The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.
Overexpression of SOD1 in Transgenic Rats Protects Vulnerable Neurons Against Ischemic Damage After Global Cerebral Ischemia and Reperfusion
Open accessAbstract
Transient global cerebral ischemia resulting from cardiac arrest is known to cause selective death in vulnerable neurons, including hippocampal CA 1 pyramidal neurons. It is postulated that oxygen radicals, superoxide in particular, are involved in cell death processes. To test this hypothesis, we first used in situ imaging of superoxide radical distribution by hydroethidine oxidation in vulnerable neurons. We then generated SOD1 transgenic (Tg) rats with a five-fold increase in copper zinc superoxide dismutase activity. The Tg rats and their non-Tg wild-type littermates were subjected to 10 min of global ischemia followed by 1 and 3 d of reperfusion. Neuronal damage, as assessed by cresyl violet staining and DNA fragmentation analysis, was significantly reduced in the hippocampal CA 1 region, cortex, striatum, and thalamus in SOD1 Tg rats at 3 d, as compared with the non-Tg littermates. There were no changes in the hippocampal CA 3 subregion and dentate gyrus, resistant areas in both SOD1 Tg and non-Tg rats. Quantitative analysis of the damaged CA 1 subregion showed marked neuroprotection against transient global cerebral ischemia in SOD1 Tg rats. These results suggest that superoxide radicals play a role in the delayed ischemic death of hippocampal CA 1 neurons. Our data also indicate that SOD1 Tg rats are useful tools for studying the role of oxygen radicals in the pathogenesis of neuronal death after transient global cerebral ischemia.
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Cites
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Self-citationSuperoxide production in rat hippocampal neurons: selective imaging with hydroethidine
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Cited by
Ischemic Cell Death in Brain Neurons
Lipton, P. (1999) · Physiological Reviews · doi:10.1152/physrev.1999.79.4.1431 · Cited by 3,043
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Free Radical Pathways in CNS Injury
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Self-citationIntrinsic oxidative stress in cancer cells: a biochemical basis for therapeutic selectivity
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Metadata
- Authors
- Chan, P. H., Kawase, M., Murakami, K., Chen, S. F., Li, Y., Calagui, B., Reola, L., Carlson, E., & Epstein, C. J.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 1998-10-15
- Volume
- 18
- Issue
- 20
- Pages
- 8292-8299
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W1527017265
- Cited by
- 340
- References
- 31
- FWCI
- 10.88
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- CoChat. (2026). Citation check: Overexpression of SOD1 in Transgenic Rats Protects Vulnerable Neurons Against Ischemic Damage After Global Cerebral Ischemia and Reperfusion. https://app.cochat.ai/papers/10.1523/jneurosci.18-20-08292.1998
- The paper
- Chan, P. H., Kawase, M., Murakami, K., Chen, S. F., Li, Y., Calagui, B., Reola, L., Carlson, E., & Epstein, C. J. (1998). Overexpression of SOD1 in Transgenic Rats Protects Vulnerable Neurons Against Ischemic Damage After Global Cerebral Ischemia and Reperfusion. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.18-20-08292.1998
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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