Inhibiting stress oxidant may be new therapy for COPD

A study in Clinical and Experimental Pharmacology and Physiology published by Wiley-Blackwell has showed that the generation of oxidative stress increases pulmonary inflammation – thus encouraging the development of airway obstruction associated with chronic obstructive pulmonary disease (COPD).

The study "Oxidative Stress is an Important Component of Airway Inflammation in Mice Exposed to Cigarette Smoke or Lipopolysaccharide" investigates the inflammatory responses in oxidative stress-deficient mice exposed to cigarette smoke. The authors employ a cigarette smoke model to understand the role of oxidative stress in the pathogenesis of COPD, and suggested that further investigations of the efficacy of new compounds that may help treat respiratory disorders.

Cigarette smoking is the main cause of respiratory disorders such as chronic bronchitis, emphysema and COPD. Smokers and patients with COPD generally display an increased oxidative stress level as compared to healthy patients.

Lead author Vincent Lagente, Professor of Pharmacology at the University of Rennes 1 in France says, "Overwhelming evidence shows that- compared to non-smokers and healthy patients smokers and patients with COPD display an increased level of oxidative stress, and suffer from an imbalance in oxidants in airway inflammation. As classic anti-inflammatory compounds are ineffective in treating respiratory disorders, and the effects of cigarette smoke on COPD are still not completely understood, we have developed a cigarette exposure protocol that results in airway inflammation to better understand the physiopathology of the inflammatory process."

In examining the response of mice exposed to cigarette smoke, researchers found that those with reduced oxidative stress showed lesser inflammatory symptoms hence suggesting the association of oxidative stress with COPD and supporting the development of anti-oxidant therapy for smoking related-diseases.

(Source: Clinical and Experimental Pharmacology and Physiology: Wiley-Blackwell: April 2008)