The DOI matches its Crossref record; 46 of the 46 references it cites were found in a registry or an index.
Reduction of CuZn-Superoxide Dismutase Activity Exacerbates Neuronal Cell Injury and Edema Formation after Transient Focal Cerebral Ischemia
Open accessAbstract
Apoptotic neuronal cell death has recently been associated with the development of infarction after cerebral ischemia. In a variety of studies, CuZn-superoxide dismutase (CuZn-SOD) has been shown to protect the brain from ischemic injury. A possible role for CuZn-SOD-related modulation of neuronal viability is suggested by the finding that CuZn-SOD inhibits apoptotic neuronal cell death in response to some forms of cellular damage. We evaluated this possibility in the model of transient focal cerebral ischemia in mice bearing a disruption of the CuZn-SOD gene (Sod1). Homozygous mutant (Sod1−/−) mice had no detectable CuZn-SOD activity, and heterozygous mutants (Sod1+/−) showed a 50% decrease compared with wild-type mice.Sod1−/− mice showed a high level of blood–brain barrier disruption soon after 1 hr of middle cerebral artery occlusion and 100% mortality at 24 hr after ischemia.Sod1+/− mice showed 30% mortality at 24 hr after ischemia, and neurological deficits were exacerbated compared with wild-type controls. The Sod1+/− animals also had increased infarct volume and brain swelling, accompanied by increased apoptotic neuronal cell death as indicated by the in situ nick-end labeling technique to detect DNA fragmentation and morphological criteria. These results suggest that oxygen-free radicals, especially superoxide anions, are an important factor for the development of infarction by brain edema formation and apoptotic neuronal cell death after focal cerebral ischemia and reperfusion.
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Cited by
Nitric Oxide and Peroxynitrite in Health and Disease
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Aquaporin-4 deletion in mice reduces brain edema after acute water intoxication and ischemic stroke
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Self-citationNeuroinflammatory mechanisms of blood-brain barrier damage in ischemic stroke
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Metadata
- Authors
- Kondo, T., Reaume, A. G., Huang, T.-T., Carlson, E., Murakami, K., Chen, S. F., Hoffman, E. K., Scott, R. W., Epstein, C. J., & Chan, P. H.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 1997-06-01
- Volume
- 17
- Issue
- 11
- Pages
- 4180-4189
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W2152494586
- Cited by
- 429
- References
- 46
- FWCI
- 20.11
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- CoChat. (2026). Citation check: Reduction of CuZn-Superoxide Dismutase Activity Exacerbates Neuronal Cell Injury and Edema Formation after Transient Focal Cerebral Ischemia. https://app.cochat.ai/papers/10.1523/jneurosci.17-11-04180.1997
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- Kondo, T., Reaume, A. G., Huang, T.-T., Carlson, E., Murakami, K., Chen, S. F., Hoffman, E. K., Scott, R. W., Epstein, C. J., & Chan, P. H. (1997). Reduction of CuZn-Superoxide Dismutase Activity Exacerbates Neuronal Cell Injury and Edema Formation after Transient Focal Cerebral Ischemia. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.17-11-04180.1997
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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