2,3, 7,8-tetrachlorodibenzo-p-dioxin (TCDD) is an environmental contaminant that mediates a variety of biological effects including the induction of several xenobiotic metabolizing enzymes. The mechanism of induction of cytochrome P-450 1A1 (CYP1A1) gene is the best understood. Induction by TCDD occurs at the level of transcription and is mediated by the Ah receptor which interacts with TCDD, gains access to the nucleus, and associates with a nuclear protein termed Amt. The study described in this fellowship will examine the induction of class 3 aldehyde dehydrogenase (ALDH) by TCDD. The concentration of TCDD required to induce transcriptional activation of ALDH is 10--fold that needed to induce CYP1A1. The main goal of this project is to analyze the mechanism responsible for the differential responsiveness of CYP1A1 and ALDH. These studies may generate new insights into the factors that determine the severity of TCDD's health effects.

Agency
National Institute of Health (NIH)
Institute
National Institute of Environmental Health Sciences (NIEHS)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
5F32ES005677-03
Application #
2444216
Study Section
Toxicology Subcommittee 2 (TOX)
Project Start
1997-07-01
Project End
Budget Start
1997-07-01
Budget End
1998-06-30
Support Year
3
Fiscal Year
1997
Total Cost
Indirect Cost
Name
Stanford University
Department
Biology
Type
Schools of Medicine
DUNS #
800771545
City
Stanford
State
CA
Country
United States
Zip Code
94305