Acrolein effects in pulmonary cells: relevance to chronic obstructive pulmonary disease
Version of Record online: 3 JUL 2012
© 2012 New York Academy of Sciences.
Annals of the New York Academy of Sciences
Volume 1259, Environmental Stressors in Biology and Medicine pages 39–46, July 2012
How to Cite
Moretto, N., Volpi, G., Pastore, F. and Facchinetti, F. (2012), Acrolein effects in pulmonary cells: relevance to chronic obstructive pulmonary disease. Annals of the New York Academy of Sciences, 1259: 39–46. doi: 10.1111/j.1749-6632.2012.06531.x
- Issue online: 3 JUL 2012
- Version of Record online: 3 JUL 2012
- stress kinases;
- oxidative stress;
Acrolein (2-propenal) is a highly reactive α,β-unsaturated aldehyde and a respiratory irritant that is ubiquitously present in the environment but that can also be generated endogenously at sites of inflammation. Acrolein is abundant in tobacco smoke, which is the major environmental risk factor for chronic obstructive pulmonary disease (COPD), and elevated levels of acrolein are found in the lung fluids of COPD patients. Its high electrophilicity makes acrolein notorious for its facile reaction with biological nucleophiles, leading to the modification of proteins and DNA and depletion of antioxidant defenses. As a consequence, acrolein results in oxidative stress as well as altered intracellular signaling and gene transcription/translation. In pulmonary cells, acrolein, at subtoxic concentrations, can activate intracellular stress kinases, alter the production of inflammatory mediators and proteases, modify innate immune response, induce mucus hypersecretion, and damage airway epithelium. A better comprehension of the mechanisms underlying acrolein effects in the airways may suggest novel treatment strategies in COPD.