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HERO ID
508845
Reference Type
Journal Article
Title
Impact of oxidative stress on lung diseases
Author(s)
Park, HS; Kim, SR; Lee, YC
Year
2009
Is Peer Reviewed?
1
Journal
Respirology
ISSN:
1323-7799
EISSN:
1440-1843
Volume
14
Issue
1
Page Numbers
27-38
Language
English
DOI
10.1111/j.1440-1843.2008.01447.x
Web of Science Id
WOS:000261839500003
Abstract
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.
Keywords
antioxidant; lung; oxidative stress; reactive oxygen species; signal; transduction; nf-kappa-b; idiopathic pulmonary-fibrosis; endothelial growth-factor; extracellular-superoxide dismutase; bronchoalveolar lavage fluid; activated protein-kinase; airway epithelial-cells; reactive oxygen; hydrogen-peroxide; free-radicals
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