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Activation of complement by hydroxyl radical in thermal injury. Surgery 1988 Aug;104(2):272-9

Date

08/01/1988

Pubmed ID

2840749

Scopus ID

2-s2.0-0023690735 (requires institutional sign-in at Scopus site)   84 Citations

Abstract

Complement activation resulting from local burn injury of skin and other soft tissues can be linked to systemic complications, such as intravascular hemolysis, neutrophil activation, and acute lung injury. This study was designed to clarify the relationship between cutaneous thermal injury, oxygen radical formation, and complement activation in vivo. A model for "selective" venous sampling from the area of a partial-thickness cutaneous burn over 25% to 30% of the total body surface in the rat was developed. Interventions involving oxygen radical scavengers, antioxidant enzymes, xanthine oxidase inhibitors, an iron chelator, complement depletion, and neutrophil depletion were used to probe the nature of the oxygen products involved in complement activation. Plasma from the area of burn was examined for total hemolytic complement activity, content of C5a-related chemotactic peptide, and relationship of oxygen products to appearance of this peptide. Xanthine oxidase inhibitors, hydroxyl radical scavengers, and complement depletion diminished the generation of C5a activity at the burn site, whereas neutrophil depletion was without effect. These data suggest that C5a activity may be related to oxygen products from xanthine oxidase. The catalase sensitivity and iron dependency of C5a generation suggest that hydroxyl radical may be related to complement activation and C5a appearance. This is the first report to directly link oxygen radical generation and complement activation in vivo.

Author List

Oldham KT, Guice KS, Till GO, Ward PA



MESH terms used to index this publication - Major topics in bold

Animals
Antioxidants
Burns
Chemotactic Factors
Complement Activation
Complement C5
Complement C5a
Complement System Proteins
Lymphocyte Depletion
Male
Neutrophils
Rats
Rats, Inbred Strains
Superoxides
Xanthine Oxidase