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How smoke induces lung damage via oxidative stress

Institution: University of California, Davis
Investigator(s): Michal Levy, Ph.D.
Award Cycle: 2006 (Cycle 15) Grant #: 15FT-0041 Award: $75,000
Subject Area: Pulmonary Disease
Award Type: Postdoctoral Fellowship Awards

Initial Award Abstract
According to the American Lung Association, chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death in America and is projected to be third by 2020, claiming the lives of 120,000 Americans in 2002. Smoking is the primary risk factor for COPD and approximately 80 to 90 percent of COPD deaths are estimated to be caused by smoking. The National Center for Health Statistics reports that in 2003, 10.7 million U.S. adults were estimated to have COPD. In 2004, the cost to the nation for COPD was approximately $37.2 billion.

Cigarette smoke contains abundant free radical species and reactive oxidants such as hydrogen peroxide (H2O2) which have been suggested to play a role in cigarette smoke-induced lung injury and to contribute to pulmonary diseases mainly through destruction of airway epithelial cells. The increased oxidant load in smokers may contribute to COPD through many biological actions including cellular injury and initiation of programmed cell death (apoptosis).

Our lab has demonstrated that H2O2 exposure leads to increases in the generation of ceramide, a lipid signaling molecule capable of initiating apoptosis in the lung. We have further demonstrated that the enzyme responsible for ceramide generation under H202 exposure is a member of the neutral sphingomyelinase family (nSMase). These results support our hypothesis that there is a tight connection between oxidative stress and the ceramide pathway that leads to the induction of apoptosis in lung epithelial cells.