Interactions of oxygen radicals with airway epithelium.
Abstract
Reactive oxygen species (ROS) have been implicated in the pathogenesis of numerous
disease processes. Epithelial cells lining the respiratory airways are uniquely vulnerable
regarding potential for oxidative damage due to their potential for exposure to both
endogenous (e.g., mitochondrial respiration, phagocytic respiratory burst, cellular
oxidases) and exogenous (e.g., air pollutants, xenobiotics, catalase negative organisms)
oxidants. Airway epithelial cells use several nonenzymatic and enzymatic antioxidant
mechanisms to protect against oxidative insult. Nonenzymatic defenses include certain
vitamins and low molecular weight compounds such as thiols. The enzymes superoxide
dismutase, catalase, and glutatione peroxidase are major sources of antioxidant protection.
Other materials associated with airway epithelium such as mucus, epithelial lining
fluid, and even the basement membrane/extracellular matrix may have protective actions
as well. When the normal balance between oxidants and antioxidants is upset, oxidant
stress ensues and subsequent epithelial cell alterations or damage may be a critical
component in the pathogenesis of several respiratory diseases. Oxidant stress may
profoundly alter lung physiology including pulmonary function (e.g., forced expiratory
volumes, flow rates, and maximal inspiratory capacity), mucociliary activity, and
airway reactivity. ROS may induce airway inflammation; the inflammatory process may
serve as an additional source of ROS in airways and provoke the pathophysiologic responses
described. On a more fundamental level, cellular mechanisms in the pathogenesis of
ROS may involve activation of intracellular signaling enzymes including phospholipases
and protein kinases stimulating the release of inflammatory lipids and cytokines.
Respiratory epithelium may be intimately involved in defense against, and pathophysiologic
changes invoked by, ROS.
Type
Journal articlePermalink
https://hdl.handle.net/10161/13741Collections
More Info
Show full item recordScholars@Duke
Bernard Martin Fischer
Associate Professor in Pediatrics
Comparative Pharmacology and Cell Biology Mechanisms of complementary-alternative
medicines and products Signal Transduction and Cell Signaling Mechanisms of inflammation
and disease Cytokine, Oxidant, and Inflammatory Mediator NetworkingIntegrative care/treatments
for HIV patientsMechanisms of chronic inflammation associated with HIV

Articles written by Duke faculty are made available through the campus open access policy. For more information see: Duke Open Access Policy
Rights for Collection: Scholarly Articles
Works are deposited here by their authors, and represent their research and opinions, not that of Duke University. Some materials and descriptions may include offensive content. More info