Program - Society of Toxicology

44 th Annual Meeting
and ToxExpo
Program Description
MONDAY
#342 12:45 INTRACARDIAC AND INTRAVASCULAR LEAD
UTILIZATION: METHODS FOR IMPROVED
DATA COLLECTION. C. Hassler. Safety
Pharmacology, Battelle Memorial Laboratories,
Columbus, OH. Sponsor: L. Kinter.
#343 1:00 OBTAINING QUALITY ECG ENDPOINTS IN
SAFETY PHARMACOLOGY AND GENERAL
TOXICOLOGY STUDIES. ARE RESTRAINT AND
SURGICAL INTERVENTION NECESSARY? M.
Zawada and L. B. Kinter. Safety Assessment,
AstraZeneca, Wilmington, DE.
Abstract 344 is located on page74.
Monday Afternoon, March 7
1:30 PM to 4:30 PM
Room RO8
INNOVATIONS IN TOXICOLOGICAL SCIENCES SESSION:
ALTERNATIVE RNA SPLICING: A MECHANISM FOR ENHANCING
DIVERSITY OF GENE EXPRESSION
Chairperson(s): Curt Omiecinski, Pennsylvania State University, University
Park, PA and Craig Marcus, University of New Mexico, Albuquerque, NM.
Endorsed by:
Carcinogenesis SS
Alternative RNA splicing is an emerging field of molecular science that has
significant impact on the toxicological considerations of gene expression and
protein function. The diversity of alternatively spliced transcripts has farreaching
significance in terms of understanding interindividual differences in
response to xenobiotics, mechanisms of toxicity at the molecular level, tissuespecific
toxicity, and the mechanisms for regulating responses to environmental
and chemical challenge. This Symposium will provide an overview of basic
mechanisms and toxicological significance of RNA alternative splicing, with a
focus on alternatively spliced xenobiotic nuclear receptors. Importantly, the
session will also address bioinformatics-related issues pertaining to the identification
of splice variants, including the design of microarray and genomics
platforms that facilitate variant transcript detection.
#286 1:30 INTRODUCTION TO SYMPOSIUM:
ALTERNATIVE RNA SPLICING: A
MECHANISM FOR ENHANCING DIVERSITY OF
GENE EXPRESSION. C. Omiecinski. Ctr Molec
Toxicology, Penn State University, University Park, PA.
#287 1:35 DISCOVERY AND TISSUE-SPECIFIC
MONITORING OF ALTERNATIVE PRE-MNRA
SPLICING WVENTS USING INK-JET
MICROARRAYS. J. M. Johnson, J. Castle, P. Garrett-
Engele, Z. Kan, L. Lim, C. Armour, C. Raymond and E.
Schadt. Informatics, Rosetta Inpharmatics, Merck &
Co., Inc., Seattle, WA. Sponsor: C. Marcus.
#288 2:10 FUNCTIONALLY DISTINCT ISOFORMS OF THE
FARNESOID X RECEPTOR (FXR). P. A. Edwards,
Y. Zhang and F. Y. Lee. Biological Chemistry, UCLA,
Los Angeles, CA. Sponsor: C. Marcus.
#289 2:45 HUMAN PXR: GENERATION OF DIVERSITY
THROUGH ALTERNATIVE SPLICING AND
POLYMORPHISM. E. G. Schuetz. Pharmaceutical
Sciences, St. Jude Children’s Research Hospital,
Memphis, TN. Sponsor: C. Marcus.
#290 3:20 FUNCTIONALLY DISTINCT ALTERNATIVE
SPLICE VARIANTS OF THE HUMAN
XENOBIOTIC RECEPTOR, CAR. C. Omiecinski, S.
Auerbach and M. Stoner. Ctr Molec Toxicology, Penn
State University, University Park, PA.
#291 3:55 STEROID RECEPTOR COACTIVATORS
PROMOTE COORDINATE TRANCRIPTION AND
ALTERNATIVE SPLICING. B. W. O’Malley.
Molecular & Cellular Biology, Baylor College of
Medicine, Houston, TX. Sponsor: C. Marcus.
Monday Afternoon, March 7
1:30 PM to 4:30 PM
Room 208
SYMPOSIUM SESSION: DIETARY ACRYLAMIDE: NEW OR
ANCIENT RISK?
Chairperson(s): Philip M. Bolger, U.S. FDA, College Park, MD and Danial
Doerge, National Center for Toxicological Research, Jefferson, AR.
Endorsed by:
Food Safety SS*
Occupational and Public Health SS
Regulatory and Safety Evaluation SS
Risk Assessment SS
Initial investigations by Swedish researchers of fried and oven-baked foods indicated
that acrylamide formation is associated with high temperature cooking
processes for certain carbohydrate-rich foods, such as potatoes and cereals.
Since then similar findings have been reported by researchers in other countries.
The discovery of acrylamide in food is a concern because acrylamide is a potential
carcinogen and genotoxicant, and a known human neurotoxicant. It does not
appear to be present in uncooked food and is present in low or undetectable
levels in foods cooked at lower temperatures, such as by boiling. One plausible
mechanism responsible for acrylamide formation in carbohydrate-rich foods
cooked at high temperatures is the Mallard reaction between asparagine and
certain sugars. However, not enough is known about acrylamide formation to
identify safe, effective, and practical modifications to food processing techniques
that will clearly prevent or reduce formation. Identifying major
mechanisms of formation is an important step in identifying ways to reduce or
prevent acrylamide formation during cooking. There are significant uncertainties
about the impact of dietary acrylamide exposure on public health, since
foods reported to contain acrylamide have been consumed for many years.
While acrylamide causes cancer in laboratory animals at high doses, it is not
clear whether a similar response would occur at the much lower levels found in
food. Several epidemiological environmental studies of workplace and dietary
exposures have failed to show an increased cancer risk with acrylamide exposure.
It is also conceivable that subtle effects can occur on the developing
nervous system at acrylamide doses lower than those that have been studied in
animals and humans. To better assess the risk of acrylamide information is
needed on dietary exposure, bioavailability from food, biomarkers of exposure,
and the potential to cause cancer and neurotoxic or neurodevelopmental effects
when consumed in food.
#292 1:30 OVERVIEW OF DIETARY ACRYLAMIDE. P. M.
Bolger. Center for Food Safety and Applied Nutrition,
US Food and Drug Administration, College Park, MD.
#293 1:35 TOXICOKINETICS OF ACRYLAMIDE AND
GLYCIDAMIDE IN B6C3F1 MICE AND FISCHER
344 RATS. D. R. Doerge 1 , J. F. Young 2 , L. McDaniel 1 ,
N. C. Twaddle 1 and M. I. Churchwell 1 . 1 Biochem.
Toxicol., NCTR, Jefferson, AR and 2 Biometry and Risk
Assessment, NCTR, Jefferson, AR. Sponsor: P. Bolger.
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SOT’s 44 th Annual Meeting