title: Increased serum catalase activity in septic patients with the adult respiratory distress syndrome.
abstract: Excessive hydrogen peroxide (H2O2) generation appears to contribute to the development of the adult respiratory distress syndrome (ARDS), but H2O2-combatting antioxidant defenses have not been evaluated. We found that serum from septic patients with ARDS scavenged more (p less than 0.05) H2O2 in vitro (82.7 +/- 3.8%) than did serum from septic patients without ARDS (56.9 +/- 3.1%) or control subjects (20.2 +/- 2.4%). Serum from septic patients with ARDS also had more (p less than 0.05) catalase activity (54.9 +/- 10.9 U/ml) than did serum from septic patients without ARDS (28.6 +/- 3.4 U/ml) or control subjects (7.3 +/- 0.8 U/ml). In contrast, serum from septic patients with or without ARDS and control subjects had the same glutathione peroxidase (GPX) activity. Serum H2O2 scavenging activity correlated with serum catalase (r = 0.77) but not GPX (r = 0.33) activity and was inhibitable (greater than 90%) by sodium azide, a catalase inhibitor. Increases in serum catalase activity did not appear to be derived from erythrocytes (RBC) because septic patients with or without ARDS and control subjects had similar RBC hemolysis in response to osmotic stress in vitro and serum haptoglobin concentrations. Serum from septic patients with ARDS also protected endothelial cells against H2O2-mediated damage (34.5 +/- 2.2% 51Cr release) better (p less than 0.05) than serum from septic patients without ARDS (47.3 +/- 7.4%) or control subjects (82.1 +/- 10.2%), but killing of bacteria by neutrophils in vitro was the same in serum from patients and control subjects. Our findings indicate that patients with sepsis and/or ARDS have increased serum catalase activity, which may alter H2O2-dependent processes.
authors.affiliation: Webb-Waring Lung Institute, Denver, CO 80262.
authors.forename: J A
authors.initials: JA
authors.lastname: Leff
authors.forename: P E
authors.initials: PE
authors.lastname: Parsons
authors.forename: C E
authors.initials: CE
authors.lastname: Day
authors.forename: E E
authors.initials: EE
authors.lastname: Moore
authors.forename: F A
authors.initials: FA
authors.lastname: Moore
authors.forename: M A
authors.initials: MA
authors.lastname: Oppegard
authors.forename: J E
authors.initials: JE
authors.lastname: Repine
mesh_terms: D001424:Bacterial Infections / Q000201:enzymology* / Q000276:immunology; D001770:Blood Bactericidal Activity / Q000276:immunology; D002374:Catalase / Q000097:blood*; D005260:Female; D005979:Glutathione Peroxidase / Q000097:blood; D006801:Humans; D006861:Hydrogen Peroxide / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000276:immunology; D012128:Respiratory Distress Syndrome / Q000201:enzymology* / Q000276:immunology
chemical_list: D006861:Hydrogen Peroxide; D002374:Catalase; D005979:Glutathione Peroxidase