Cold‐induced brain edema and infarction are reduced in transgenic mice overexpressing CuZn‐Superoxide dismutase

Cold‐induced brain edema and infarction are reduced in transgenic mice overexpressing... It has been proposed that oxygen‐derived radicals, superoxide in particular, are involved in the alteration of blood‐brain barrier permeability and the pathogenesis of brain edema following trauma, ischemia, and reperfusion injury. Using transgenic mice that overexpress the human gene for copper‐zinc‐superoxide dismutase, we studied the role of superoxide radicals in the blood‐brain permeability changes, edema development, and delayed infarction resulting from cold‐trauma brain injury. At 2 hours after a 30‐second cold injury, cerebral water and Evans blue contents were reduced, respectively, from 80 ± 0.2% and 132.7 ± 12.9 m̈g/gm of dry weight for nontransgenic mice to 78.5 ± 0.3% and 87.1 ± 9.9% m̈g/gm of dry weight for transgenic mice. Infarction, as measured by 2,3,5‐triphenyltetrazolium chloride staining, was reduced by 52% in transgenic brains. These data indicate that an increased level of superoxide dismutase activity in the brain reduces the development of vasogenic brain edema and infarction. Superoxide radicals play an important role in the pathogenesis of these lesions in cold‐traumatized brain. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annals of Neurology Wiley

Cold‐induced brain edema and infarction are reduced in transgenic mice overexpressing CuZn‐Superoxide dismutase

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Publisher
Wiley
Copyright
Copyright © 1991 American Neurological Association
ISSN
0364-5134
eISSN
1531-8249
DOI
10.1002/ana.410290506
pmid
1859179
Publisher site
See Article on Publisher Site

Abstract

It has been proposed that oxygen‐derived radicals, superoxide in particular, are involved in the alteration of blood‐brain barrier permeability and the pathogenesis of brain edema following trauma, ischemia, and reperfusion injury. Using transgenic mice that overexpress the human gene for copper‐zinc‐superoxide dismutase, we studied the role of superoxide radicals in the blood‐brain permeability changes, edema development, and delayed infarction resulting from cold‐trauma brain injury. At 2 hours after a 30‐second cold injury, cerebral water and Evans blue contents were reduced, respectively, from 80 ± 0.2% and 132.7 ± 12.9 m̈g/gm of dry weight for nontransgenic mice to 78.5 ± 0.3% and 87.1 ± 9.9% m̈g/gm of dry weight for transgenic mice. Infarction, as measured by 2,3,5‐triphenyltetrazolium chloride staining, was reduced by 52% in transgenic brains. These data indicate that an increased level of superoxide dismutase activity in the brain reduces the development of vasogenic brain edema and infarction. Superoxide radicals play an important role in the pathogenesis of these lesions in cold‐traumatized brain.

Journal

Annals of NeurologyWiley

Published: May 1, 1991

References

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