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2586 ENHANCED NRF2 ACTIVATION ATTENUATES FASTING-INDUCED FATTY LIVER. J. Xu 1 , J. Moscovitz 1 , M. Yamamoto 2 and A. L. Slitt 1 . 1 Biomedical and Pharmaceutical Sciences, University of Rhode Island, Kingston, RI and 2 Medical Biochemistry, Tohoku University Graduate School of Medicine, Sendai, Japan. Non-Alcoholic fatty liver disease (NAFLD) affects 20% of the U.S. population. Approximately 15 to 20% of patients with fatty liver develop a severe form of hepatic disease known as nonalcoholic steatohepatitis (NASH). The high prevalence of fatty liver and NASH warrants research into the signaling mechanisms responsible for hepatic lipid accumulation. Nuclear factor-erythroid 2-related factor 2 (Nrf2, Nfe2l2), a bZIP family transcription factor, is protective against xenobioticrelated toxicity and chemical-induced carcinogenesis. However little information about Nrf2 function on lipid metabolism is available. Male C57BL/6 and Keap1- KD mice were fed ad libitum or withheld food (fasted) for 24 hours to determine whether enhanced Nrf2 activation in liver could prevent fasting-induced steatosis. In C57BL/6 mice, fasting increased hepatic triglyceride content 240%, and serum triglyceride concentrations 21% compared to fed mice. In contrast, Keap1-KD mice were resistant to fasting, with hepatic triglyceride increased 1.3 fold, and serum triglyceride levels decreased about 6% compared to fed Keap-KD mice. Fasting increased serum free fatty acid levels 110% in C57BL/6, but only 61% Keap1-KD mice. Keap1-KD mice exhibit decreased basal expression of FAS, ACC-1 and SCD-1 in liver, genes important for regulating lipid synthesis, compared to C57BL/6 mice. Fasting decreased FAS, ACC-1 and SCD-1 mRNA expression in liver to a much greater degree in Keap1-KD compared to C57BL/6 mice, 54%, 31% and 81% respectively. These data demonstrated that Keap1-KD mice are resistant to fasting-induced steatosis. Future work will focus on the mechanism by which Nrf2 activity modulates fatty acid synthesis gene expression in liver and promotes resistance to fasting. In conclusion, enhances Nrf2 activation by Keap1 knockdown prevents fasting induced steatosis, pointing to an important function on lipid metabolism (NIH 3R01ES016042-02S2). 2587 PROTECTION OF RETINAL VESSELS FROM HYPEROXIC INJURY BY β-NAPHTHOFLAVONE (BNF) IN NEWBORN RATS. X. Couroucli, Y. W. Liang, L. Wang, W. Jiang and B. Moorthy. Pediatrics, Baylor College of Medicine, Houston, TX. Supplemental oxygen administration, which is routinely encountered in the treatment of premature infants suffering from respiratory distress, contributes to retinopathy of prematurity (ROP). In this study, we tested the hypothesis that exposure of newborn rats to a combination of β-napthoflavone (BNF) and hyperoxia would alleviate retinopathy and abnormal neovascularization compared to those exposed to hyperoxia alone. Newborn Fisher 344 rats were maintained in room air or exposed to hyperoxia ([gt] than 95% O2) for 7 days. Some animals were treated i.p. with BNF (20 mg/kg) or vehicle (saline), once daily for the first 4 days of hyperoxic exposures, and were sacrificed at selected time points after termination of hyperoxia. Vascular densities of flat mounted retinas were assessed. mRNA expression of VEGF, its receptors (VEGFR-1/sFLT-1 and VEGFR-2), and cytochrome P4501B1 (CYP1B1) was determined by real time RT-PCR. Immediately after 7 days of exposure to hyperoxia, we observed severe vaso-obliteration, compared to the hyperoxia + BNF. Seven to thirty days after termination of hyperoxia, the animals displayed abnormal retinal vessels, whereas those given BNF+ hyperoxia showed significantly lesser extent of neovascularization. At the later time points, VEGF mRNA expression in the hyperoxia group was much higher than that of the BNF+ hyperoxia group. On the other hand, the expression of VEGFR-1 and sFLT-1, but not VEGFR2, was upregulated by BNF + hyperoxia, compared to the hyperoxia only group. Interestingly, retinal CYP1B1 expression was also augmented in the BNF + hyperoxia group. Our study supported the hypothesis that BNF protects retinas from oxygen-induced retinopathy, and that upregulation of VEGFR1 as well as CYP1B1 contributes to the retinoprotective effects of BNF. Further studies are needed to elucidate the mechanisms of the protective action of BNF, which could lead to clinical trials in infants who are at risk of developing ROP. 2588 HYPOXIA-ISCHEMIA TRIGGERS BAX PHOSPHORYLATION, TRANSLOCATION, AND RESULTANT CELL DEATH PHENOTYPE. S. Krishnan 1 , M. Gill 2 and R. Perez-Polo 1 . 1 Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, TX and 2 Northwestern University, Chicago, IL. Sponsor: J. Ward. Hypoxia-ischemia (HI) in the neonatal brain can lead to DNA damage, inflammation, and cell death, all of which ultimately produce neurodevelopmental deficits. Neuronal cell death caused by HI is characterized by an array of cell death pheno- 554 SOT 2011 ANNUAL MEETING types with necrotic and/or apoptotic characteristics, in which the Bcl-2 family of proteins, including Bax, play a role. Here, we use well-established in vivo and in vitro models of neonatal cerebral HI, and standard molecular techniques to investigate whether HI-dependent phosphorylation of Bax at Ser163, Thr167, and/or Ser184 residues determines Bax multi-organelle localization and correlation with organelle-specific cell death signaling after HI. In rotenone-treated SH-SY5Y cells, a significant increase in p-BaxThr167 was found in mitochondrial fractions when compared to control ½ hour after treatment. In vivo, we also found an increase in p-BaxThr167 in the nucleus at 1 hour after treatment, which correlates with a decrease in mitochondrial p-BaxThr167. This may indicate that phosphorylation of BaxThr167 leads to Bax translocation to the nucleus from mitochondria. We also observed an increase of p-BaxThr167 in cytosolic fractions at 1 hour, indicating that phosphorylation of BaxThr167 may be generally responsible for Bax translocation out of mitochondria. Lastly, no significant changes in p-BaxSer163 were observed up to 6 hours after HI. Interestingly, we observed a decreasing trend in cytosolic p-BaxSer163 gradually from 0 to 6 hours, as well as a significant decrease in p-BaxSer163 in the mitochondrial fraction at 6 hours after HI. These data suggest a role for phosphorylation in the translocation of Bax after HI. Understanding the mechanisms of Bax translocation will aid in the rational design of specified therapeutic strategies which could potentially involve altering Bax subcellular redistribution to decrease the irreversible trauma resulting from a prolonged inflammatory response. 2589 ESTIMATING THE GLOBAL PUBLIC HEALTH IMPLICATIONS OF ELECTRICITY AND COAL CONSUMPTION. J. M. Gohlke 1, 4 , R. Thomas 4 , A. Woodward 3 , D. Campbell-Lendrum 2 , A. Pruss-Ustun 2 , S. Hales 2 and C. J. Portier 4 . 1 Environmental Health Sciences, University of Alabama at Birmingham, Birmingham, AL, 2 Public Health and Environment, World Health Organization, Geneva, Switzerland, 3 Population Health, University of Auckland, Auckland, New Zealand and 4 Laboratory of Molecular Toxicology, NIEHS, Research Triangle Park, NC. The growing health risks associated with greenhouse gas emissions has resulted in a global call for development of new energy policies emphasizing efficiency and lowcarbon energy cycles, yet the economic and social development often associated with access to affordable energy are important considerations for improving health in developing nations. Here we assess the relationship between electricity consumption and health outcomes. Using time-series datasets across 41 countries with varying development trajectories between 1965 and 2005, an autoregressive model of life expectancy (LE) and infant mortality (IM) was developed based on electricity consumption, coal consumption, and previous year’s LE or IM. The model predicts increased electricity consumption is associated with reduced IM for countries starting with relatively high IM (above 100 per 1000 births), whereas LE was not significantly associated with electricity consumption in any of the models. In addition, the model suggests increasing coal consumption that is not explained by electricity use is associated with increased IM and reduced LE. These results are compared with previously published estimates of disease burdens attributable to energy-related environmental factors including indoor and outdoor air pollution, and water and sanitation. In addition, prediction of health impacts from an integrated air pollution emissions health impact model for coal-fired power plants is compared to the time-series model results. Consistency across analyses of historical time-series and health impact models suggest health benefits may be related to increasing electricity consumption in those countries with very high IM, while negative health impacts of coal consumption are predicted across all countries. 2590 SELENIUM FROM OCEAN FISH PREVENTS METHYLMERCURY TOXICITY. L. Raymond and N. Ralston. Energy & Environmental Research Center, University of North Dakota, Grand Forks, ND. Supplemental selenium (Se) has been known to counteract mercury (Hg) toxicity since 1967, but the mechanisms of this protective effect have only recently become clear. Methylmercury (MeHg) is a highly specific irreversible inhibitor of Se-dependent enzymes (Se-enzymes). Supplemental dietary Se replenishes Se lost to MeHg binding, thereby maintaining normal Se-enzyme activities. Rationale and scope; Our prior animal studies have shown that the normal range of dietary Se (as sodium selenite) is effective in preventing and reversing MeHg toxicity. Since ocean fish are among the richest sources of dietary Se, we hypothesized that their Se contents would protect against the adverse effects otherwise associated with MeHg exposures from seafood consumption. Experimental procedure; In this study, 120 weanling male Long Evans rats were fed diets containing either low or high MeHg (0.5 or 50 nmol MeHg/g). These diets were augmented with either sodium selenite (~0.1, 1.0, or 10 nmol Se/g) or Se from delipidated protein isolates from bigeye
tuna, swordfish, or mako shark (3.5, 2.3, and 2.1 nmol Se/g respectively). Diets were prepared with torula yeast protein or delipidated fish protein isolates added as 10% of the total diet to replace an equivalent amount of torula yeast protein; (2 Hg levels x 6 Se diets = 12 dietary treatments, 10 rats per group). Contributions of MeHg from the tuna, swordfish, and shark supplemented diets were (1.6, 2.3, and 3.6 nmol MeHg/g respectively). Rats were fed low Se torula yeast based diets for 5 weeks to deplete their tissue Se reserves. Rats were then switched to their assigned dietary treatments for the duration of the study. Results; Rats fed high MeHg, low Se diets showed growth inhibition after 4 weeks, and hind limb crossing after 9 weeks. Rats fed all other dietary treatments grew normally and did not show symptoms of MeHg toxicity. Conclusion; The Se in ocean fish prevented MeHg toxicity in rats fed otherwise toxic levels of MeHg, even though ocean fish contributed additional MeHg levels in the diets. 2591 IS CHELATION THE MECHANISM OF ACTION OF P- AMINOSALICYLIC ACID (PAS) IN THE TREATMENT OF MANGANISM? V. Petion, J. Rios, J. Mayne, J. Hilaire, D. Nicholson, D. Skeete, K. Ruddock, M. A. Carroll and E. J. Catapane. Biology, Medgar Evers College, Brooklyn, NY. Manganese (Mn) is potentially toxic in high concentrations. Mining, welding and steel manufacturing can expose workers to high levels of Mn leading to Manganism, a Parkinsons-like disorder. The mechanism of toxicity is not fully understood and effective treatments are still being developed. Studies indicate the chelator EDTA is effective in alleviating Manganism. Recently another drug, paminosalicylic acid (PAS), is being used for treatment. However, the mechanism of action is unclear and is debated whether effects of PAS are due to anti-inflammation or chelation. We used dialysis tubing with a 100-500 MWCO pore size to mimic the passive elements of Mn movements across the blood-brain barrier. Tubing was set up with Mn plus PAS, EDTA, diaminocyclohexane (DACH) or glucose. Samples were taken outside the bags over time. Mn was measured with an Atomic Absorption Spectrometer. Less Mn was found to pass across bags containing Mn and EDTA as compared to control. The amounts of Mn outside of bags containing Mn with PAS or DACH was higher than controls. The paradoxical results with PAS and DACH are most likely explained because the Mn-PAS and Mn- DACH chelation complex is able to pass through the pore size, while the Mn- EDTA complex can not. Therefore, Mn is diffusing out of the bags by 2 driving forces, that driven by the free Mn concentration gradient and that driven by the Mn-PAS or Mn-DACH chelation complex gradients. We also used a spectrophotometric assay to determine Mn chelating properties of PAS. Mn solutions were exposed to varying concentrations of PAS. Free Mn was converted to permanganate. Levels of permanganate were measured spectrophotometrically. Results indicate PAS is an effective chelator of Mn. Increasing concentrations of PAS reduced levels of free Mn in solution. This information can be of importance with respect to passive transport mechanisms of the blood-brain barrier and can help to clarify the mechanism of action of PAS in alleviating the symptoms of Manganism. 2592 NEUROIMAGING OF MANGANESE TOXICITY: THERAPEUTIC EFFECT OF PARA-AMINO SALICYLIC ACID IN A RAT MODEL. A. Epur 1, 2 , J. Xu 1, 2 , W. Zheng 1 and U. Dydak 1, 2 . 1 School of Health Sciences, Purdue University, West Lafayette, IN and 2 Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, IN. Excessive exposure to Manganese (Mn) is known to cause parkinsonism. Earlier studies have shown that para-aminosalicylic acid (PAS) effectively alleviates symptoms in Mn-induced parkinsonism patients and reduces Mn levels in the rat brain. To study the underlying mechanism, changes in the neurochemical profile of the rat brain with or without PAS treatment after Mn exposure were studied using magnetic resonance spectroscopy (MRS) at 9.4T. The rats (220g at start) were divided into three groups: Group P (N=8) received 6 weeks of ip Mn injections (6 mg Mn/kg bodyweight, 5 d/wk), followed by 4 weeks of sc PAS injections at 200 mg/kg, 7 d/wk. Group M (N=8) also received 6 weeks of Mn injections, followed by 4 weeks of saline injections. Group C (controls, N=4) received saline injections throughout the study. Short echo-time MRS data was acquired in all animals at baseline, wk 6 and wk 10 in the thalamus, frontal cortex and hippocampus. Our data showed a significant decrease of the antioxidant glutathione (GSH) with Mn exposure in the thalamus (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
Page 505 and 506:
2330 THE ROLE OF TRANSFORMING GROWT
Page 507 and 508: ined following up to 96 h continuou
Page 509 and 510: effect doses obtained with the rat
Page 511 and 512: diated transcriptional response of
Page 513 and 514: docrine disruptor activities of EDC
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: nology to develop improved methods.
Page 561 and 562: nificantly reduce circulating thyro
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 609 and 610:
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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