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PMID: 7603981 Published · ppublish English Comparative Study Journal Article Research Support, Non-U.S. Gov't

Mice lacking extracellular superoxide dismutase are more sensitive to hyperoxia.

Carlsson LM, Jonsson J, Edlund T, Marklund SL

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.

MeSH Terms
Animals Cells, Cultured Chimera Embryo, Mammalian Hyperoxia/genetics,physiopathology Isoenzymes/deficiency,genetics,metabolism Macromolecular Substances Mice Mice, Mutant Strains Molecular Sequence Data Organ Specificity Stem Cells Superoxide Dismutase/deficiency,genetics,metabolism
Chemicals
Isoenzymes Macromolecular Substances Superoxide Dismutase
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Carlsson L M
Department of Clinical Chemistry, Umeå University Hospital, Sweden.
Jonsson J
Edlund T
Marklund S L
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Article Info
Journal
Proceedings of the National Academy of Sciences of the United States of America
Abbr.
Proc Natl Acad Sci U S A
ISSN
0027-8424
Published
1995-07-03
Pages
6264-8
Language
English
Region
United States
NLM ID
7505876
PMCID
PMC41498
Subset
IM
Databases
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