MRS of brain metabolite levels demonstrates the ability of scavenging of excess brain glutamate to protect against nerve agent induced seizures
This study describes the use of in vivo magnetic resonance spectrocopy (MRS) to monitor brain glutamate and lactate levels in a paraoxon (PO) intoxication model. Our results show that the administration of recombinant glutamate-oxaloacetate transaminase (rGOT) in combination with oxaloacetate (OxAc)...
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| Veröffentlicht in: | International journal of molecular sciences 2015-02, Vol.16 (2), p.3226-3236 |
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| container_title | International journal of molecular sciences |
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| creator | Ruban, Angela Biton, Inbal E Markovich, Arik Mirelman, David |
| description | This study describes the use of in vivo magnetic resonance spectrocopy (MRS) to monitor brain glutamate and lactate levels in a paraoxon (PO) intoxication model. Our results show that the administration of recombinant glutamate-oxaloacetate transaminase (rGOT) in combination with oxaloacetate (OxAc) significantly reduces the brain-accumulated levels of glutamate. Previously we have shown that the treatment causes a rapid decrease of blood glutamate levels and creates a gradient between the brain and blood glutamate levels which leads to the efflux of excess brain glutamate into the blood stream thereby reducing its potential to cause neurological damage. The fact that this treatment significantly decreased the brain glutamate and lactate levels following PO intoxication suggests that it could become a new effective neuroprotective agent. |
| doi_str_mv | 10.3390/ijms16023226 |
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Our results show that the administration of recombinant glutamate-oxaloacetate transaminase (rGOT) in combination with oxaloacetate (OxAc) significantly reduces the brain-accumulated levels of glutamate. Previously we have shown that the treatment causes a rapid decrease of blood glutamate levels and creates a gradient between the brain and blood glutamate levels which leads to the efflux of excess brain glutamate into the blood stream thereby reducing its potential to cause neurological damage. 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Our results show that the administration of recombinant glutamate-oxaloacetate transaminase (rGOT) in combination with oxaloacetate (OxAc) significantly reduces the brain-accumulated levels of glutamate. Previously we have shown that the treatment causes a rapid decrease of blood glutamate levels and creates a gradient between the brain and blood glutamate levels which leads to the efflux of excess brain glutamate into the blood stream thereby reducing its potential to cause neurological damage. The fact that this treatment significantly decreased the brain glutamate and lactate levels following PO intoxication suggests that it could become a new effective neuroprotective agent.</description><subject>Animals</subject><subject>Aspartate Aminotransferases - administration & dosage</subject><subject>Aspartate Aminotransferases - genetics</subject><subject>Aspartate Aminotransferases - metabolism</subject><subject>Brain</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>Communication</subject><subject>Glutamic Acid - metabolism</subject><subject>Humans</subject><subject>Lactic Acid - metabolism</subject><subject>Magnetic Resonance Imaging</subject><subject>Magnetic Resonance Spectroscopy</subject><subject>Male</subject><subject>Metabolome</subject><subject>Metabolomics - methods</subject><subject>NMR</subject><subject>Nuclear magnetic resonance</subject><subject>Oxaloacetic Acid - administration & dosage</subject><subject>Paraoxon - adverse effects</subject><subject>Rats</subject><subject>Seizures - chemically induced</subject><subject>Seizures - diagnosis</subject><subject>Seizures - drug therapy</subject><subject>Seizures - genetics</subject><subject>Seizures - metabolism</subject><subject>Spectrum analysis</subject><subject>Studies</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkk2L1TAYhYsozji6cy0BNy7matJ8diPI4KgwIvixLmn6tpNLm1zzphfHP-FfNmWuw9WN2SThPOfwJpyqesroS84b-spvZ2SK1ryu1b3qlIm63lCq9P2j80n1CHFLV0g2D6uTWiphiuG0-vXx8xcSB9Il6wOZIdsuTj4DmWAPE5Ie5hgwJ5sBSb4GYjtf9JvVg87uIYw-jOsNfjhAPASN05LtXEwkR7JLMYPLxI5FwkwCpH0JGiFk4kO_OOgJgv-5JMDH1YPBTghPDvtZ9e3y7deL95urT-8-XLy52jghZN702lErjaCODRwaANMpIcQwSE170_NG8AGYYZ2zHZV2XRpsZ1Wnjeo142fV69vc3dLN0LsyS7JTu0t-tummjda3fyvBX7dj3LeCC2WaNeDFISDF7wtgbmePDqbJBogLtkxLLjTV3PwfVbIWgplaFvT5P-g2LimUnyiU4lxI0dSFOr-lXIqICYa7uRlt11K0x6Uo-LPjt97Bf1rAfwMHzbbV</recordid><startdate>20150202</startdate><enddate>20150202</enddate><creator>Ruban, Angela</creator><creator>Biton, Inbal E</creator><creator>Markovich, Arik</creator><creator>Mirelman, David</creator><general>MDPI AG</general><general>MDPI</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>7TK</scope><scope>5PM</scope></search><sort><creationdate>20150202</creationdate><title>MRS of brain metabolite levels demonstrates the ability of scavenging of excess brain glutamate to protect against nerve agent induced seizures</title><author>Ruban, Angela ; Biton, Inbal E ; Markovich, Arik ; Mirelman, David</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c445t-d7c0a5840c1f3e9ee8b6444ff570d8d3943fe181bcab05aaaaa7eaba6b786d713</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Aspartate Aminotransferases - administration & dosage</topic><topic>Aspartate Aminotransferases - genetics</topic><topic>Aspartate Aminotransferases - metabolism</topic><topic>Brain</topic><topic>Brain - metabolism</topic><topic>Brain - pathology</topic><topic>Communication</topic><topic>Glutamic Acid - metabolism</topic><topic>Humans</topic><topic>Lactic Acid - metabolism</topic><topic>Magnetic Resonance Imaging</topic><topic>Magnetic Resonance Spectroscopy</topic><topic>Male</topic><topic>Metabolome</topic><topic>Metabolomics - methods</topic><topic>NMR</topic><topic>Nuclear magnetic resonance</topic><topic>Oxaloacetic Acid - administration & dosage</topic><topic>Paraoxon - adverse effects</topic><topic>Rats</topic><topic>Seizures - chemically induced</topic><topic>Seizures - diagnosis</topic><topic>Seizures - drug therapy</topic><topic>Seizures - genetics</topic><topic>Seizures - metabolism</topic><topic>Spectrum analysis</topic><topic>Studies</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ruban, Angela</creatorcontrib><creatorcontrib>Biton, Inbal E</creatorcontrib><creatorcontrib>Markovich, Arik</creatorcontrib><creatorcontrib>Mirelman, David</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ruban, Angela</au><au>Biton, Inbal E</au><au>Markovich, Arik</au><au>Mirelman, David</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MRS of brain metabolite levels demonstrates the ability of scavenging of excess brain glutamate to protect against nerve agent induced seizures</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2015-02-02</date><risdate>2015</risdate><volume>16</volume><issue>2</issue><spage>3226</spage><epage>3236</epage><pages>3226-3236</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>This study describes the use of in vivo magnetic resonance spectrocopy (MRS) to monitor brain glutamate and lactate levels in a paraoxon (PO) intoxication model. 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| source | MEDLINE; MDPI - Multidisciplinary Digital Publishing Institute; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Animals Aspartate Aminotransferases - administration & dosage Aspartate Aminotransferases - genetics Aspartate Aminotransferases - metabolism Brain Brain - metabolism Brain - pathology Communication Glutamic Acid - metabolism Humans Lactic Acid - metabolism Magnetic Resonance Imaging Magnetic Resonance Spectroscopy Male Metabolome Metabolomics - methods NMR Nuclear magnetic resonance Oxaloacetic Acid - administration & dosage Paraoxon - adverse effects Rats Seizures - chemically induced Seizures - diagnosis Seizures - drug therapy Seizures - genetics Seizures - metabolism Spectrum analysis Studies |
| title | MRS of brain metabolite levels demonstrates the ability of scavenging of excess brain glutamate to protect against nerve agent induced seizures |
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