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Molecular targets for tobacco oxidants in lung cell death

Institution: University of California, Davis
Investigator(s): Tommer Ravid, Ph.D.
Award Cycle: 2001 (Cycle 10) Grant #: 10FT-0134 Award: $70,000
Subject Area: Pulmonary Disease
Award Type: Postdoctoral Fellowship Awards

Initial Award Abstract
Tobacco smoke is a major risk factor for lung disease. Nevertheless, the biological effects of tobacco smoke are poorly understood. Cigarette smoke contains molecules called “free radical species” or “oxidants” that damage lung tissues and lead to abnormal lung function or diseases like emphysema or chronic obstructive pulmonary disease.

Our long-term goal is to determine how these deleterious molecules in tobacco smoke damage lung cells and change their ability to survive. The proposed project will focus on the study of the cellular pathways by which these tobacco smoke oxidants cause cell death or “apoptosis”. In particular, we will study how these oxidants affect ceramides, which are lipid molecules found in cells that transmit signals for the lung cells to, among other functions, die. Previous work in our laboratory has provided evidence that oxidants in tobacco smoke increase ceramide production and therefore, lead to cell death and subsequent lung injury.

Understanding how tobacco oxidants induce cell death is crucial to the development of therapeutic and pharmacological strategies to block the destructive properties of tobacco reactive oxidants, thereby reducing damage to the respiratory tract of cigarette smokers.

Ceramide-mediated apoptosis in lung epithelial cells is regulated by glutathione.
Periodical: American Journal of Respiratory Cell and Molecular Biology Index Medicus:
Authors: Lavrentiadou SN, Chan C, Kawcak, T, Ravid T, Tsaba A, vanDer Vliet A, Rasooly R et al ART
Yr: 2001 Vol: 25 Nbr: Abs: Pg: 676-684