Increased Serum Catalase Activity in Septic Patients with the Adult Respiratory Distress Syndrome

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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 < 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 < 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 (> 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 < 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.