This project hypothesizes that acrolein exposure in second hand smoke is associated with the formation of stable premutagenic adducts leading to the development of arteriosclerotic plaques. A significant component of the vapor phase is allylamine that can be metabolized acrolein, which in turn has a potential for forming DNA adducts. Such adducts have been identified in human and rodent cells. The principal investigator proposes to expose a sensitive animal model (cockerel) to levels of acrolein that mimic the levels one might expect from metabolism of vapor phase, second hand cigarette smoke components. There are two specific aims: The first is whether or not there are detectable changes in arteriosclerotic plaque development as a consequence of acrolein exposure; the second is whether or not acrolein-DNA adducts levels are different in DNA from aortas of acrolein treated and air control cockerels and correlation of this with accelerated plaque development. If it occurs, the adduct levels will be measured by P32-postlabeling and will be correlated with accelerated plaque development.

Agency
National Institute of Health (NIH)
Institute
National Institute of Environmental Health Sciences (NIEHS)
Type
Small Research Grants (R03)
Project #
1R03ES008624-01
Application #
2019049
Study Section
Special Emphasis Panel (ZES1-EBJ-C (01))
Project Start
1996-10-28
Project End
1998-02-28
Budget Start
1996-10-28
Budget End
1998-02-28
Support Year
1
Fiscal Year
1997
Total Cost
Indirect Cost
Name
New York University
Department
Public Health & Prev Medicine
Type
Schools of Medicine
DUNS #
City
New York
State
NY
Country
United States
Zip Code
10016
Penn, A; Nath, R; Pan, J et al. (2001) 1,N(2)-propanodeoxyguanosine adduct formation in aortic DNA following inhalation of acrolein. Environ Health Perspect 109:219-24