Acrolein effects in pulmonary cells: relevance to chronic obstructive pulmonary disease.

Abstract

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.

• Authors: Nadia Moretto, Giorgia Volpi, Fiorella Pastore, Fabrizio Facchinetti
• Journal: Annals of the New York Academy of Sciences (Ann N Y Acad Sci) Vol. 1259 Pg. 39-46 (Jul 2012) ISSN: 1749-6632 [Electronic] United States
• PMID: 22758635 (Publication Type: Journal Article, Review)
• Copyright: © 2012 New York Academy of Sciences.

Chemical References

• Air Pollutants
• Tobacco Smoke Pollution
• Acrolein

Topics

• Acrolein (pharmacology, toxicity)
• Air Pollutants (pharmacology, toxicity)
• Animals
• Humans
• Inflammation (chemically induced, complications)
• Lung (cytology, drug effects)
• Models, Biological
• Pulmonary Disease, Chronic Obstructive (etiology, immunology, therapy)
• Tobacco Smoke Pollution (adverse effects)