Mechanisms and Modifications of Pulmonary and Systemic Epithelia Function and Structure by Reactive Oxygen Species and Proteases
Abstract
A number of pathologic conditions including battle field injuries, skin burns, decreased organ perfusion, sepsis and hemorrhagic shock, result in the release of reactive oxygen species (ROS) in the circulation. In addition, activated neutrophils, aggregating in the site of injury, also release ROS and proteases. Epithelial tissues are prime targets for these species. This injury may lead to electrolyte imbalance, edema, and ultimately death. Our general goal is to identify the mechanisms by which ROS and proteases injure the intestinal and lung epithelia. Active sodium (Na+) transport is a seminal function of epithelial tissues, and sodium channels are the primary regulated proteins through which Na(+) enters most epithelial cells. Recent evidence from our laboratories indicates the existence of a new type of channel in alveolar epithelial cells. The main goals of the proposed research are to: (1) characterize the biophysical and functional properties of the alveolar Na(+) channels and compare them to those found in intestine and kidney; (2) identify their molecular structure; (3) quantify the effects of intracellular and extracellular increases in reactive oxygen species and proteases on the function and structure of epithelial and intestinal Na(+) channels; and (4) understand the important of active Na(+) transport in limiting pulmonary edema in healthy and diseased lungs in vivo. Finally, we will test the hypothesis that an increase in epithelial antioxidant defenses, by the delivery of liposome- encapsulated superoxide dismutase and catalase, mitigate the onset and progression of reactive oxygen species induced injury.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jan 01, 1991
- Accession Number
- ADA246635
Entities
People
- Sadis Matalon
Organizations
- University of Alabama