Impact of oxidative stress on lung diseases

被引：242

作者：

Park, Hee Sun ^{[2
]}

Kim, So Ri ^{[1
]}

Lee, Yong Chul ^{[1
]}

机构：

[1] Chonbuk Natl Univ, Sch Med, Dept Internal Med, Airway Remodeling Lab, Jeonju 561180, Jeonbuk, South Korea

[2] Chungnam Natl Univ, Sch Med, Dept Internal Med, Taejon, South Korea

来源：

RESPIROLOGY | 2009年 / 14卷 / 01期

关键词：

antioxidant; lung; oxidative stress; reactive oxygen species; signal transduction; NF-KAPPA-B; GROWTH-FACTOR-BETA; EXTRACELLULAR-SUPEROXIDE DISMUTASE; BRONCHOALVEOLAR LAVAGE FLUID; AIRWAY EPITHELIAL-CELLS; PROTEIN-KINASE-C; REACTIVE OXYGEN; HYDROGEN-PEROXIDE; FREE-RADICALS; TRANSCRIPTION FACTOR;

D O I：

10.1111/j.1440-1843.2008.01447.x

中图分类号：

R56 [呼吸系及胸部疾病];

学科分类号：

摘要：

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.

引用

页码：27 / 38

页数：12

共 174 条

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