Biochemical and Metabolic Response to Nitrogen Dioxide-Induced Endothelial Injury

Nitrogen dioxide is a ubiquitous air pollutant resulting from the combustion of fossil fuels. Since NO₂ is a reactive free radical, one postulated mechanism on NO₂ pulmonary injury involves peroxidation of membrane lipids. Dr. Patel and colleagues at the University of Florida evaluated the dose- and time-dependent effects of NO₂ exposure by measuring metabolic function, biochemical and biophysical parameters. The porcine pulmonary artery and aortic endothelial cells in monoculture cells were exposed to 3 or 5ppm of NO₂ or air for 3-24 hours. To measure biochemical changes GSH-reductase, GSH-peroxidase, G6PDH activities, lipid peroxide formation, and lactate dehydrogenase release were measured. To evaluate biophysical changes lipid fluidity in the hydrophobic and hydrophilic regions of the plasma membrane were monitored.