre
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ats. The majority of the studies fo
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in the China Jintan Child Cohort St
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corneum thickness, cellular epiderm
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645 EVALUATION OF THE IN VITRO EPIS
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654 TCDD ADSORBED ONTO NATURAL AND
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tion revealed no test article-relat
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671 INFLAMMATION AND TISSUE DAMAGE
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model, ethanol was found to inhibit
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689 ENHANCED SUPPRESSIVE FUNCTION O
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NAC + LPS yielded different levels
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707 LIFE-STAGE PBPK MODELS FOR MULT
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downstream of the apical endpoint o
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726 UPDATED ALUMINUM PHARMACOKINETI
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global parameter sensitivity analys
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and renal inflammation induced by 2
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754 PLASMA, URINE, AND TISSUE CONCE
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cently characterized transporter OA
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exposure system was developed from
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lood cell mass and decrease in urin
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practical alternatives to MC in non
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imals dosed with 167 mg/kg THU alon
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and organ weights, clinical signs a
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yet is induced in most bladder and
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830 RISK ASSESSMENT OF THE SPILL: C
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knowledgebase creation. Results are
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852 UNDERSTANDING STRUCTURAL AND PH
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for integrating epidemiology and an
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motor activity, including age of th
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y partial purification of urine (fr
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pacity for self-renewal and may dif
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sue. The depth of our analysis led
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910 IMPLEMENTING CALIFORNIA’S GRE
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concentrations in six tissues and b
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934 THE FDA’S LIVER TOXICITY KNOW
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943 GENOME-WIDE DNA METHYLATION DIF
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membrane localization and subsequen
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trols, respectively. Subtoxic and t
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survival using both smoking regimes
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as non-, weak, moderate, or strong
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988 NNK-INDUCED CYTOKINE ALTERATION
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group (one-way ANOVA, p90 % viabili
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ered as an organ involved in xenobi
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Transport of CPZ across the Caco-2
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estrous cycle and sexual behavior d
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mRNA expression levels. Collectivel
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1043 THE EFFECTS OF ENDOCRINE DISRU
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1052 MONO-2-ETHYLHEXYL PHTHALATE IN
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Results: MC was variable within and
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UtSMCs. Phosphorylation of FoxO1 wa
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nonpregnant and pregnant diabetic m
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1089 PFOA-INDUCED LIVER EFFECTS IN
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events in the liver. AZD9056 was ev
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The peppermint oil caused a concent
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OA did not affect food consumption.
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1126 PERSISTENT DEVELOPMENTAL ARYLH
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1135 BACH2 BINDING TO Prdm1 AS A ME
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The purpose of this project was to
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one marrow. Since Chk1 is an attrac
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1163 THE MRNA AND MIRNA PROFILE OF
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have now compared the IC50 values b
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1181 ELUCIDATION OF FACTORS DETERMI
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enced by pre-exposure to cigarette
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if abnormal PF was associated with
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weight (P=0.016) and small for gest
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portant cause of death, compared to
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posure groups. However, the differe
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Naphthalene is routinely analyzed i
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1245 SEASONAL CHARACTERIZATION OF H
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1255 URINARY T, T MUCONIC ACID LEVE
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modating a reliable data evaluation
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enzoquinone generate ROS and arylat
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teins (e.g. C3, 4, and 5, APOB, VDB
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1293 TRANSFORMING GROWTH FACTOR BET
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mation was decreased to the same le
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1312 EVALUATION OF THE SENSITIVITY
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luted OFR and CRL. Culture media ex
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urinary TCPy levels, blood and brai
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activity. The dose-response curves
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mice, each with 4 dose groups. One
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exposure to both ATR and DACT has a
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third tetratricopeptide repeats (TP
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7d. 28d after TMT injury there was
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subunits. Each cell type was treate
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1394 COMPARATIVE EFFECTS OF METHYLM
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1403 GENOTOXICITY AND PRE-NEOPLASTI
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vated only in high-dose-treated ani
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1421 DOSE-RESPONSE OF NAPHTHALENE-I
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cisplatin; 1.2-, 1.9- and 2.9-fold
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Day 11 and started to recover on Da
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1448 DEVELOPMENT OF A METHOD FOR QU
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1457 GLOBAL GENE PROFILING REVEALS
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cluding mouse and human macrophage,
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model of lung inflammation and host
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1484 NANOTOXICOLOGY AND NANOHEALTH
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throughput in vitro approach was us
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1502 IMMUNOLOGICAL ASPECTS OF AN AN
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(CIA) and the Streptococcal cell wa
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sitizers were 100% concordant among
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1530 MINIMAL RISK LEVELS FOR STYREN
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ical groups in the field of regulat
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vitro with this potentially insect-
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their performance on toxicological
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need for a better understanding of
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1577 AN IN VITRO MODEL SYSTEM FOR A
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gene expression post-transcriptiona
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1595 GENE EXPRESSION PROFILE OF RAT
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to confirm a hepatotoxic property o
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1613 AN INVESTIGATION OF THE CLEARA
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its nuclear translocation was reduc
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were collected from TK animals at d
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egulated targets were selected for
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U/L after tetracycline. Minocycline
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peri-pubertal FasL-/- mice show a d
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showed similar levels of apoptosis
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1676 TWO BIOMARKERS FOR EVALUATION
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motifs selected. This system was ap
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1693 VOC SERUM LEVELS IN THE GENERA
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1702 DOES THE CLOCK MAKE THE POISON
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those with high nickel content are
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isk assessment. However, unique cha
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model of APAP metabolism and glutat
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logically & morphologically similar
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posure, blood chemistry was analyze
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elated to oxidative stress by measu
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ostasis), but work is needed to tra
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tokine products during carcinogenes
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ways as chemical stressors and, the
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toxicity of nanomaterials relates s
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1815 MEASURING COMPOUND SELECTIVITY
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1825 EFFECTS OF METABOLISM BY INTES
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cyanoacetic acid increased 2-3 fold
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1845 IS THE PROMISCUITY OF THE ARYL
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crorarray analysis. RT-PCR results
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are a family of phase-II biotransfo
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ous labs. As a result of positive s
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down the doses may produce more tox
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spectively. Below 100 mg/l of gemfi
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1900 GENERATION OF PRECISION CUT LI
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iomarkers or observation of lesions
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creased reticulocytes and lymphocyt
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statistically significant interacti
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monize sample preparation and analy
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NPC and sinonasal cancer in neighbo
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showed incidences of lung and nasal
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utylbenzenes, exhibited most simila
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1975 DIFFERENTIAL MODULATION OF CYP
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organic As to MMA(V) and a lower ca
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ole in invasion and metastasis of c
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3T3-L1 cells to low-levels of arsen
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2011 IDENTIFICATION OF A NOVEL VX M
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This work was supported by Cooperat
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2029 EFFICACY OF ENDOTRACHEAL ADMIN
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Diazepam injections and its combina
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2047 ESTERASE ACTIVITIES AND HEMOST
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nanoparticle-induced toxicity progr
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house, were iv infused into rats ov
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een explored. This study investigat
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croscopic analysis revealed that on
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egg yolk collected from turtles inh
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consistency of results in both expe
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2111 CYTOCHROME P450 3A5 GENOTYPE I
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esidues of organophosphates or thei
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manganism. Recent work from our lab
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Aβ1-40 in CSF and hippocampus in P
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2147 CATALASE MANIPULATIONS MODIFY
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ation based on real-world exposure
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NPs. Aggregation of citrate-stabili
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2175 THE ROLE OF SURFACE CHEMISTRY
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seen rapid uptake in biological ima
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effect on uterine weight or vaginal
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dicating widespread exposure. While
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components into the liver parenchym
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2223 ISOLATION AND DETECTION OF RIC
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stored (-20 celsius degree). The co
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2241 DDA, A BIOMARKER FOR ENVIRONME
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2249 INTERACTION BETWEEN DIETARY SE
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2258 PHARMACOKINETICS, EXCRETION BA
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2267 SENSITIVE AND SPECIFIC FLUORES
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2276 METABOLISM AND DISPOSITION OF
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ment of hypertension in companion a
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for the propyl series can be used f
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2304 IN VITRO EXPOSURE AND EVALUATI
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2313 THE SYNERGISTIC EFFECT OF SODI
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genes that play a crucial role in M
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2330 THE ROLE OF TRANSFORMING GROWT
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ined following up to 96 h continuou
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Page 515 and 516: individuals. Week 6 results were qu
Page 517 and 518: functionality of photosystem II and
Page 519 and 520: wild mice (Mus musculus) from areas
Page 521 and 522: 2406 TOXICITY AND BIOACCUMULATION O
Page 523 and 524: Isocitric acid is the acid in the h
Page 525 and 526: 2425 EFFECTS OF FUMONISINS IN ETHAN
Page 527 and 528: centration(μg/g) were: 5.1-95.3; 2
Page 529 and 530: 2445 AUTOPHAGY IN DEVELOPMENT: A LI
Page 531 and 532: sures to inhaled Mn in dust. Nevert
Page 533 and 534: 2466 CRITICAL EVALUATION OF ANIMAL
Page 535 and 536: elationships predict that resting r
Page 537 and 538: 2489 COMPARATIVE TOXICITY OF BIODIE
Page 539 and 540: 2497 TRANSCRIPTIONAL REGULATION OF
Page 541 and 542: 2506 TOXICOLOGICAL CONSIDERATIONS O
Page 543 and 544: launched with the aim of developing
Page 545 and 546: forms mRNA expression levels were a
Page 547 and 548: 2534 CUTANEOUS WOUND HEALING IN THE
Page 549 and 550: wells (0, 1, 5, 10, 25, 50, 100, an
Page 551 and 552: 2553 AN ORGANOTYPIC MICROLIVER PLAT
Page 553 and 554: serum-free media. At 24 hrs, the gr
Page 555 and 556: 2572 INCREASED ARSENIC BIOACCESSIBI
Page 557 and 558: nology to develop improved methods.
Page 559: tuna, swordfish, or mako shark (3.5
Page 563 and 564: grouped into 9 observation periods
Page 565 and 566: histopathological or biochemical ev
Page 567 and 568: exhibited a hyperactive phenotype,
Page 569 and 570: the search of effective drugs for e
Page 571 and 572: 2644 COVALENT BINDING OF 14 C 2-MET
Page 573 and 574: aries targeting all transcription f
Page 575 and 576: (p 9 weeks) and CSC phenotype acqui
Page 577 and 578: 2673 IMMUNE-MEDIATED VASCULAR INJUR
Page 579 and 580: for risk identification and charact
Page 581 and 582: to control toxicant delivery in tob
Page 583 and 584: Author Index (Continued) The numera
Page 611 and 612:
Keyword Index (Continued) Arsenite
Page 613 and 614:
Keyword Index (Continued) Covalent
Page 615 and 616:
Keyword Index (Continued) flow cyto
Page 617 and 618:
Keyword Index (Continued) innate im
Page 619 and 620:
Keyword Index (Continued) nanoparti
Page 621 and 622:
Keyword Index (Continued) preservat
Page 623 and 624:
Keyword Index (Continued) Thrombocy
Page 625 and 626:
Toxicological Sciences The Official
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The Toxicologist - Society of Toxicology

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