Impact of oxidative stress on lung diseases
Version of Record online: 17 DEC 2008
© 2009 The Authors; Journal compilation © 2009 Asian Pacific Society of Respirology
Volume 14, Issue 1, pages 27–38, January 2009
How to Cite
PARK, H. S., KIM, S. R. and LEE, Y. C. (2009), Impact of oxidative stress on lung diseases. Respirology, 14: 27–38. doi: 10.1111/j.1440-1843.2008.01447.x
- Issue online: 17 DEC 2008
- Version of Record online: 17 DEC 2008
- Received 8 June 2008; invited to revise 16 July 2008; revised 8 August 2008; accepted 2 September 2008 (Associate Editor: Yuben Moodley).
- oxidative stress;
- reactive oxygen species;
- signal transduction
Reactive oxygen species (ROS) are products of normal cellular metabolism and are known to act as second messengers. Under physiological conditions, ROS participate in maintenance of cellular ‘redox homeostasis’ in order to protect cells against oxidative stress through various redox-regulatory mechanisms. Overproduction of ROS, most frequently due to excessive stimulation of either reduced nicotinamide adenine dinucleotide phosphate by cytokines or the mitochondrial electron transport chain and xanthine oxidase, results in oxidative stress. Oxidative stress is a deleterious process that leads to lung damage and consequently to various disease states. Knowledge of the mechanisms of ROS regulation could lead to the pharmacological manipulation of antioxidants in lung inflammation and injury.