Annual Meeting Program - Society of Toxicology

Society of Toxicology 2008
Program Description (Continued)
Tuesday Afternoon, March 18
1:30 PM to 4:30 PM
Hyatt
E. Anderson Amphitheater
K–12 Paracelsus Goes to the Classroom—The TEAMS
Project: Toxicologists Educating and Mentoring
Students
Chairperson(s): Katie Sprugel, Amgen, Seattle, WA and Vanessa
Fitsanakis, King College, Bristol, TN
Continuing the tradition of providing public outreach in conjunction
with the Annual Meeting, the Committee on K–12 Education will host a
symposium for high school students by videoconferencing from the Annual
Meeting to classrooms around the state of Washington. Twelve groups of
students will present their projects to one another and to a panel of toxicologists
in a morning and an afternoon session. Other students will have
the opportunity to submit an electronic version of their project for a virtual
poster session. The presentations will educate other students about a health
or environmental health issue of importance to the students or their community.
Toxicologists from SOT will also serve as mentors in the months
preceding the meeting as the students develop their presentations.
Tuesday Afternoon, March 18
1:30 PM to 2:30 PM
Exhibit Hall 4C-3
Exhibitor Hosted Session: Covance: Outsourcing
Preclinical Safety Assessment—How to Create a
Strategy for Success
Presented by: Covance
The consideration to outsource your preclinical safety assessment studies
cannot be approached without consideration of many factors—your
strengths and resources, identifying what you need in an outsourcing
partner, your timelines and options to successfully meet your milestones,
and deciding on the right combination of available options. Learn more
about critical considerations that will contribute to your success in developing
the right outsourcing strategy for your program.
Tuesday Afternoon, March 18
1:30 PM to 2:30 PM
Exhibit Hall 4C-4
Exhibitor Hosted Session: Global Metabolomic
Analysis in Drug Discovery and Development
Presented by: Metabolon, Inc.
Small molecule biomarkers are the most common approach to diagnose and
monitor human disease. Detection of endogenous biochemicals and xenobiotics
also provides solutions for compound profiling and optimization,
toxicology, drug discovery, and drug safety. Metabolon’s analytical mass
spectrometry platform and proprietary data analysis software provides a
method for the detection and identification of small molecules across a
wide array of sample types. An overview of the technology and numerous
case study examples will be provided.
Abstract #
Tuesday Afternoon, March 18
1:30 PM to 4:15 PM
Room 605
Oxidative Signaling AND Redox Biology
SYMPOSIUM SESSION: ENDOTHELIAL DYSFUNCTION:
MORE THAN JUST A ‘NO NO̓ PHENOMENON
Chairperson(s): Matthew Campen, Lovelace Respiratory Research
Institute, Albuquerque, NM and Daniel Conklin, University of Louisville,
Louisville, KY.
Endorsed by:
Inhalation and Respiratory Specialty Section*
Mechanisms Specialty Section
Various environmental and anthropomorphic toxins can cause direct or
indirect injury to the vasculature, resulting in endothelial cell dysfunction.
Endothelial dysfunction is thought to be an early marker of vascular injury
and precedes overt macro- and microvascular pathology (e.g., atherosclerosis,
peripheral artery disease, angiopoathy), and may even be a crucial
factor in end-stage lung disease. Endothelial dysfunction has been measured
in many forms such as decreased endothelium-dependent relaxation,
increased expression of endothelial cell adhesion molecules (e. g., ICAM-1,
VCAM-1, selectins, etc), increased circulating endothelial-derived products
(e.g., sICAM-1, ET-1, vWF, etc…), and increased vascular permeability.
Endothelial dysfunction is often linked to a generalized decrease in bioavailable
or bioactive nitric oxide (NO), which could result from diminished
eNOS expression, decreased eNOS activity due to decreased co-factor availability
or protein uncoupling, and/or increased superoxide production, which
can sequester NO to form peroxynitrite. In addition, as toxicants combine
with pre-existing disease conditions to amplify vascular oxidative stress,
endothelial dysfunction is typically evidenced by increased superoxide
production, increased iNOS and cytokine expression, and increased protein
modification by peroxynitrite, which could result in protein inactivation.
Despite inconsistencies among methodologies across laboratories, and some
variation among findings, data largely indicate that a variety of inhaled and
ingested xenobiotics can adversely impact endothelial function, especially in
the setting of pre-existing disease.
#1251 1:30 ENDOTHELIAL DYSFUNCTION: MORE
THAN JUST A ‘NO NO̓ PHENOMENON.
M. J. Campen 1 and D. J. Conklin 2 . 1 Cardiovascular
and Respiratory Physiology, Lovelace Respiratory
Research Institute, Albuquerque, NM and 2 Institute
of Molecular Cardiology, University of Louisville,
Louisville, KY.
#1252 1:41 MECHANISMS OF ENDOTHELIAL
DYSFUNCTION: RELEVANCE TO INHALED
PM. S. Rajagopalan. Ohio State University Medical
Center, Columbus, OH. Sponsor: D. Conklin.
#1253 2:03 EFFECTS OF INHALED DIESEL EXHAUST
ON VASCULAR OXIDATIVE STRESS
AND ENOS FUNCTION. T. L. Knuckles 1 , S.
Lucas 1 , A. Lund 1 , T. Cherng 2 , N. Kanagy 2 and M.
Campen 1 . 1 Lovelace Respiratory Research Institute,
Albuquerque, NM and 2 University of New Mexico,
Albuquerque, NM.
#1254 2:25 REGULATION OF ENDOTHELIAL CELL
ADHESION MOLECULES BY ACROLEIN,
AN ENVIRONMENTAL ALDEHYDE. S. E.
D’Souza 1 , S. D. Sithu 1 , E. N. Vladykovskaya 2 ,
D. J. Conklin 2 , A. Bhatnagar 2 and S. Srivastava 2 .
1
Physiology, University of Louisville, Louisville, KY
and 2 Molecular Cardiology, University of Louisville,
Louisville, KY.
Tuesday
up-to-date information at www.toxicology.org 195