Extracellular superoxide dismutase deficiency worsens outcome from focal cerebral ischemia in the mouse
The role of endogenous extracellular superoxide dismutase (EC-SOD) was examined in a murine model of transient focal cerebral ischemia. Homozygous EC-SOD deficient (EC-SOD −/−; n=18) and wild type (EC-SOD +/+; n=19) littermates were anesthetized with halothane and subjected to 50 min of intraluminal...
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| Veröffentlicht in: | Neuroscience letters 1999-05, Vol.267 (1), p.13-16 |
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| creator | Sheng, Huaxin Brady, Todd C. Pearlstein, Robert D. Crapo, James D. Warner, David S. |
| description | The role of endogenous extracellular superoxide dismutase (EC-SOD) was examined in a murine model of transient focal cerebral ischemia. Homozygous EC-SOD deficient (EC-SOD
−/−;
n=18) and wild type (EC-SOD
+/+;
n=19) littermates were anesthetized with halothane and subjected to 50 min of intraluminal middle cerebral artery occlusion with pericranial temperature maintained at 37.0°C. After 24 h of reperfusion, resultant hemiparesis and cerebral infarct size were measured. Total infarct volume was 81% greater (
P=0.03) and hemiparesis was more severe (
P=0.01) in EC-SOD
−/− versus EC-SOD
+/+ mice. The worsened ischemic outcome observed in EC-SOD
−/− mice is consistent with prior work which found transgenic EC-SOD overexpressing mice to exhibit enhanced tolerance to focal ischemia. The results suggest that endogenous antioxidant activity in the extracellular compartment plays an important role in the histologic/neurologic response to focal cerebral ischemia. |
| doi_str_mv | 10.1016/S0304-3940(99)00316-X |
| format | Article |
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−/−;
n=18) and wild type (EC-SOD
+/+;
n=19) littermates were anesthetized with halothane and subjected to 50 min of intraluminal middle cerebral artery occlusion with pericranial temperature maintained at 37.0°C. After 24 h of reperfusion, resultant hemiparesis and cerebral infarct size were measured. Total infarct volume was 81% greater (
P=0.03) and hemiparesis was more severe (
P=0.01) in EC-SOD
−/− versus EC-SOD
+/+ mice. The worsened ischemic outcome observed in EC-SOD
−/− mice is consistent with prior work which found transgenic EC-SOD overexpressing mice to exhibit enhanced tolerance to focal ischemia. The results suggest that endogenous antioxidant activity in the extracellular compartment plays an important role in the histologic/neurologic response to focal cerebral ischemia.</description><identifier>ISSN: 0304-3940</identifier><identifier>EISSN: 1872-7972</identifier><identifier>DOI: 10.1016/S0304-3940(99)00316-X</identifier><identifier>PMID: 10400237</identifier><identifier>CODEN: NELED5</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>Animals ; Biological and medical sciences ; Brain ; Cerebral Infarction - enzymology ; Cerebral Infarction - genetics ; Cerebral Infarction - physiopathology ; Disease Models, Animal ; Extracellular Matrix - enzymology ; Extracellular superoxide dismutase ; Ischemia ; Ischemic Attack, Transient - enzymology ; Ischemic Attack, Transient - genetics ; Ischemic Attack, Transient - physiopathology ; Male ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mouse ; Neurology ; Superoxide Dismutase - deficiency ; Superoxide Dismutase - genetics ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Neuroscience letters, 1999-05, Vol.267 (1), p.13-16</ispartof><rights>1999 Elsevier Science Ireland Ltd</rights><rights>1999 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c421t-ae68dd34a70011e380719e4aacfbdb565cb4af24715aee9151b1cc7882ea7b9d3</citedby><cites>FETCH-LOGICAL-c421t-ae68dd34a70011e380719e4aacfbdb565cb4af24715aee9151b1cc7882ea7b9d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0304-3940(99)00316-X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1792295$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10400237$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sheng, Huaxin</creatorcontrib><creatorcontrib>Brady, Todd C.</creatorcontrib><creatorcontrib>Pearlstein, Robert D.</creatorcontrib><creatorcontrib>Crapo, James D.</creatorcontrib><creatorcontrib>Warner, David S.</creatorcontrib><title>Extracellular superoxide dismutase deficiency worsens outcome from focal cerebral ischemia in the mouse</title><title>Neuroscience letters</title><addtitle>Neurosci Lett</addtitle><description>The role of endogenous extracellular superoxide dismutase (EC-SOD) was examined in a murine model of transient focal cerebral ischemia. Homozygous EC-SOD deficient (EC-SOD
−/−;
n=18) and wild type (EC-SOD
+/+;
n=19) littermates were anesthetized with halothane and subjected to 50 min of intraluminal middle cerebral artery occlusion with pericranial temperature maintained at 37.0°C. After 24 h of reperfusion, resultant hemiparesis and cerebral infarct size were measured. Total infarct volume was 81% greater (
P=0.03) and hemiparesis was more severe (
P=0.01) in EC-SOD
−/− versus EC-SOD
+/+ mice. The worsened ischemic outcome observed in EC-SOD
−/− mice is consistent with prior work which found transgenic EC-SOD overexpressing mice to exhibit enhanced tolerance to focal ischemia. The results suggest that endogenous antioxidant activity in the extracellular compartment plays an important role in the histologic/neurologic response to focal cerebral ischemia.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Brain</subject><subject>Cerebral Infarction - enzymology</subject><subject>Cerebral Infarction - genetics</subject><subject>Cerebral Infarction - physiopathology</subject><subject>Disease Models, Animal</subject><subject>Extracellular Matrix - enzymology</subject><subject>Extracellular superoxide dismutase</subject><subject>Ischemia</subject><subject>Ischemic Attack, Transient - enzymology</subject><subject>Ischemic Attack, Transient - genetics</subject><subject>Ischemic Attack, Transient - physiopathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Mouse</subject><subject>Neurology</subject><subject>Superoxide Dismutase - deficiency</subject><subject>Superoxide Dismutase - genetics</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><issn>0304-3940</issn><issn>1872-7972</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU9v1DAQxS1ERZfCRwD5gBA9BMaOHccnhKr-kypxaJF6sxx7Ql0l8dZOoP32uLsr2ltPM4ffzLx5j5APDL4yYM23S6hBVLUW8EXrQ4CaNdX1K7JireKV0oq_Jqv_yD55m_MtAEgmxRuyz0AA8FqtyO_j-zlZh8OwDDbRvKwxxfvgkfqQx2W2uXTYBxdwcg_0b0wZp0zjMrs4Iu1THGkfnR2ow4RdKk3I7gbHYGmY6HyDdIxLxndkr7dDxve7ekB-nRxfHZ1VFz9Pz49-XFROcDZXFpvW-1pYBcAY1i0oplFY6_rOd7KRrhO250IxaRE1k6xjzqm25WhVp319QD5v965TvFswz2Ysesp7dsKiwzS6sHWrXgSZEtBoyQsot6BLMeeEvVmnMNr0YBiYxyjMJgrz6LPR2myiMNdl7uPuwNKN6J9Nbb0vwKcdYHMxsE92ciE_cUpzrmXBvm8xLLb9CZhM3oSBPiR0s_ExvKDkH7WMp-A</recordid><startdate>19990521</startdate><enddate>19990521</enddate><creator>Sheng, Huaxin</creator><creator>Brady, Todd C.</creator><creator>Pearlstein, Robert D.</creator><creator>Crapo, James D.</creator><creator>Warner, David S.</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</general><scope>IQODW</scope><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>7X8</scope></search><sort><creationdate>19990521</creationdate><title>Extracellular superoxide dismutase deficiency worsens outcome from focal cerebral ischemia in the mouse</title><author>Sheng, Huaxin ; Brady, Todd C. ; Pearlstein, Robert D. ; Crapo, James D. ; Warner, David S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c421t-ae68dd34a70011e380719e4aacfbdb565cb4af24715aee9151b1cc7882ea7b9d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Brain</topic><topic>Cerebral Infarction - enzymology</topic><topic>Cerebral Infarction - genetics</topic><topic>Cerebral Infarction - physiopathology</topic><topic>Disease Models, Animal</topic><topic>Extracellular Matrix - enzymology</topic><topic>Extracellular superoxide dismutase</topic><topic>Ischemia</topic><topic>Ischemic Attack, Transient - enzymology</topic><topic>Ischemic Attack, Transient - genetics</topic><topic>Ischemic Attack, Transient - physiopathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Mouse</topic><topic>Neurology</topic><topic>Superoxide Dismutase - deficiency</topic><topic>Superoxide Dismutase - genetics</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sheng, Huaxin</creatorcontrib><creatorcontrib>Brady, Todd C.</creatorcontrib><creatorcontrib>Pearlstein, Robert D.</creatorcontrib><creatorcontrib>Crapo, James D.</creatorcontrib><creatorcontrib>Warner, David S.</creatorcontrib><collection>Pascal-Francis</collection><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>MEDLINE - Academic</collection><jtitle>Neuroscience letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sheng, Huaxin</au><au>Brady, Todd C.</au><au>Pearlstein, Robert D.</au><au>Crapo, James D.</au><au>Warner, David S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Extracellular superoxide dismutase deficiency worsens outcome from focal cerebral ischemia in the mouse</atitle><jtitle>Neuroscience letters</jtitle><addtitle>Neurosci Lett</addtitle><date>1999-05-21</date><risdate>1999</risdate><volume>267</volume><issue>1</issue><spage>13</spage><epage>16</epage><pages>13-16</pages><issn>0304-3940</issn><eissn>1872-7972</eissn><coden>NELED5</coden><abstract>The role of endogenous extracellular superoxide dismutase (EC-SOD) was examined in a murine model of transient focal cerebral ischemia. Homozygous EC-SOD deficient (EC-SOD
−/−;
n=18) and wild type (EC-SOD
+/+;
n=19) littermates were anesthetized with halothane and subjected to 50 min of intraluminal middle cerebral artery occlusion with pericranial temperature maintained at 37.0°C. After 24 h of reperfusion, resultant hemiparesis and cerebral infarct size were measured. Total infarct volume was 81% greater (
P=0.03) and hemiparesis was more severe (
P=0.01) in EC-SOD
−/− versus EC-SOD
+/+ mice. The worsened ischemic outcome observed in EC-SOD
−/− mice is consistent with prior work which found transgenic EC-SOD overexpressing mice to exhibit enhanced tolerance to focal ischemia. The results suggest that endogenous antioxidant activity in the extracellular compartment plays an important role in the histologic/neurologic response to focal cerebral ischemia.</abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>10400237</pmid><doi>10.1016/S0304-3940(99)00316-X</doi><tpages>4</tpages></addata></record> |
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| ispartof | Neuroscience letters, 1999-05, Vol.267 (1), p.13-16 |
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| language | eng |
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| subjects | Animals Biological and medical sciences Brain Cerebral Infarction - enzymology Cerebral Infarction - genetics Cerebral Infarction - physiopathology Disease Models, Animal Extracellular Matrix - enzymology Extracellular superoxide dismutase Ischemia Ischemic Attack, Transient - enzymology Ischemic Attack, Transient - genetics Ischemic Attack, Transient - physiopathology Male Medical sciences Mice Mice, Inbred C57BL Mice, Knockout Mouse Neurology Superoxide Dismutase - deficiency Superoxide Dismutase - genetics Vascular diseases and vascular malformations of the nervous system |
| title | Extracellular superoxide dismutase deficiency worsens outcome from focal cerebral ischemia in the mouse |
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