Biomarkers of Oxidative Stress in Adult Respiratory Distress Syndrome

Abstract

Oxidative stress is considered as a significant component in the pathogenesis of the adult respiratory distress syndrome (ARDS) (1-3). Oxidative stress can be defined as the pathogenic outcome created by the oxidation of critical tissue targets by reactive species which are generated at rates that exceed tissue antioxidant capacity. Evidence for the presence of oxidative stress in ARDS patients is scarce. A major limitation for measuring reactive species in biological systems is their short half life. Since reactive species modify biological molecules such as proteins, lipids and DNA measurement of the modified targets provide the experimental tools for their detection and quantification. Previously we identified plasma proteins as a suitable target for quantification of oxidative stress in humans. Therefore the purpose of this study was to measure modified plasma proteins in ARDS patients as well as patients with sepsis. Two protein modifications were measured; protein carbonyl adducts and 3-nitrotyrosine. Protein carbonyls are derived by the direct oxidation of amino acid residues or conjugation of aldehydes that are formed by the oxidation of unsaturated lipids or sugars. Overall, plasma protein carbonyls indicate the formation of oxidants. Nitration of protein tyrosine residues by nitrating species results in the formation of 3-nitrotyrosine. The data collected indicated that elevation in protein carbonyls is associated with ARDS but not sepsis whereas plasma protein 3-nitrotyrosine was found to be elevated in both ARDS and septic patients.