Title:Reactive Oxygen Species, Inflammation, and Lung Diseases
Volume: 18
Issue: 26
Author(s): Di Paola Rosanna and Cuzzocrea Salvatore
Affiliation:
Keywords:
Oxidative stress, inflammation, DNA damage, lung diseases, Reactive oxygen species (ROS), cellular metabolism, airways, apoptosis, protooncogenes, signal transduction pathways.
Abstract: Reactive oxygen species (ROS) are well recognized for playing a dual role as both deleterious and beneficial species. ROS are
products of normal cellular metabolism and under physiological conditions, participate in maintenance of cellular ‘redox homeostasis.
Overproduction of ROS, results in oxidative stress. Oxidative stress is a deleterious process that leads to lung damage and consequently
to various disease states. The lung is a highly specialized organ that facilitates uptake of oxygen and release of carbon dioxide.
Persistent inhalation of the invading pathogens or toxic agents may result in overwhelming production of ROS. Oxidants initiate a number
of pathologic processes, including inflammation of the airways, which may contribute to the pathogenesis and/or exacerbation of airways
disease.
During inflammation, enhanced ROS production may induce recurring DNA damage, inhibition of apoptosis, and activation of protooncogenes
by initiating signal transduction pathways. Therefore, it is conceivable that chronic inflammation-induced production of ROS
in the lung may predispose individuals to lung diseases. In this review, we discuss mechanisms of oxidant stress in the lung, the role of
oxidants in lung disease pathogenesis and exacerbation.
