Program - Society of Toxicology

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44 th Annual Meeting and ToxExpo Program Description WEDNESDAY #1648 3:40 EFFECTS OF ENVIRONMENTAL AIR POLLUTANTS ON POSTNATAL LUNG DEVELOPMENT. M. Fanucchi. School of Veterinary Medicine, University of California, Davis, CA. Wednesday Afternoon, March 9 1:30 PM to 4:30 PM Room RO3 SYMPOSIUM SESSION: ROLE OF CELL-CELL AND CELL-MATRIX INTERACTIONS IN REGULATION OF TOXICANT-MEDIATED CELL DEATH Chairperson(s): Ronald Tjalkens, Colorado State University, Fort Collins, CO. Endorsed by: Carcinogenesis SS* Mechanisms SS Neurotoxicology SS Cell-cell interactions are key for the regulation of cell survival, cell death and cell proliferation. Thus, an understanding of the interdependency between different tissue cellular compartments is key to elucidating mechanisms of cell death in response to toxicants. This symposium will provide a timely update on the molecular mechanisms of cell death and its regulation, including the role played by cell-cell and cell-matrix interactions. This will be illustrated by three examples of the role these pathways play in toxicant response in diverse tissues. The first speaker will consider how hepatic Kupffer cells are implicated in normal homeostasis and in hepatocarcinogenesis and can mediate both hepatocyte survival or cell death, depending on the toxic insult. The second speaker will address how gap junctional intercellular communication and cell adhesion are interrelated processes using the example of hexachlorobenzene which induces a down-regulation of connexins and E-cadherin in the liver of female but not male rats. The third speaker brings an external perspective and will discuss how the cell detects and signals damage leading to survival or cell death. The fourth speaker will address how neuronal trophic and communication functions are maintained by intricate coupling with associated astroglial cells with emphasis on neurotoxicants that selectively target astroglial cells, rendering neurons vulnerable to both physiologic and pathophysiologic stresses. The forth speaker will also summarise the symposium by uncovering similarities and common themes in the role of the cellular environment in determining cell fate after toxicant insult. This symposium will be of interest both to non-experts looking to understand this field and those with a specific interest in cell biology, carcinogenesis, neurotoxicology, apoptosis or cell-cell communication. #1649 1:30 ROLE OF CELL-CELL AND CELL-MATRIX INTERACTIONS IN REGULATION OF TOXICANT-MEDIATED CELL DEATH. R. Roberts 1 and R. Tjalkens 2 . 1 Safety Assessment, AstraZeneca, Alderley Park, United Kingdom and 2 Department of Environmental and Radiological Health Sciences, Colorado State University, Fort Collins, CO. #1650 1:40 CELL-CELL INTERACTIONS AND THEIR ROLE IN TOXICANT-INDUCED HEPATIC CELL DEATH. R. Roberts. Safety Assessment, AstraZeneca, Alderley Park, United Kingdom. #1651 2:20 MODULATION OF CELL-CELL INTERACTIONS BY EPIGENETIC HEPATOCARCINOGENS. M. Charbonneau, I. Plante, N. Raynal and D. G. Cyr. INRS-Institut Armand-Frappier, Universite du Quebec, Pointe-Claire, Montreal, QC, Canada. #1652 3:00 THE REGULATION OF APOPTOSIS: SURVIVAL SIGNALLING AND THE IMPORTANCE OF CELL TO CELL COMMUNICATION. C. Dive 1,2 , J. T. Erler 1 , I. J. Stratford 2 , D. A. Tennant 1,3 and D. R. Tomlinson 3 . 1 Cellular and Molecular Pharmacology Group, Cancer Research UK Paterson Institute, Manchester, United Kingdom, 2 School of Pharmacy and Pharmaceutical sciences, University of Manchester, Manchester, United Kingdom and 3 School of Biological Sciences, University of Manchester, Manchester, United Kingdom. Sponsor: R. Roberts. #1653 3:40 NEURO-GLIAL INTERACTIONS IN BASAL GANGLIA DYSFUNCTION: INSIGHTS FROM MANGANESE NEUROTOXICITY. R. Tjalkens. Toxicology Section, Department of Environmental and Radiological Health Sciences, Colorado State University, Fort Collins, CO. Wednesday Afternoon, March 9 1:30 PM to 4:30 PM Room RO4 SYMPOSIUM SESSION: THE UBIQUITIN- PROTEASOME SYSTEM AS A BIOLOGICAL TARGET IN TOXIC RESPONSES AND DISEASE Chairperson(s): Richard Pollenz, University of South Florida, Tampa, FL and Elaine M. Faustman, Institute for Risk Analysis & Risk Communication, Seattle, WA. Endorsed by: Mechanisms SS Neurotoxicology SS The ubiquitin-proteasome system is an essential pathway involved in covalently modifying proteins to influence their function and turnover. The cascade is initiated by an activating enzyme (E1), that binds to the 76 amino acid ubiquitin protein (UB). The E1 then transfers the UB to an E2 carrier protein. Following this transfer, a UB ligase enzyme (E3) covalently links the UB to a target protein. It is the E3, or E3/E2 complex that supplies the target specificity of the ubiquitination event. Genome mining has identified 530 possible genes encoding E1, E2, E3, UB and deubiquitinating enzymes (DUB). Ubiquinated substrates are usually recognized by the 20S or 26S proteasome complexes and destroyed, although recent studies suggest that UB or UB-like modification does not always result in destruction. The proteasomes are huge multiprotein complexes that can be found in both the cytoplasm and nucleus. Overall, the proteasome accounts for 1% of a cells protein. Due to the number of gene products required for the ubiquitin-proteasome system, it is a prime target in various human diseases states and cancer. Defects in the system have been implicated in neurodegenerative diseases such as Parkinsons and Alzheimers. In addition, studies continue to suggest that that the various enzymes of the pathway may be targets for toxicologically relevant compounds typified by arsenic, cadmium, TCDD and ethanol. In addition, the ubiquitin-proteasome system is implicated in the ligand mediated degradation of important transcription factors such as p53, steroid hormone receptors and the aryl hydrocarbon receptor (AHR). Due to these findings, the enzymes of the ubiquitin-proteasome pathway have become important targets in toxicology screens and in drug discovery paradigms. #1654 1:30 THE UBIQUITIN- PROTEASOME SYSTEM AS A BIOLOGICAL TARGET IN TOXIC RESPONSES AND DISEASE. R. S. Pollenz. Biology, University of South Florida, Tampa, FL. 176 SOT’s 44 th Annual Meeting
44 th Annual Meeting and ToxExpo Program Description #1655 1:37 TOXICANT AFFECTS ON UBIQUITIN- PROTEOSOME SYSTEMS: LESSONS FROM CROSS-COMPOUND AND CROSS-SYSTEM ASSESSMENTS. E. Faustman, X. Yu, J. Sidhu and J. Robinson. Department of Environmental and Occupational Health Sciences, University of Washingotn, Seattle, WA. #1656 2:17 ENVIRONMENTAL FACTORS, UBIQUITIN- PROTEOSOME DYSFUNCTION AND PARKINSON’S DISEASE. A. G. Kanthasamy. Biomedical Sciences, Iowa State University, Ames, IA. #1657 2:57 EFFECT OF ETHANOL ADMINISTRATION ON PROTEASOME ACTIVITY IN LIVER AND IN CULTURED HEPATOMA CELLS. T. M. Donohue, N. A. Osna and D. L. Clemens. Research, VA Medical Center, Omaha, NE. Sponsor: R. Pollenz. #1658 3:37 THE UBIQUITIN-PROTEASOME SYSTEM IN REGULATION OF NUCLEAR TRANSCRIPTION FACTORS AND SIGNAL TRANSDUCTION PATHWAYS. R. S. Pollenz, J. Popat, M. de la Pena and J. McQuown. Biology, University of South Florida, Tampa, FL. Wednesday Afternoon, March 9 1:30 PM to 4:30 PM La Louisiane Ballroom B #1659 1:30 WHY METALS BECOME NEUROTOXIC. W. Zheng. School of Health Sciences, Purdue University, West Lafayette, IN. #1660 1:50 SELECTIVE BLOOD-BRAIN BARRIER TRANSPORT OF ALUMINUM, MANGANESE, AND OTHER METALS IN METAL-INDUCED NEURODEGENERATION. R. A. Yokel. College of Pharmacy, University of Kentucky Medical Center, Lexington, KY. #1661 2:30 INTERACTION OF COPPER AND ZINC WITH β- AMYLOID IN PATHOGENESIS OF ALZHEIMER’S DISEASE. A. I. Bush. Genetics and Aging Research Unit, Harvard Medical School and Massachusetts General Hospital, Charlestown, MA. Sponsor: W. Zheng. #1662 3:10 BINDING TO SUBCELLULAR STRUCTURES IN METHYLMERCURY-INDUCED NEURODEGENERATIVE DAMAGE. K. R. Reuhl. Pharmacology & Toxicology, Rutgers University, Piscataway, NJ. #1663 3:50 METAL-METAL INTERACTIONS IN MANGANESE-INDUCED PARKINSONISM. W. Zheng. School of Health Sciences, Purdue University, West Lafayette, IN. Abstract 1664 is located on page 199. SYMPOSIUM SESSION: WHAT MAKES METALS NEUROTOXIC IN NEURODEGENERATIVE DISORDERS? Chairperson(s): Wei Zheng, Purdue University, West Lafayette, IN and Robert A. Yokel, University of Kentucky, Lexington, KY. Endorsed by: Metals SS* Neurotoxicology SS Risk Assessment SS Neurodegenerative diseases are characterized by progressive atrophy and dysfunction of anatomically or physiologically related neurological systems.Cumulative evidence suggests a role of metals in the etiology of numerous such diseases.For example, excess manganese (Mn) and iron (Fe) in particular brain regions have been associated with Parkinsonism; copper (Cu) and zinc (Zn) have been implicated in extracellular deposits of amyloid plaques in Alzheimer’s brains; overload of aluminum (Al) in the brain has also been controversially related to Alzheimer’s disease.Moreover, exposure to organic metals such as methylmercury (MeHg) has been linked to persistent psychomotor disturbances. However, the imminent question remains as to what factors may render metals, either essential or xenobiotic, more prone to being harmful in sporadic or hereditary neurodegenerative diseases. Understandably, interactions of these metals with genetic components, proteins, metal transport machineries, and cellular redox mechanisms, may signify some of the key factors in metal-induced neurotoxicities. This symposium will address the current understanding of biochemical characteristics of metals that are implicated in neurodegenerative disorders, including (1) metal-protein interaction such as Cu and Zn in beta-amyloid aggregation, (2) metal-metal interaction such as Mn in alteration of brain Fe functions, (3) metal-subcellular structure interaction such as MeHg and microtubules, (4) metal-transporter interaction such as Al speciation in brain Al metabolomics, and (5) metal-redox pathway interaction implicated in metal-induced oxidative stress. The symposium will be of interest to those who are engaged in metal toxicology, neuroscience, neurotoxicology, risk assessment, regulatory management, occupational health, and toxicology education. WEDNESDAY up-to-date information at www.toxicology.org 177
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Contents Program Overview .........
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Annual Meeting Events Calendar (Con
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INTERNATIONAL HARMONIZATION OF TECH
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Saturday Afternoon, March 5 2:00 PM
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Program - Society of Toxicology

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