Review article
Role of oxidants/antioxidants in smoking-induced lung diseases

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Abstract

An imbalance between oxidants and antioxidants has been considered in the pathogenesis of smoking-induced lung diseases, such as chronic obstructive pulmonary disease (COPD), particularly emphysema. Recent evidence indicates that increased neutrophil sequestration and activation occurs in the pulmonary microvasculature in smokers and in patients with COPD, with the potential to release reactive oxygen species (ROS). ROS generated by airspace phagocytes or inhaled directly from the environment also increase the oxidant burden and may contribute to the epithelial damage. Although much research has focused on the protease/antiprotease theory of the pathogenesis of emphysema, less attention has been paid to the role of ROS in this condition. The injurious effects of the increased oxidant burden in smokers and in patients with COPD are opposed by the lung antioxidant defences. Hence, determining the mechanisms regulating the antioxidant responses is critical to our understanding of the role of oxidants in the pathogenesis of smoking-induced lung diseases and to devising future strategies for antioxidant therapy. In this article we have reviewed the evidence for the presence of an oxidant/antioxidant imbalance in smoking-induced lung disease and its relevance to therapy in these conditions.

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  • Cited by (0)

    1

    Dr. Irfan Rahman obtained a Ph.D. in Biochemistry in 1989 from the University of Nagpur, India, on the topic of “certain biochemical alterations of human polymorphonuclear leukocytes in essential hypertension.” He then joined Prof. D. Massaro's laboratory as a post-doctoral fellow and studied on lung antioxidant gene expression, in response to oxidants (ozone and hyperoxia) at the University of Miami, and Georgetown University, Washington, DC. In 1993, he moved to the UK to work with Dr. W. MacNee's group on the role of oxidant/antioxidant mechanisms in the pathogenesis of airways diseases. His research interests include the transcriptional regulation of antioxidant gene expression, inhalation toxicology, and oxidant mediated programmed cell death.

    2

    Dr. William MacNee is a reader in Medicine in the University of Edinburgh, Clinical Director of the Respiratory Medicine Unit at the Royal Infirmary of Edinburgh and visiting Professor, in Napier University, Edinburgh. He received his M.B. Ch.B. and M.D. degrees from the University of Glasgow. He was an MRC Travelling Fellow at the Pulmonary Research Laboratory, University of British Columbia, Vancouver. His research interests include neutrophil kinetics in the lungs, epithelial cell biology, and oxidant/antioxidant mechanisms in the pathogenesis of airways diseases. He is the author of over 80 scientific articles, chapters, and has been an invited speaker at numerous international conferences.

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