title: Mice lacking extracellular superoxide dismutase are more sensitive to hyperoxia.
abstract: Extracellular superoxide dismutase (EC-SOD; superoxide:superoxide oxidoreductase, EC 1.15.1.1) is a secreted Cu- and Zn-containing tetrameric glycoprotein, the bulk of which is bound to heparan sulfate proteoglycans in the interstitium of tissues. To test the function of EC-SOD in vivo, mice carrying a targeted disruption of the EC-SOD gene were generated. The EC-SOD null mutant mice develop normally and remain healthy until at least 14 months of age. No compensatory induction of other SOD isoenzymes or other antioxidant enzymes was observed. When stressed by exposure to > 99% oxygen, the EC-SOD null mutant mice display a considerable reduction in survival time compared to wild-type mice and an earlier onset of severe lung edema. These findings suggest that while under normal physiological conditions other antioxidant systems may substitute for the loss of EC-SOD; when the animal is stressed these systems are unable to provide adequate protection.
authors.affiliation: Department of Clinical Chemistry, Umeå University Hospital, Sweden.
authors.forename: L M
authors.initials: LM
authors.lastname: Carlsson
authors.forename: J
authors.initials: J
authors.lastname: Jonsson
authors.forename: T
authors.initials: T
authors.lastname: Edlund
authors.forename: S L
authors.initials: SL
authors.lastname: Marklund
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D002678:Chimera; D004622:Embryo, Mammalian; D018496:Hyperoxia / Q000235:genetics / Q000503:physiopathology; D007527:Isoenzymes / Q000172:deficiency / Q000235:genetics / Q000378:metabolism; D046911:Macromolecular Substances; D051379:Mice; D008817:Mice, Mutant Strains; D008969:Molecular Sequence Data; D009928:Organ Specificity; D013234:Stem Cells; D013482:Superoxide Dismutase / Q000172:deficiency* / Q000235:genetics / Q000378:metabolism
chemical_list: D007527:Isoenzymes; D046911:Macromolecular Substances; D013482:Superoxide Dismutase