title: Impact of oxidative stress on lung diseases.
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.
authors.affiliation: Department of Internal Medicine, Chungnam National University Medical School, Daejeon, Korea.
authors.forename: Hee Sun
authors.initials: HS
authors.lastname: Park
authors.forename: So Ri
authors.initials: SR
authors.lastname: Kim
authors.forename: Yong Chul
authors.initials: YC
authors.lastname: Lee
mesh_terms: D000975:Antioxidants; D006801:Humans; D008171:Lung Diseases / Q000188:drug therapy / Q000503:physiopathology*; D018384:Oxidative Stress / Q000235:genetics / Q000276:immunology; D017382:Reactive Oxygen Species / Q000737:chemistry / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D000975:Antioxidants; D017382:Reactive Oxygen Species