ABSTRACT
Oxidative stress as a result of cigarette smoking is an important etiological factor in the pathogenesis of chronic obstructive pulmonary disease (COPD). Various reports are available on the imbalance of oxidant-antioxidant in the lungs as a result of cigarette smoke and airborne particulate matter. Abnormal in•ammation is the hallmark of chronic airway diseases (COPD and asthma), which is caused by oxidative stress. Keeping in mind that only about 15-20% of smokers develop COPD, a new paradigm in COPD research has now emerged that suggests that epigenetic alterations might be a clue for understanding the pathophysiology of COPD and other chronic lung disorders such as asthma. At present, no effective treatment exists to halt the progressive decline in lung function of smokers who get the disease. Since COPD is considered to be a result of oxidative stress imposed by smoking, treatment with dietary antioxidants has been in vogue for some time. Other than thiols, and vitamins such as C and E, the most prominent antioxidant candidate of choice has been dietary polyphenols. Besides thiols, which are mucolytic, vitamins C and E are less efˆcacious as antioxidants in the lung. Recently, a unique role of dietary polyphenols is described via modulation of redox signaling in in•ammation. In this chapter, a brief overview of the pathophysiology of COPD and asthma is given in light of oxidative stress and in•ammatory response, followed by information on epigenetic changes due to environmental factors linked to oxidative stress and in•ammation, and mechanisms of epigenetic alterations in chronic lung diseases. Furthermore, how polyphenols may be beneˆcial and have in•uence in modulating/ intervening the epigenetic changes and associated pathophysiological alterations in chronic airway disorders is explored.
