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.
| 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 |
