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were given IDB at dosages of 0, 30, 300, or 1000 mg/kg by oral gavage on a daily basis from GD 6 through 15. Effects in the 1000 mg/kg dose group included a transient body weight (bwt) loss for the dams, a slight decrease in mean fetal bwt, and a reduction in the incidence of cervical centrum #1 ossification. This study showed that IDB does not cause any significant developmental or maternal effects and the NOAEL for the minor effects observed was 300 mg/kg/day. In the two-generation reproductive toxicity study, IDB was given by dietary administration at 0, 1000, 3000, or 10000 ppm. There were no effects on reproductive performance (mating, fertility, copulation, and/or conception indices) or estrous cyclicity and no differences in spermatogenic parameters. Accordingly, the reproductive NOAEL was the highest dose tested of 10,000 ppm (equivalent to ~ 676 mg/kg/day for males and 641-1469 mg/kg/day for females). The NOAEL for minor offspring effects was 3000 ppm (equivalent to parental doses of ~195 mg/kg/day for males and 191-440 mg/kg/day for females) based on lower birth weights (PND 1) in the F1 and F2 offspring (10000 ppm) with lower bwt in the pre-weaning period. There were no effects on areola retention (male offspring) or ano-genital distance. Balanopreputial separation was delayed in the offspring from the 10000 ppm group, most likely due to the lower body weights in this group. These data showed that IDB does not influence endocrine-mediated reproductive processes. The overall conclusion from these studies was that IDB does not cause any significant developmental or reproductive effects. 1030 EXTENDED ONE GENERATION REPRODUCTIVE TOXICITY TEST WITH LEAD ACETATE. R. Kubaszky 1 , D. J. Esdaile 1 , T. Hanley 2 , P. Maslej 1 , D. Minnema 2 , J. Wright 3 and R. Lewis 3 . 1 Lab. Research Ltd., Veszprem, Hungary, 2 Syngenta Crop Protection, LLC, Greensboro, NC and 3 Syngenta, Jealotts Hill, Bracknell, United Kingdom. This study was designed to demonstrate the utility of an extended one-generation reproduction study in rats as proposed by draft OECD guideline and the Agricultural Chemical Safety Assessment (ACSA) Technical Committee of the ILSI Health and Environmental Sciences Institute (HESI) and by Cooper, et al (2006). Lead Acetate was provided in drinking water to the F0 adult Wistar rats throughout pre-mating, gestation, and lactation, and to the F1 generation to adulthood. The adults (24 rats/sex/group) were given concentrations of 0 (sodium acetate control), 100, 800 and 1700 ppm Pb, beginning 2 to 4 weeks prior to mating. Adults were mated and evaluated for standard in-life parameters, reproductive evaluations and histopathology. Resulting litters were culled and then assigned to 3 subgroups for clinical pathology/thyroid function/neurotoxicity, immunotoxicity and reproductive toxicity assessments. Selected pups were evaluated for developmental milestones, growth, neurobehavior assessments (FOB, grip strength, landing foot splay, motor activity), TDAR (sRBC) immunotoxicity, thyroid hormones, standard pathology and neurohistopathology. Dose-related decreases in water consumption were observed in F0 adults and F1 offspring at all concentrations. Decreases in sperm parameters (sperm counts, motility, and morphology) were observed in the F0 and F1 males. At the high dose, effects on early post-natal survival, lower pup body weights throughout lactation, decreases in anogenital distance, and delayed vaginal opening and preputial separation were observed. Although not statistically significant from control, slightly lower serum IgM levels were noted for the 1700 ppm males. Despite minimal evidence of neurobehavioral changes, neuropathological examination indicates a treatment-related peripheral neuropathology. This outcome illustrates the utility of using an integrated study design to investigate the various aspects of developmental neurotoxicity, immunotoxocity, and reprotoxicity. 1031 DISTRIBUTION OF ATRAZINE (ATR) AND METABOLITES IN THE WISTAR RAT FOLLOWING GESTATIONAL/LACTATIONAL EXPOSURES. T. E. Stoker 1 , A. Kamel 2 , Y. Qian 2 , L. Podhorniak 2 , R. Cooper 1 and L. Strader 1 . 1 Endocrinology Branch, U.S. EPA, Research Triangle Park, NC and 2 Analytical Chemistry Branch, U.S. EPA, Ft. Meade, DC. Gestational/lactational exposure to ATR is reported to alter reproductive/developmental function, yet our understanding of the transfer of ATR and/or its metabolites from the dam to the fetus/offspring is limited. Previously we examined the lactational transfer of C14-ATR, but specific ATR metabolites were not determined. In the current study, the distribution of atrazine and certain metabolites were determined in the dam, fetus and neonate following gavage exposure. Groups of dams were exposed to 0, 5 and 25 mg/kg ATR from (1) gestation day (GD) 18-20, (2) GD 14-20 or (3) GD 14- postnatal day (PND) 10. Two hours after the last dose, blood was drawn by cardiac puncture and the dam perfused with saline. GD20 fetuses were collected, along with the plasma, brain, adrenal glands and mammary glands of the dam. On PND 10 pups were separated from the dam for 2.5 h and 220 SOT 2011 ANNUAL MEETING then allowed to nurse 30 minutes before plasma, brain, adrenal and milk samples were collected. We measured ATR, desethyl ATR (DEA), desisopropyl ATR (DIA), diaminochlorotriazine (DACT), and hydroxyl ATR (OH-ATR) using LC/MS/MS. In the dams DACT accounted for the highest concentration in plasma and tissues, followed by DIA and DEA, with similar amounts present after both the 3 and 7 day exposure. ATR was present in very low amounts. OH-ATR was not detected in the majority of the samples. There was transfer of ATR from the dam to the fetus on GD 20 following both exposures and doses. Although all analytes were present in the GD20 fetus, DACT contributed to over 75% of the total. In the PND10 pups DACT accounted for 99% of the analytes which correlated well with the 91% of DACT found in the milk. This study demonstrates that DACT was the primary metabolite found in the dam and fetus/neonate at 2 h after the last dose and that ATR crossed both the placental and blood-brain barrier of the dam/neonate. This study does not reflect EPA policy. 1032 LOW-DOSE, GESTATIONAL EXPOSURE TO ATRAZINE DOES NOT ALTER POSTNATAL REPRODUCTIVE DEVELOPMENT OF MALE OFFSPRING. M. J. Fraites, D. S. Best, M. G. Narotsky and R. L. Cooper. Toxicology Assessment Division, NHEERL, ORD, U.S. EPA, Research Triangle Park, NC. There is growing evidence that xenobiotic exposure during the perinatal period may result in a variety of adverse outcomes when the developing organism attains adulthood. Maternal stress and subsequent exposure of the fetus to excess glucocorticoids may underlie these effects. Previous studies have demonstrated that high gestational doses of the chlorotriazine herbicide, atrazine (ATR), alter reproductive development of the male rat. ATR also acutely increases circulating glucocorticoids in adult rats. Therefore, the current studies investigated the development of male Sprague Dawley rat offspring following 1) lower doses of ATR during gestation and 2) an ATR dosing regimen designed to increase daily maternal glucocorticoid exposure. Timed-pregnant dams were administered 1, 5, 20, or 100 mg/kg/d ATR from gestation day 14–21 in a single oral gavage dose once per day (s.i.d) or the same dosage of ATR split into two doses per day (b.i.d.) to elevate glucocorticoid levels during the nadir and peak of the diurnal rhythm. Lower doses of ATR (1–20 mg/kg/d) administered s.i.d. or b.i.d. did not alter offspring body weight, neonatal testosterone production, timing of puberty, anogenital distance, adult testosterone or luteinizing hormone levels, or adult androgen-sensitive tissue weights. A similar level of maternal toxicity was observed at 100 mg/kg/d in both studies; however, this dosage administered b.i.d. resulted in significantly higher mortality of offspring after birth. Although birth weight was significantly reduced in high-dose litters of both studies (and remained lower through PND 59 in s.i.d. offspring), the reproductive development of these offspring was not altered. We conclude that gestational exposure to ATR at lower dosages (≤20 mg/kg/d) has no significant effect on pup survival or the male developmental endpoints assessed in these studies. Significant offspring mortality may have precluded observations of altered development in high-dose litters. This abstract does not necessarily reflect EPA policy. 1033 BISPHENOL A INDUCES ATRESIA IN MOUSE ANTRAL FOLLICLES. J. Peretz, R. K. Gupta and J. A. Flaws. Comparative Biosciences, University of Illinois Urbana-Champaigne, Urbana, IL. Bisphenol A (BPA) is a prominent chemical in the manufacturing of plastics and consumer goods. In a government funded human study (NHANES), BPA, with a half-life of at least 4-6 hours, was present in 95% of random urine samples, indicating that humans are constantly exposed to this chemical. Further, BPA has been found to cause adverse effects in numerous tissues throughout the human body, including ovarian antral follicles. Previous studies in our lab have shown that exposure to BPA inhibits antral follicle growth and steroidogenesis in the adult mouse ovary. However, the health of these BPA-treated antral follicles has not been evaluated. Thus, this study tested the hypothesis that BPA exposure (4.4μM to 440μM) induces atresia in antral follicles. To test this hypothesis, antral follicles were isolated from adult mice on postnatal day (PND) 32 and cultured continuously with either vehicle (dimethylsulfoxide; DMSO) or BPA (4.4, 44, or 440μM) in supplemented α–minimum essential media for 120h. After culture, the follicles were evaluated for atresia. Further, RNA was isolated from follicles, reverse transcribed into cDNA, and subjected to real-time PCR for various genes known to regulate atresia. The results indicate that BPA (440μM) significantly induced atresia in the antral follicles (DMSO: 1.3±0.15; BPA440μM: 4.0±0.0), significantly increased mRNA expression levels of the anti-apoptotic factor B-cell lymphoma 2 (Bcl2) (DMSO: 0.08±0.01; BPA440μM: 1.5±0.46ge; genomic equivalents (ge);n=3;p=0.02) and significantly decreased mRNA expression of the antioxidant superoxide dismutase (SOD) (DMSO: 0.27±0.15; BPA440μM: 0.07±0.33 ge;n=3;p=0.02) compared to DMSO controls. BPA exposure did not affect Bcl2-associated X protein or catalase
mRNA expression levels. Collectively, these data indicate that BPA causes atresia and alters some antioxidant factors in antral follicles. Support: NIHR01 ES019178, P20ES018163. 1034 EVALUATION OF A COMBINED DERMAL DEVELOPMENTAL AND PERINATAL/POSTNATAL REPRODUCTION TOXICITY STUDY OF PEA (PHENETHYL ALCOHOL) IN RATS—INCLUDING AN EXAMINATION SKELETAL VARIANTS POSTNATALLY. V. T. Politano 1 , E. M. Lewis 2 , A. M. Hoberman 2 , R. M. Diener 3 and A. Api 1 . 1 Research Institute for Fragrance Materials, Inc., Woodcliff Lake, NJ, 2 Charles River Laboratories Preclinical Services, Horsham, PA and 3 Argus International, Inc., Horsham, PA. The purpose of this study was to determine the reversibility of fetal skeletal alterations and delays in skeletal ossification following percutaneous, occluded application of neat doses of 140, 430 or 1400 mg/kg/day Phenethyl Alcohol (PEA) to four groups of 40 Crl:CD(SD) female rats on Gestation Days 7 through 20 (GDs 7 through 20). Twenty rats in each group were Caesarean-sectioned, while the remaining 20 rats in each group were allowed to deliver their litters. The highest dosage, 1400 mg/kg/day, was maternally and developmentally toxic. The developmental No-Observable-Effect-Level (NOEL) for Caesarean-delivered fetuses on GD 21 was 140 mg/kg/day. Higher dosages caused reductions in fetal weight and delays in skeletal ossification. The No-Observable-Adverse-Effect-Level (NOAEL) in the naturally delivered pups at Postpartum Day 21 (PPD 21) was 430 mg/kg/day. All delays in ossification and increased incidences of cervical ribs at the 7th cervical vertebrae observed on GD 21 in the Caesarean-delivered fetuses at 430 mg/kg/day were resolved by PPD 21 in the naturally delivered pups at 430 mg/kg/day. 1035 PREGNENOLONE CO-TREATMENT DOES NOT RESTORE GROWTH OF MOUSE ANTRAL FOLLICLES TREATED IN VITRO WITH THE MONO- HYDROXYLATED METABOLITE OF METHOXYCHLOR. Z. R. Craig, P. R. Hannon and J. A. Flaws. Comparative Biosciences, University of Illinois, Urbana, IL. Antral follicles are the functional units of the ovary and are responsible for ovarian steroidogenesis and ovulation of oocytes for fertilization. Chemicals that disrupt antral follicle function have the potential to lead to infertility. Mono-OH methoxychlor (mono-OH) is a metabolite of the model endocrine disruptor, methoxychlor (MXC). Mono-OH has been shown to inhibit growth, increase follicular death, and decrease steroidogenesis by cultured mouse antral follicles. Because synthesis of pregnenolone is considered the rate-limiting step in ovarian steroidogenesis, we hypothesized that co-treating antral follicles with pregnenolone would prevent mono- OH induced inhibition of follicle growth. To test this hypothesis, antral follicles isolated from female CD-1 mice (32-35 days old) were either untreated or exposed in vitro to dimethylsulfoxide (DMSO, vehicle control), or mono-OH (10 μg/mL) with and without pregnenolone (1 μg/mL) for 96 hours. Follicle diameters were monitored every 24 h and used to measure the rate of follicular growth (% change) over the 96-h culture period. In agreement with previous reports, antral follicles treated with mono-OH did not grow during the 96-h culture period when compared to DMSO-treated follicles (DMSO: 36.24 ± 6.7 % change; mono-OH: 6.10 ± 1.8 % change; P≤0.05, n=3). Co-treatment of antral follicles with pregnenolone did not prevent inhibition of growth in antral follicles treated with mono-OH (- 6.84 ± 1.8 % change; P>0.05; n=3). Finally, pregnenolone treatment did not affect growth of follicles treated with DMSO vehicle (30.93 ± 2.7 % change; P>0.05). Collectively, these results suggest that mono-OH potentially inhibits follicular growth by a mechanism independent of availability of pregnenolone for steroidogenesis. Funded by NIH R01 ES012893, ES019178 and Billie A. Field Fellowship in Reproductive Physiology. 1036 DI-(2-ETHYLHEXYL) PHTHALATE AND MONO-(2- ETHYLHEXYL) PHTHALATE INHIBIT GROWTH OF OVARIAN ANTRAL FOLLICLES THROUGH AN OXIDATIVE STRESS PATHWAY. W. Wang, Z. R. Craig, M. S. Basavarajappa, R. K. Gupta and J. A. Flaws. Comparative Bioscience, University of Illinois, Urbana, Urbana, IL. Phthalates are synthetic plasticizers used widely in plastics and many other common consumer products. Exposure to these chemicals can cause developmental and reproductive toxicity. Our previous studies show that di-(2-ethylhexyl) phthalate (DEHP) and its active metabolite, mono-(2-ethylhexyl) phthalate (MEHP), can inhibit follicle growth and cause atresia of antral follicles. However, the mechanisms by which DEHP and MEHP inhibit growth and cause atresia are not fully understood. Oxidative stress has been linked to phthalate-induced toxicity in non-reproductive tissues. Thus, we tested the hypothesis that DEHP and MEHP inhibit the growth of antral follicles through an oxidative stress pathway. Antral follicles were isolated from ovaries of adult CD-1 mice (age 30-35 days) and cultured with vehicle control (dimethylsulfoxide [DMSO]), DEHP (1-100μg/ml) or MEHP (0.1- 10μg/ml) ± N-acetyl cysteine (NAC, an antioxidant) (0.5-2mM) for 96h. During culture, follicle size was evaluated daily as a measurement of follicle growth. At the end of culture, follicles were subjected to measurement of the expression of various key antioxidant enzymes: Cu/Zn superoxide dismutase (SOD1), glutathione peroxidase (GPX), and catalase (CAT) by quantitative real-time PCR. The results indicate that DEHP (1-100μg/ml) and MEHP (1-10μg/ml) inhibited the growth of follicles compared to DMSO controls and that NAC (0.5-2mM) blocked the ability of DEHP and MEHP to inhibit follicle growth. DEHP and MEHP reduced the expression of SOD1, whereas NAC blocked the effects of DEHP and MEHP on SOD1 expression. However, the expression of GPX and CAT were not affected by the treatments. Collectively, these data suggest that DEHP and its active metabolite, MEHP, inhibit follicle growth by inducing oxidative stress. (Supported by R01 ES 019178) 1037 METHOXYCHLOR ALTERS STEROIDOGENIC ENZYMES IN CULTURED MOUSE ANTRAL FOLLICLES. M. Basavarajappa, Z. Craig, B. Karman, W. Wang and J. Flaws. Comparative Biosciences, University of Illinois, Urbana, IL. The organochlorine pesticide methoxychlor (MXC) is a known endocrine disruptor that affects adult female rodents by causing reduced fertility, persistent estrus, and ovarian atrophy. MXC is widely used in many countries to prevent and kill the various species of insects that attack crops, vegetables, fruits, and animals. Previously, we demonstrated that MXC reduces estradiol, testosterone, and androstenedione levels in antral follicles. The goal of the present study was to determine whether MXC reduces estradiol and its biosynthetic hormone intermediates by altering steroidogenic enzymes present in the antral follicles of the ovary. To accomplish this goal, antral follicles were mechanically isolated from ovaries of CD1 female mice aged 35-40 days. The isolated antral follicles (10-15 per treatment) were cultured in supplemented α-minimum essential media in the presence of dimethylsulfoxide (control; DMSO) or MXC (1, 10, 100 μg/ml) for 96 h at 37°C and 5%CO2. At the end of the culture, follicles were snap frozen, RNA was isolated, cDNA was synthesized, and quantitative real time PCR was performed to measure the levels of steroidogenic enzymes present in antral follicles. Results were expressed as a ratio of starting quantity (SQ) of each gene mRNA to β-actin (Actn). The data indicate that MXC significantly decreases the expression of steroid acute regulatory protein (Star; DMSO=1.57±0.32, MXC10=0.31±0.03, MXC100=0.70±0.12 SQ; 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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modating a reliable data evaluation
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enzoquinone generate ROS and arylat
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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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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
Page 399 and 400:
1845 IS THE PROMISCUITY OF THE ARYL
Page 401 and 402:
crorarray analysis. RT-PCR results
Page 403 and 404:
are a family of phase-II biotransfo
Page 405 and 406:
ous labs. As a result of positive s
Page 407 and 408:
down the doses may produce more tox
Page 409 and 410:
spectively. Below 100 mg/l of gemfi
Page 411 and 412:
1900 GENERATION OF PRECISION CUT LI
Page 413 and 414:
iomarkers or observation of lesions
Page 415 and 416:
creased reticulocytes and lymphocyt
Page 417 and 418:
statistically significant interacti
Page 419 and 420:
monize sample preparation and analy
Page 421 and 422:
NPC and sinonasal cancer in neighbo
Page 423 and 424:
showed incidences of lung and nasal
Page 425 and 426:
utylbenzenes, exhibited most simila
Page 427 and 428:
1975 DIFFERENTIAL MODULATION OF CYP
Page 429 and 430:
organic As to MMA(V) and a lower ca
Page 431 and 432:
ole in invasion and metastasis of c
Page 433 and 434:
3T3-L1 cells to low-levels of arsen
Page 435 and 436:
2011 IDENTIFICATION OF A NOVEL VX M
Page 437 and 438:
This work was supported by Cooperat
Page 439 and 440:
2029 EFFICACY OF ENDOTRACHEAL ADMIN
Page 441 and 442:
Diazepam injections and its combina
Page 443 and 444:
2047 ESTERASE ACTIVITIES AND HEMOST
Page 445 and 446:
nanoparticle-induced toxicity progr
Page 447 and 448:
house, were iv infused into rats ov
Page 449 and 450:
een explored. This study investigat
Page 451 and 452:
croscopic analysis revealed that on
Page 453 and 454:
egg yolk collected from turtles inh
Page 455 and 456:
consistency of results in both expe
Page 457 and 458:
2111 CYTOCHROME P450 3A5 GENOTYPE I
Page 459 and 460:
esidues of organophosphates or thei
Page 461 and 462:
manganism. Recent work from our lab
Page 463 and 464:
Aβ1-40 in CSF and hippocampus in P
Page 465 and 466:
2147 CATALASE MANIPULATIONS MODIFY
Page 467 and 468:
ation based on real-world exposure
Page 469 and 470:
NPs. Aggregation of citrate-stabili
Page 471 and 472:
2175 THE ROLE OF SURFACE CHEMISTRY
Page 473 and 474:
seen rapid uptake in biological ima
Page 475 and 476:
effect on uterine weight or vaginal
Page 477 and 478:
dicating widespread exposure. While
Page 479 and 480:
components into the liver parenchym
Page 481 and 482:
2223 ISOLATION AND DETECTION OF RIC
Page 483 and 484:
stored (-20 celsius degree). The co
Page 485 and 486:
2241 DDA, A BIOMARKER FOR ENVIRONME
Page 487 and 488:
2249 INTERACTION BETWEEN DIETARY SE
Page 489 and 490:
2258 PHARMACOKINETICS, EXCRETION BA
Page 491 and 492:
2267 SENSITIVE AND SPECIFIC FLUORES
Page 493 and 494:
2276 METABOLISM AND DISPOSITION OF
Page 495 and 496:
ment of hypertension in companion a
Page 497 and 498:
for the propyl series can be used f
Page 499 and 500:
2304 IN VITRO EXPOSURE AND EVALUATI
Page 501 and 502:
2313 THE SYNERGISTIC EFFECT OF SODI
Page 503 and 504:
genes that play a crucial role in M
Page 505 and 506:
2330 THE ROLE OF TRANSFORMING GROWT
Page 507 and 508:
ined following up to 96 h continuou
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 and 558:
nology to develop improved methods.
Page 559 and 560:
tuna, swordfish, or mako shark (3.5
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 585 and 586:
Page 587 and 588:
Page 589 and 590:
Page 591 and 592:
Page 593 and 594:
Page 595 and 596:
Page 597 and 598:
Page 599 and 600:
Page 601 and 602:
Page 603 and 604:
Page 605 and 606:
Page 607 and 608:
Page 609 and 610:
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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