Creatine decreases convulsions and neurochemical alterations induced by glutaric acid in rats
Abstract Glutaric acidemia type I (GA-I) is an inherited metabolic disease characterized by striatal degeneration, seizures, and accumulation of glutaric acid (GA). Considering that GA impairs energy metabolism and induces reactive species generation, we investigated whether the acute administration...
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| Veröffentlicht in: | Brain research 2007-12, Vol.1185, p.336-345 |
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| creator | Magni, Danieli Valnes Oliveira, Mauro Schneider Furian, Ana Flávia Fiorenza, Natália Gindri Fighera, Michele Rechia Ferreira, Juliano Mello, Carlos Fernando Royes, Luiz Fernando Freire |
| description | Abstract Glutaric acidemia type I (GA-I) is an inherited metabolic disease characterized by striatal degeneration, seizures, and accumulation of glutaric acid (GA). Considering that GA impairs energy metabolism and induces reactive species generation, we investigated whether the acute administration of creatine, an amino acid with antioxidant and ergogenic properties, protects against the seizures and neurochemical alterations (inhibition of Na+ ,K+ -ATPase and increased protein carbonylation) induced by the intrastriatal injection of GA (4 μmol/striatum). We also investigated whether creatine protected against the GA-induced inhibition of glutamate uptake in vitro . Creatine administration (300 mg/kg, p.o.) decreased seizures (evidenced by electrographic changes), protein carbonylation and Na+ ,K+ -ATPase inhibition induced by GA. However, creatine, at a dose capable of fully preventing GA-induced protein carbonylation (50 and 150 mg/kg, p.o.), did not prevent convulsions and Na+ ,K+ -ATPase inhibition, suggesting that the anticonvulsant activity of creatine in this experimental model is not related to its antioxidant action. Creatine also protected against the GA-induced inhibition of l -[3 H]glutamate uptake in synaptosomes, suggesting that creatine may reduce the deleterious effects of GA by maintaining glutamate uptake in the synaptic cleft. Therefore, considering that creatine significantly attenuates the deleterious effects of GA assessed by behavioral and neurochemical measures, it is plausible to propose the use of this amino acid as an adjuvant therapy in the management of glutaric acidemia. |
| doi_str_mv | 10.1016/j.brainres.2007.09.023 |
| format | Article |
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Considering that GA impairs energy metabolism and induces reactive species generation, we investigated whether the acute administration of creatine, an amino acid with antioxidant and ergogenic properties, protects against the seizures and neurochemical alterations (inhibition of Na+ ,K+ -ATPase and increased protein carbonylation) induced by the intrastriatal injection of GA (4 μmol/striatum). We also investigated whether creatine protected against the GA-induced inhibition of glutamate uptake in vitro . Creatine administration (300 mg/kg, p.o.) decreased seizures (evidenced by electrographic changes), protein carbonylation and Na+ ,K+ -ATPase inhibition induced by GA. However, creatine, at a dose capable of fully preventing GA-induced protein carbonylation (50 and 150 mg/kg, p.o.), did not prevent convulsions and Na+ ,K+ -ATPase inhibition, suggesting that the anticonvulsant activity of creatine in this experimental model is not related to its antioxidant action. Creatine also protected against the GA-induced inhibition of l -[3 H]glutamate uptake in synaptosomes, suggesting that creatine may reduce the deleterious effects of GA by maintaining glutamate uptake in the synaptic cleft. Therefore, considering that creatine significantly attenuates the deleterious effects of GA assessed by behavioral and neurochemical measures, it is plausible to propose the use of this amino acid as an adjuvant therapy in the management of glutaric acidemia.</description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/j.brainres.2007.09.023</identifier><identifier>PMID: 17950259</identifier><identifier>CODEN: BRREAP</identifier><language>eng</language><publisher>London: Elsevier B.V</publisher><subject>Analysis of Variance ; Animals ; Anticonvulsants - therapeutic use ; Behavior, Animal - drug effects ; Biochemistry and metabolism ; Biological and medical sciences ; Brain Chemistry - drug effects ; Central nervous system ; Convulsion ; Creatine ; Creatine - therapeutic use ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Drug Interactions ; Electric Stimulation - adverse effects ; Electroencephalography - methods ; Fundamental and applied biological sciences. Psychology ; Glutamate ; Glutarates ; Glutaric acid ; Male ; Neurology ; Oxidative damage ; Protein Carbonylation - drug effects ; Rats ; Rats, Wistar ; Seizures - chemically induced ; Seizures - drug therapy ; Seizures - metabolism ; Sodium-Potassium-Exchanging ATPase - metabolism ; Striatum ; Synaptosomes - drug effects ; Synaptosomes - metabolism ; Vertebrates: nervous system and sense organs</subject><ispartof>Brain research, 2007-12, Vol.1185, p.336-345</ispartof><rights>Elsevier B.V.</rights><rights>2007 Elsevier B.V.</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c482t-b2c66459ba59216eea0989bc98d0101623616c6bc4f66d7556b08749366b54853</citedby><cites>FETCH-LOGICAL-c482t-b2c66459ba59216eea0989bc98d0101623616c6bc4f66d7556b08749366b54853</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.brainres.2007.09.023$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19900936$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17950259$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Magni, Danieli Valnes</creatorcontrib><creatorcontrib>Oliveira, Mauro Schneider</creatorcontrib><creatorcontrib>Furian, Ana Flávia</creatorcontrib><creatorcontrib>Fiorenza, Natália Gindri</creatorcontrib><creatorcontrib>Fighera, Michele Rechia</creatorcontrib><creatorcontrib>Ferreira, Juliano</creatorcontrib><creatorcontrib>Mello, Carlos Fernando</creatorcontrib><creatorcontrib>Royes, Luiz Fernando Freire</creatorcontrib><title>Creatine decreases convulsions and neurochemical alterations induced by glutaric acid in rats</title><title>Brain research</title><addtitle>Brain Res</addtitle><description>Abstract Glutaric acidemia type I (GA-I) is an inherited metabolic disease characterized by striatal degeneration, seizures, and accumulation of glutaric acid (GA). Considering that GA impairs energy metabolism and induces reactive species generation, we investigated whether the acute administration of creatine, an amino acid with antioxidant and ergogenic properties, protects against the seizures and neurochemical alterations (inhibition of Na+ ,K+ -ATPase and increased protein carbonylation) induced by the intrastriatal injection of GA (4 μmol/striatum). We also investigated whether creatine protected against the GA-induced inhibition of glutamate uptake in vitro . Creatine administration (300 mg/kg, p.o.) decreased seizures (evidenced by electrographic changes), protein carbonylation and Na+ ,K+ -ATPase inhibition induced by GA. However, creatine, at a dose capable of fully preventing GA-induced protein carbonylation (50 and 150 mg/kg, p.o.), did not prevent convulsions and Na+ ,K+ -ATPase inhibition, suggesting that the anticonvulsant activity of creatine in this experimental model is not related to its antioxidant action. Creatine also protected against the GA-induced inhibition of l -[3 H]glutamate uptake in synaptosomes, suggesting that creatine may reduce the deleterious effects of GA by maintaining glutamate uptake in the synaptic cleft. Therefore, considering that creatine significantly attenuates the deleterious effects of GA assessed by behavioral and neurochemical measures, it is plausible to propose the use of this amino acid as an adjuvant therapy in the management of glutaric acidemia.</description><subject>Analysis of Variance</subject><subject>Animals</subject><subject>Anticonvulsants - therapeutic use</subject><subject>Behavior, Animal - drug effects</subject><subject>Biochemistry and metabolism</subject><subject>Biological and medical sciences</subject><subject>Brain Chemistry - drug effects</subject><subject>Central nervous system</subject><subject>Convulsion</subject><subject>Creatine</subject><subject>Creatine - therapeutic use</subject><subject>Disease Models, Animal</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug Interactions</subject><subject>Electric Stimulation - adverse effects</subject><subject>Electroencephalography - methods</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Glutamate</subject><subject>Glutarates</subject><subject>Glutaric acid</subject><subject>Male</subject><subject>Neurology</subject><subject>Oxidative damage</subject><subject>Protein Carbonylation - drug effects</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Seizures - chemically induced</subject><subject>Seizures - drug therapy</subject><subject>Seizures - metabolism</subject><subject>Sodium-Potassium-Exchanging ATPase - metabolism</subject><subject>Striatum</subject><subject>Synaptosomes - drug effects</subject><subject>Synaptosomes - metabolism</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFksFu1DAQQC0EotvCL1S-wC1h7DhOfEGgVaFIlTgAR2TZzix4yTrFk1Tav8fRLqrEhZNtzRvP-HkYuxZQCxD6zb722cWUkWoJ0NVgapDNE7YRfScrLRU8ZRsA0FVvTHPBLon25dg0Bp6zC9GZFmRrNuz7NqObY0I-YChbQuJhSg_LSHFKxF0aeMIlT-EnHmJwI3fjjLmkrNGYhiXgwP2R_xiX2eUYuAtxKAFeGHrBnu3cSPjyvF6xbx9uvm5vq7vPHz9t399VQfVyrrwMWqvWeNcaKTSiA9MbH0w_wPpa2Wihg_ZB7bQeurbVHvpOmUZr36q-ba7Y69O993n6vSDN9hAp4Di6hNNCVoKSWilVQH0CQ56IMu7sfY4Hl49WgF1L2b39K9auYi0YW8SWxOtzhcUfcHhMO5sswKsz4Kho2mWXQqRHzhiA0nDh3p04LD4eImZLIWIqFmPGMNthiv_v5e0_V4QxpvVzfuERaT8tORXbVliSFuyXdQzWKYAOZNELzR9Dm68F</recordid><startdate>20071214</startdate><enddate>20071214</enddate><creator>Magni, Danieli Valnes</creator><creator>Oliveira, Mauro Schneider</creator><creator>Furian, Ana Flávia</creator><creator>Fiorenza, Natália Gindri</creator><creator>Fighera, Michele Rechia</creator><creator>Ferreira, Juliano</creator><creator>Mello, Carlos Fernando</creator><creator>Royes, Luiz Fernando Freire</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></search><sort><creationdate>20071214</creationdate><title>Creatine decreases convulsions and neurochemical alterations induced by glutaric acid in rats</title><author>Magni, Danieli Valnes ; Oliveira, Mauro Schneider ; Furian, Ana Flávia ; Fiorenza, Natália Gindri ; Fighera, Michele Rechia ; Ferreira, Juliano ; Mello, Carlos Fernando ; Royes, Luiz Fernando Freire</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c482t-b2c66459ba59216eea0989bc98d0101623616c6bc4f66d7556b08749366b54853</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Analysis of Variance</topic><topic>Animals</topic><topic>Anticonvulsants - therapeutic use</topic><topic>Behavior, Animal - drug effects</topic><topic>Biochemistry and metabolism</topic><topic>Biological and medical sciences</topic><topic>Brain Chemistry - drug effects</topic><topic>Central nervous system</topic><topic>Convulsion</topic><topic>Creatine</topic><topic>Creatine - therapeutic use</topic><topic>Disease Models, Animal</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drug Interactions</topic><topic>Electric Stimulation - adverse effects</topic><topic>Electroencephalography - methods</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Glutamate</topic><topic>Glutarates</topic><topic>Glutaric acid</topic><topic>Male</topic><topic>Neurology</topic><topic>Oxidative damage</topic><topic>Protein Carbonylation - drug effects</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Seizures - chemically induced</topic><topic>Seizures - drug therapy</topic><topic>Seizures - metabolism</topic><topic>Sodium-Potassium-Exchanging ATPase - metabolism</topic><topic>Striatum</topic><topic>Synaptosomes - drug effects</topic><topic>Synaptosomes - metabolism</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Magni, Danieli Valnes</creatorcontrib><creatorcontrib>Oliveira, Mauro Schneider</creatorcontrib><creatorcontrib>Furian, Ana Flávia</creatorcontrib><creatorcontrib>Fiorenza, Natália Gindri</creatorcontrib><creatorcontrib>Fighera, Michele Rechia</creatorcontrib><creatorcontrib>Ferreira, Juliano</creatorcontrib><creatorcontrib>Mello, Carlos Fernando</creatorcontrib><creatorcontrib>Royes, Luiz Fernando Freire</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><jtitle>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Magni, Danieli Valnes</au><au>Oliveira, Mauro Schneider</au><au>Furian, Ana Flávia</au><au>Fiorenza, Natália Gindri</au><au>Fighera, Michele Rechia</au><au>Ferreira, Juliano</au><au>Mello, Carlos Fernando</au><au>Royes, Luiz Fernando Freire</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Creatine decreases convulsions and neurochemical alterations induced by glutaric acid in rats</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>2007-12-14</date><risdate>2007</risdate><volume>1185</volume><spage>336</spage><epage>345</epage><pages>336-345</pages><issn>0006-8993</issn><eissn>1872-6240</eissn><coden>BRREAP</coden><abstract>Abstract Glutaric acidemia type I (GA-I) is an inherited metabolic disease characterized by striatal degeneration, seizures, and accumulation of glutaric acid (GA). Considering that GA impairs energy metabolism and induces reactive species generation, we investigated whether the acute administration of creatine, an amino acid with antioxidant and ergogenic properties, protects against the seizures and neurochemical alterations (inhibition of Na+ ,K+ -ATPase and increased protein carbonylation) induced by the intrastriatal injection of GA (4 μmol/striatum). We also investigated whether creatine protected against the GA-induced inhibition of glutamate uptake in vitro . Creatine administration (300 mg/kg, p.o.) decreased seizures (evidenced by electrographic changes), protein carbonylation and Na+ ,K+ -ATPase inhibition induced by GA. However, creatine, at a dose capable of fully preventing GA-induced protein carbonylation (50 and 150 mg/kg, p.o.), did not prevent convulsions and Na+ ,K+ -ATPase inhibition, suggesting that the anticonvulsant activity of creatine in this experimental model is not related to its antioxidant action. Creatine also protected against the GA-induced inhibition of l -[3 H]glutamate uptake in synaptosomes, suggesting that creatine may reduce the deleterious effects of GA by maintaining glutamate uptake in the synaptic cleft. Therefore, considering that creatine significantly attenuates the deleterious effects of GA assessed by behavioral and neurochemical measures, it is plausible to propose the use of this amino acid as an adjuvant therapy in the management of glutaric acidemia.</abstract><cop>London</cop><cop>Amsterdam</cop><cop>New York, NY</cop><pub>Elsevier B.V</pub><pmid>17950259</pmid><doi>10.1016/j.brainres.2007.09.023</doi><tpages>10</tpages></addata></record> |
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| subjects | Analysis of Variance Animals Anticonvulsants - therapeutic use Behavior, Animal - drug effects Biochemistry and metabolism Biological and medical sciences Brain Chemistry - drug effects Central nervous system Convulsion Creatine Creatine - therapeutic use Disease Models, Animal Dose-Response Relationship, Drug Drug Interactions Electric Stimulation - adverse effects Electroencephalography - methods Fundamental and applied biological sciences. Psychology Glutamate Glutarates Glutaric acid Male Neurology Oxidative damage Protein Carbonylation - drug effects Rats Rats, Wistar Seizures - chemically induced Seizures - drug therapy Seizures - metabolism Sodium-Potassium-Exchanging ATPase - metabolism Striatum Synaptosomes - drug effects Synaptosomes - metabolism Vertebrates: nervous system and sense organs |
| title | Creatine decreases convulsions and neurochemical alterations induced by glutaric acid in rats |
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