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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.

This paper is published in the May/June 2008 issue of Clinical and Experimental Pharmacology and Physiology(Vol. 35, Issue 5-6, pg. 601-605).
The article abstract is available free online at:

Media wishing to receive a PDF or schedule media interviews with the authors should contact Alina Boey, PR & Communications Manager Asia at or phone 65-96565580.

About Wiley-Blackwell
Wiley-Blackwell was formed in February 2007 as a result of the acquisition of Blackwell Publishing Ltd. by John Wiley & Sons, Inc., and its merger with Wiley’s Scientific, Technical, and Medical business. Together, the companies have created a global publishing business with deep strength in every major academic and professional field. Wiley-Blackwell publishes approximately 1,400 scholarly peer-reviewed journals and an extensive collection of books with global appeal. For more information on Wiley-Blackwell, please visit or
About Wiley
Founded in 1807, John Wiley & Sons, Inc. has been a valued source of information and understanding for 200 years, helping people around the world meet their needs and fulfill their aspirations. Since 1901, Wiley and its acquired companies have published the works of more than 350 Nobel laureates in all categories: Literature, Economics, Physiology/Medicine, Chemistry and Peace.

Our core businesses include scientific, technical, medical and scholarly journals, encyclopedias, books, and online products and services; professional/trade publishes books, subscription products, training materials, and online applications and websites; and educational materials for undergraduate and graduate students and lifelong learners. Wiley's global headquarters are located in Hoboken, New Jersey, with operations in the U.S., Europe, Asia, Canada, and Australia. The Company’s Web site can be accessed at The Company is listed on the New York Stock Exchange under the symbols JWa and JWb.

Alina Boey | alfa
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