You are not currently logged in.
Access your personal account or get JSTOR access through your library or other institution:
If You Use a Screen ReaderThis content is available through Read Online (Free) program, which relies on page scans. Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Mice Lacking Extracellular Superoxide Dismutase are More Sensitive to Hyperoxia
L. M. Carlsson, J. Jonsson, T. Edlund and S. L. Marklund
Proceedings of the National Academy of Sciences of the United States of America
Vol. 92, No. 14 (Jul. 3, 1995), pp. 6264-6268
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/2367823
Page Count: 5
Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Preview not available
Extracellular superoxide dismutase (EC-SOD; superoxide:superoxide oxidoreductase, EC 184.108.40.206) 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.
Proceedings of the National Academy of Sciences of the United States of America © 1995 National Academy of Sciences