Preconditioning with prolonged normobaric hyperoxia induces ischemic tolerance partly by upregulation of antioxidant enzymes in rat brain tissue
Abstract Recent studies suggest that normobaric hyperoxia (HO) results in brain ischemic tolerance (BIT), reducing ischemic brain injury. We have attempted to determine the time course of HO-induced upregulation of antioxidant enzymes. Rodents comprised five groups, breathing room air (RA; O2 = 21%)...
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| description | Abstract Recent studies suggest that normobaric hyperoxia (HO) results in brain ischemic tolerance (BIT), reducing ischemic brain injury. We have attempted to determine the time course of HO-induced upregulation of antioxidant enzymes. Rodents comprised five groups, breathing room air (RA; O2 = 21%), or 95% oxygen (hyperoxia, HO) for 4, 8, 16, and 24 h (RA, 4HO, 8HO, 16HO, 24HO respectively) in the same chamber. Each main group was subdivided to MCAO-operated (middle cerebral artery occlusion), and intact (without any surgery) subgroups. After 24 h, MCAO-operated subgroups were subjected to 60 min of right MCAO. After 24 h reperfusion, neurologic deficit score (NDS), mortality rate, and infarct volume were measured in MCAO-operated subgroups. 48 h after pretreatment, antioxidant enzymes activities were assessed in MCAO-operated, sham-operated, and intact subgroups. Preconditioning with 16HO and 24HO decreased NDS, mortality rate, infarct volume, and increased antioxidant enzymes activities (superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase) significantly. Although further studies are needed to clarify the mechanisms of ischemic tolerance, the prolonged HO seems to partly exert their effects via increase in antioxidant enzymes activities. |
| doi_str_mv | 10.1016/j.brainres.2008.12.065 |
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We have attempted to determine the time course of HO-induced upregulation of antioxidant enzymes. Rodents comprised five groups, breathing room air (RA; O2 = 21%), or 95% oxygen (hyperoxia, HO) for 4, 8, 16, and 24 h (RA, 4HO, 8HO, 16HO, 24HO respectively) in the same chamber. Each main group was subdivided to MCAO-operated (middle cerebral artery occlusion), and intact (without any surgery) subgroups. After 24 h, MCAO-operated subgroups were subjected to 60 min of right MCAO. After 24 h reperfusion, neurologic deficit score (NDS), mortality rate, and infarct volume were measured in MCAO-operated subgroups. 48 h after pretreatment, antioxidant enzymes activities were assessed in MCAO-operated, sham-operated, and intact subgroups. Preconditioning with 16HO and 24HO decreased NDS, mortality rate, infarct volume, and increased antioxidant enzymes activities (superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase) significantly. Although further studies are needed to clarify the mechanisms of ischemic tolerance, the prolonged HO seems to partly exert their effects via increase in antioxidant enzymes activities.</description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/j.brainres.2008.12.065</identifier><identifier>PMID: 19167368</identifier><identifier>CODEN: BRREAP</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>Analysis of Variance ; Animals ; Antioxidants - metabolism ; Biological and medical sciences ; Brain - blood supply ; Brain - enzymology ; Brain - pathology ; Brain ischemia tolerance ; Catalase ; Catalase - metabolism ; Glutathione peroxidase ; Glutathione Peroxidase - metabolism ; Glutathione reductase ; Glutathione Reductase - metabolism ; Infarction, Middle Cerebral Artery - metabolism ; Infarction, Middle Cerebral Artery - pathology ; Infarction, Middle Cerebral Artery - physiopathology ; Ischemic Preconditioning ; Laser-Doppler Flowmetry ; Male ; Medical sciences ; Motor Activity ; Neurology ; Neuroprotection ; Normobaric hyperoxia ; Oxygen - metabolism ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury - prevention & control ; Stroke ; Superoxide dismutase ; Superoxide Dismutase - metabolism ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Brain research, 2009-03, Vol.1260, p.47-54</ispartof><rights>Elsevier B.V.</rights><rights>2008 Elsevier B.V.</rights><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c482t-9bc05c1a02989129c351a37e5fa4817937e6a8d908e844d51e6f24038fc303333</citedby><cites>FETCH-LOGICAL-c482t-9bc05c1a02989129c351a37e5fa4817937e6a8d908e844d51e6f24038fc303333</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0006899308030977$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21257737$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19167368$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bigdeli, Mohammad Reza</creatorcontrib><title>Preconditioning with prolonged normobaric hyperoxia induces ischemic tolerance partly by upregulation of antioxidant enzymes in rat brain tissue</title><title>Brain research</title><addtitle>Brain Res</addtitle><description>Abstract Recent studies suggest that normobaric hyperoxia (HO) results in brain ischemic tolerance (BIT), reducing ischemic brain injury. We have attempted to determine the time course of HO-induced upregulation of antioxidant enzymes. Rodents comprised five groups, breathing room air (RA; O2 = 21%), or 95% oxygen (hyperoxia, HO) for 4, 8, 16, and 24 h (RA, 4HO, 8HO, 16HO, 24HO respectively) in the same chamber. Each main group was subdivided to MCAO-operated (middle cerebral artery occlusion), and intact (without any surgery) subgroups. After 24 h, MCAO-operated subgroups were subjected to 60 min of right MCAO. After 24 h reperfusion, neurologic deficit score (NDS), mortality rate, and infarct volume were measured in MCAO-operated subgroups. 48 h after pretreatment, antioxidant enzymes activities were assessed in MCAO-operated, sham-operated, and intact subgroups. Preconditioning with 16HO and 24HO decreased NDS, mortality rate, infarct volume, and increased antioxidant enzymes activities (superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase) significantly. Although further studies are needed to clarify the mechanisms of ischemic tolerance, the prolonged HO seems to partly exert their effects via increase in antioxidant enzymes activities.</description><subject>Analysis of Variance</subject><subject>Animals</subject><subject>Antioxidants - metabolism</subject><subject>Biological and medical sciences</subject><subject>Brain - blood supply</subject><subject>Brain - enzymology</subject><subject>Brain - pathology</subject><subject>Brain ischemia tolerance</subject><subject>Catalase</subject><subject>Catalase - metabolism</subject><subject>Glutathione peroxidase</subject><subject>Glutathione Peroxidase - metabolism</subject><subject>Glutathione reductase</subject><subject>Glutathione Reductase - metabolism</subject><subject>Infarction, Middle Cerebral Artery - metabolism</subject><subject>Infarction, Middle Cerebral Artery - pathology</subject><subject>Infarction, Middle Cerebral Artery - physiopathology</subject><subject>Ischemic Preconditioning</subject><subject>Laser-Doppler Flowmetry</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Motor Activity</subject><subject>Neurology</subject><subject>Neuroprotection</subject><subject>Normobaric hyperoxia</subject><subject>Oxygen - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reperfusion Injury - prevention & control</subject><subject>Stroke</subject><subject>Superoxide dismutase</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUk1v1DAQjRCIbgt_ofIFbln8kTj2BYEqKEiVQALOlteZ7HpJ7MVOSsOv4CczYReQuPQ0Y_nNm5n3piguGV0zyuSL_XqTrA8J8ppTqtaMr6msHxQrphpeSl7Rh8WKUipLpbU4K85z3uNTCE0fF2dMM9kIqVbFz48JXAytH30MPmzJdz_uyCHFPoYttCTENMSNTd6R3XyAFO-8JT60k4NMfHY7GPBrjD0kGxyQg01jP5PNTKZDgu3U24WYxI7YgNmdbzESCD_mYSEIJNmR_F6FjD7nCZ4UjzrbZ3h6ihfFl7dvPl-9K28-XL-_en1TukrxsdQbR2vHLOVaaca1EzWzooG6s5VijcZUWtVqqkBVVVszkB2KIlTnBKogxEXx_MiLu36bII9mwHWg722AOGUjpW4Yr_i9QE4rKqumQaA8Al2KOSfozCH5wabZMGoW08ze_DHNLKYZxg2ahoWXpw7TZoD2X9nJJQQ8OwFsdrbvFql9_ovjjNfYf5ng1REHKNyth2Sy84C2tB5dHk0b_f2zvPyPwvU-eOz6FWbI-zilgLYYZjIWmE_LiS0XRhUVVOMUvwBcp9EE</recordid><startdate>20090313</startdate><enddate>20090313</enddate><creator>Bigdeli, Mohammad Reza</creator><general>Elsevier B.V</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>20090313</creationdate><title>Preconditioning with prolonged normobaric hyperoxia induces ischemic tolerance partly by upregulation of antioxidant enzymes in rat brain tissue</title><author>Bigdeli, Mohammad Reza</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c482t-9bc05c1a02989129c351a37e5fa4817937e6a8d908e844d51e6f24038fc303333</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Analysis of Variance</topic><topic>Animals</topic><topic>Antioxidants - metabolism</topic><topic>Biological and medical sciences</topic><topic>Brain - blood supply</topic><topic>Brain - enzymology</topic><topic>Brain - pathology</topic><topic>Brain ischemia tolerance</topic><topic>Catalase</topic><topic>Catalase - metabolism</topic><topic>Glutathione peroxidase</topic><topic>Glutathione Peroxidase - metabolism</topic><topic>Glutathione reductase</topic><topic>Glutathione Reductase - metabolism</topic><topic>Infarction, Middle Cerebral Artery - metabolism</topic><topic>Infarction, Middle Cerebral Artery - pathology</topic><topic>Infarction, Middle Cerebral Artery - physiopathology</topic><topic>Ischemic Preconditioning</topic><topic>Laser-Doppler Flowmetry</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Motor Activity</topic><topic>Neurology</topic><topic>Neuroprotection</topic><topic>Normobaric hyperoxia</topic><topic>Oxygen - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reperfusion Injury - prevention & control</topic><topic>Stroke</topic><topic>Superoxide dismutase</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bigdeli, Mohammad Reza</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>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bigdeli, Mohammad Reza</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Preconditioning with prolonged normobaric hyperoxia induces ischemic tolerance partly by upregulation of antioxidant enzymes in rat brain tissue</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>2009-03-13</date><risdate>2009</risdate><volume>1260</volume><spage>47</spage><epage>54</epage><pages>47-54</pages><issn>0006-8993</issn><eissn>1872-6240</eissn><coden>BRREAP</coden><abstract>Abstract Recent studies suggest that normobaric hyperoxia (HO) results in brain ischemic tolerance (BIT), reducing ischemic brain injury. We have attempted to determine the time course of HO-induced upregulation of antioxidant enzymes. Rodents comprised five groups, breathing room air (RA; O2 = 21%), or 95% oxygen (hyperoxia, HO) for 4, 8, 16, and 24 h (RA, 4HO, 8HO, 16HO, 24HO respectively) in the same chamber. Each main group was subdivided to MCAO-operated (middle cerebral artery occlusion), and intact (without any surgery) subgroups. After 24 h, MCAO-operated subgroups were subjected to 60 min of right MCAO. After 24 h reperfusion, neurologic deficit score (NDS), mortality rate, and infarct volume were measured in MCAO-operated subgroups. 48 h after pretreatment, antioxidant enzymes activities were assessed in MCAO-operated, sham-operated, and intact subgroups. Preconditioning with 16HO and 24HO decreased NDS, mortality rate, infarct volume, and increased antioxidant enzymes activities (superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase) significantly. Although further studies are needed to clarify the mechanisms of ischemic tolerance, the prolonged HO seems to partly exert their effects via increase in antioxidant enzymes activities.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>19167368</pmid><doi>10.1016/j.brainres.2008.12.065</doi><tpages>8</tpages></addata></record> |
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| subjects | Analysis of Variance Animals Antioxidants - metabolism Biological and medical sciences Brain - blood supply Brain - enzymology Brain - pathology Brain ischemia tolerance Catalase Catalase - metabolism Glutathione peroxidase Glutathione Peroxidase - metabolism Glutathione reductase Glutathione Reductase - metabolism Infarction, Middle Cerebral Artery - metabolism Infarction, Middle Cerebral Artery - pathology Infarction, Middle Cerebral Artery - physiopathology Ischemic Preconditioning Laser-Doppler Flowmetry Male Medical sciences Motor Activity Neurology Neuroprotection Normobaric hyperoxia Oxygen - metabolism Rats Rats, Sprague-Dawley Reperfusion Injury - prevention & control Stroke Superoxide dismutase Superoxide Dismutase - metabolism Vascular diseases and vascular malformations of the nervous system |
| title | Preconditioning with prolonged normobaric hyperoxia induces ischemic tolerance partly by upregulation of antioxidant enzymes in rat brain tissue |
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