Reduction of CuZn-Superoxide Dismutase Activity Exacerbates Neuronal Cell Injury and Edema Formation after Transient Focal Cerebral Ischemia
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 v...
Gespeichert in:
Veröffentlicht in: | The Journal of neuroscience 1997-06, Vol.17 (11), p.4180-4189 |
---|---|
Hauptverfasser: | , , , , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 4189 |
---|---|
container_issue | 11 |
container_start_page | 4180 |
container_title | The Journal of neuroscience |
container_volume | 17 |
creator | Kondo, Takeo Reaume, Andrew G Huang, Ting-Ting Carlson, Elaine Murakami, Kensuke Chen, Sylvia F Hoffman, Eric K Scott, Richard W Epstein, Charles J Chan, Pak H |
description | 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. |
doi_str_mv | 10.1523/jneurosci.17-11-04180.1997 |
format | Article |
fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6573543</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>16253241</sourcerecordid><originalsourceid>FETCH-LOGICAL-c552t-b5da599a6d433043438e97c7f9ab28ba20c35f05691ad05267b14d51b74002c03</originalsourceid><addsrcrecordid>eNpVUctu1DAUtRCoDAOfgGSxgFWKn_GEBVIVpjBV1Up9bNhYjnPT8ShxBjvpdP6Bj8bzUFVW90rncY_uQegTJadUMv515WEMfbTulKqM0owIOktQUahXaJIYRcYEoa_RhDBFslwo8Ra9i3FFCFGEqhN0UlBJFZcT9PcG6tEOrve4b3A5_vbZ7biG0D-5GvAPF7txMBHwWeI8umGL50_GQqjMABFf7WJ40-IS2hYv_GoMW2x8jec1dAaf96Eze2vTDBDwXTA-OvBDQuxeFaAKaVlEu4TOmffoTWPaCB-Oc4ruz-d35a_s8vrnojy7zKyUbMgqWRtZFCavBedEcMFnUCirmsJUbFYZRiyXDZF5QU1NJMtVRUUtaaUEIcwSPkXfD77rseqgtilSiqHXwXUmbHVvnP4f8W6pH_pHncv0tHR0ij4fDUL_Z4Q46M5Fm55gPPRj1DRnkjNBE_HbgWhTXzFA83yEEr3rUl9cze9vrm_LhaZKU6r3Xepdl0n88WXMZ-mxvIR_OeBL97DcuAA6dqZtE5vqzWZz8NvZ8X-gM61h</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>16253241</pqid></control><display><type>article</type><title>Reduction of CuZn-Superoxide Dismutase Activity Exacerbates Neuronal Cell Injury and Edema Formation after Transient Focal Cerebral Ischemia</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><creator>Kondo, Takeo ; Reaume, Andrew G ; Huang, Ting-Ting ; Carlson, Elaine ; Murakami, Kensuke ; Chen, Sylvia F ; Hoffman, Eric K ; Scott, Richard W ; Epstein, Charles J ; Chan, Pak H</creator><creatorcontrib>Kondo, Takeo ; Reaume, Andrew G ; Huang, Ting-Ting ; Carlson, Elaine ; Murakami, Kensuke ; Chen, Sylvia F ; Hoffman, Eric K ; Scott, Richard W ; Epstein, Charles J ; Chan, Pak H</creatorcontrib><description>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.</description><identifier>ISSN: 0270-6474</identifier><identifier>EISSN: 1529-2401</identifier><identifier>DOI: 10.1523/jneurosci.17-11-04180.1997</identifier><identifier>PMID: 9151735</identifier><language>eng</language><publisher>United States: Soc Neuroscience</publisher><subject>Animals ; Apoptosis - physiology ; Biotin ; Blood-Brain Barrier - physiology ; Cell Death - physiology ; Cerebral Infarction - physiopathology ; Deoxyuracil Nucleotides ; DNA Fragmentation ; Edema - physiopathology ; Evans Blue - pharmacokinetics ; Ischemic Attack, Transient - enzymology ; Ischemic Attack, Transient - mortality ; Ischemic Attack, Transient - physiopathology ; Mice ; Mice, Mutant Strains ; Neurologic Examination ; Neurons - enzymology ; Neurons - pathology ; Oxidative Stress - physiology ; Prosencephalon - blood supply ; Prosencephalon - enzymology ; Prosencephalon - pathology ; Reactive Oxygen Species - physiology ; Staining and Labeling ; Superoxide Dismutase - genetics ; Superoxide Dismutase - metabolism</subject><ispartof>The Journal of neuroscience, 1997-06, Vol.17 (11), p.4180-4189</ispartof><rights>Copyright © 1997 Society for Neuroscience 1997</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c552t-b5da599a6d433043438e97c7f9ab28ba20c35f05691ad05267b14d51b74002c03</citedby><cites>FETCH-LOGICAL-c552t-b5da599a6d433043438e97c7f9ab28ba20c35f05691ad05267b14d51b74002c03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6573543/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6573543/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,315,729,782,786,887,27931,27932,53798,53800</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9151735$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kondo, Takeo</creatorcontrib><creatorcontrib>Reaume, Andrew G</creatorcontrib><creatorcontrib>Huang, Ting-Ting</creatorcontrib><creatorcontrib>Carlson, Elaine</creatorcontrib><creatorcontrib>Murakami, Kensuke</creatorcontrib><creatorcontrib>Chen, Sylvia F</creatorcontrib><creatorcontrib>Hoffman, Eric K</creatorcontrib><creatorcontrib>Scott, Richard W</creatorcontrib><creatorcontrib>Epstein, Charles J</creatorcontrib><creatorcontrib>Chan, Pak H</creatorcontrib><title>Reduction of CuZn-Superoxide Dismutase Activity Exacerbates Neuronal Cell Injury and Edema Formation after Transient Focal Cerebral Ischemia</title><title>The Journal of neuroscience</title><addtitle>J Neurosci</addtitle><description>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.</description><subject>Animals</subject><subject>Apoptosis - physiology</subject><subject>Biotin</subject><subject>Blood-Brain Barrier - physiology</subject><subject>Cell Death - physiology</subject><subject>Cerebral Infarction - physiopathology</subject><subject>Deoxyuracil Nucleotides</subject><subject>DNA Fragmentation</subject><subject>Edema - physiopathology</subject><subject>Evans Blue - pharmacokinetics</subject><subject>Ischemic Attack, Transient - enzymology</subject><subject>Ischemic Attack, Transient - mortality</subject><subject>Ischemic Attack, Transient - physiopathology</subject><subject>Mice</subject><subject>Mice, Mutant Strains</subject><subject>Neurologic Examination</subject><subject>Neurons - enzymology</subject><subject>Neurons - pathology</subject><subject>Oxidative Stress - physiology</subject><subject>Prosencephalon - blood supply</subject><subject>Prosencephalon - enzymology</subject><subject>Prosencephalon - pathology</subject><subject>Reactive Oxygen Species - physiology</subject><subject>Staining and Labeling</subject><subject>Superoxide Dismutase - genetics</subject><subject>Superoxide Dismutase - metabolism</subject><issn>0270-6474</issn><issn>1529-2401</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVUctu1DAUtRCoDAOfgGSxgFWKn_GEBVIVpjBV1Up9bNhYjnPT8ShxBjvpdP6Bj8bzUFVW90rncY_uQegTJadUMv515WEMfbTulKqM0owIOktQUahXaJIYRcYEoa_RhDBFslwo8Ra9i3FFCFGEqhN0UlBJFZcT9PcG6tEOrve4b3A5_vbZ7biG0D-5GvAPF7txMBHwWeI8umGL50_GQqjMABFf7WJ40-IS2hYv_GoMW2x8jec1dAaf96Eze2vTDBDwXTA-OvBDQuxeFaAKaVlEu4TOmffoTWPaCB-Oc4ruz-d35a_s8vrnojy7zKyUbMgqWRtZFCavBedEcMFnUCirmsJUbFYZRiyXDZF5QU1NJMtVRUUtaaUEIcwSPkXfD77rseqgtilSiqHXwXUmbHVvnP4f8W6pH_pHncv0tHR0ij4fDUL_Z4Q46M5Fm55gPPRj1DRnkjNBE_HbgWhTXzFA83yEEr3rUl9cze9vrm_LhaZKU6r3Xepdl0n88WXMZ-mxvIR_OeBL97DcuAA6dqZtE5vqzWZz8NvZ8X-gM61h</recordid><startdate>19970601</startdate><enddate>19970601</enddate><creator>Kondo, Takeo</creator><creator>Reaume, Andrew G</creator><creator>Huang, Ting-Ting</creator><creator>Carlson, Elaine</creator><creator>Murakami, Kensuke</creator><creator>Chen, Sylvia F</creator><creator>Hoffman, Eric K</creator><creator>Scott, Richard W</creator><creator>Epstein, Charles J</creator><creator>Chan, Pak H</creator><general>Soc Neuroscience</general><general>Society for Neuroscience</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>5PM</scope></search><sort><creationdate>19970601</creationdate><title>Reduction of CuZn-Superoxide Dismutase Activity Exacerbates Neuronal Cell Injury and Edema Formation after Transient Focal Cerebral Ischemia</title><author>Kondo, Takeo ; Reaume, Andrew G ; Huang, Ting-Ting ; Carlson, Elaine ; Murakami, Kensuke ; Chen, Sylvia F ; Hoffman, Eric K ; Scott, Richard W ; Epstein, Charles J ; Chan, Pak H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c552t-b5da599a6d433043438e97c7f9ab28ba20c35f05691ad05267b14d51b74002c03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Animals</topic><topic>Apoptosis - physiology</topic><topic>Biotin</topic><topic>Blood-Brain Barrier - physiology</topic><topic>Cell Death - physiology</topic><topic>Cerebral Infarction - physiopathology</topic><topic>Deoxyuracil Nucleotides</topic><topic>DNA Fragmentation</topic><topic>Edema - physiopathology</topic><topic>Evans Blue - pharmacokinetics</topic><topic>Ischemic Attack, Transient - enzymology</topic><topic>Ischemic Attack, Transient - mortality</topic><topic>Ischemic Attack, Transient - physiopathology</topic><topic>Mice</topic><topic>Mice, Mutant Strains</topic><topic>Neurologic Examination</topic><topic>Neurons - enzymology</topic><topic>Neurons - pathology</topic><topic>Oxidative Stress - physiology</topic><topic>Prosencephalon - blood supply</topic><topic>Prosencephalon - enzymology</topic><topic>Prosencephalon - pathology</topic><topic>Reactive Oxygen Species - physiology</topic><topic>Staining and Labeling</topic><topic>Superoxide Dismutase - genetics</topic><topic>Superoxide Dismutase - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kondo, Takeo</creatorcontrib><creatorcontrib>Reaume, Andrew G</creatorcontrib><creatorcontrib>Huang, Ting-Ting</creatorcontrib><creatorcontrib>Carlson, Elaine</creatorcontrib><creatorcontrib>Murakami, Kensuke</creatorcontrib><creatorcontrib>Chen, Sylvia F</creatorcontrib><creatorcontrib>Hoffman, Eric K</creatorcontrib><creatorcontrib>Scott, Richard W</creatorcontrib><creatorcontrib>Epstein, Charles J</creatorcontrib><creatorcontrib>Chan, Pak H</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kondo, Takeo</au><au>Reaume, Andrew G</au><au>Huang, Ting-Ting</au><au>Carlson, Elaine</au><au>Murakami, Kensuke</au><au>Chen, Sylvia F</au><au>Hoffman, Eric K</au><au>Scott, Richard W</au><au>Epstein, Charles J</au><au>Chan, Pak H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reduction of CuZn-Superoxide Dismutase Activity Exacerbates Neuronal Cell Injury and Edema Formation after Transient Focal Cerebral Ischemia</atitle><jtitle>The Journal of neuroscience</jtitle><addtitle>J Neurosci</addtitle><date>1997-06-01</date><risdate>1997</risdate><volume>17</volume><issue>11</issue><spage>4180</spage><epage>4189</epage><pages>4180-4189</pages><issn>0270-6474</issn><eissn>1529-2401</eissn><abstract>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.</abstract><cop>United States</cop><pub>Soc Neuroscience</pub><pmid>9151735</pmid><doi>10.1523/jneurosci.17-11-04180.1997</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0270-6474 |
ispartof | The Journal of neuroscience, 1997-06, Vol.17 (11), p.4180-4189 |
issn | 0270-6474 1529-2401 |
language | eng |
recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6573543 |
source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
subjects | Animals Apoptosis - physiology Biotin Blood-Brain Barrier - physiology Cell Death - physiology Cerebral Infarction - physiopathology Deoxyuracil Nucleotides DNA Fragmentation Edema - physiopathology Evans Blue - pharmacokinetics Ischemic Attack, Transient - enzymology Ischemic Attack, Transient - mortality Ischemic Attack, Transient - physiopathology Mice Mice, Mutant Strains Neurologic Examination Neurons - enzymology Neurons - pathology Oxidative Stress - physiology Prosencephalon - blood supply Prosencephalon - enzymology Prosencephalon - pathology Reactive Oxygen Species - physiology Staining and Labeling Superoxide Dismutase - genetics Superoxide Dismutase - metabolism |
title | Reduction of CuZn-Superoxide Dismutase Activity Exacerbates Neuronal Cell Injury and Edema Formation after Transient Focal Cerebral Ischemia |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-08T12%3A59%3A19IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Reduction%20of%20CuZn-Superoxide%20Dismutase%20Activity%20Exacerbates%20Neuronal%20Cell%20Injury%20and%20Edema%20Formation%20after%20Transient%20Focal%20Cerebral%20Ischemia&rft.jtitle=The%20Journal%20of%20neuroscience&rft.au=Kondo,%20Takeo&rft.date=1997-06-01&rft.volume=17&rft.issue=11&rft.spage=4180&rft.epage=4189&rft.pages=4180-4189&rft.issn=0270-6474&rft.eissn=1529-2401&rft_id=info:doi/10.1523/jneurosci.17-11-04180.1997&rft_dat=%3Cproquest_pubme%3E16253241%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=16253241&rft_id=info:pmid/9151735&rfr_iscdi=true |