Mitochondrial complex I inhibition in cerebral cortex of immature rats following homocysteic acid-induced seizures
The major finding of the present study concerns the marked decrease of respiratory chain complex I activity in the cerebral cortex of immature rats following seizures induced by bilateral intracerebroventricular infusion of dl-homocysteic acid (600 nmol/side). This decrease was already evident durin...
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| Veröffentlicht in: | Experimental neurology 2007-04, Vol.204 (2), p.597-609 |
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| creator | Folbergrová, Jaroslava Ješina, Pavel Drahota, Zdeněk Lisý, Václav Haugvicová, Renata Vojtíšková, Alena Houštěk, Josef |
| description | The major finding of the present study concerns the marked decrease of respiratory chain complex I activity in the cerebral cortex of immature rats following seizures induced by bilateral intracerebroventricular infusion of
dl-homocysteic acid (600 nmol/side). This decrease was already evident during the acute phase of seizures (60–90 min after infusion) and persisted for at least 20 h after the seizures. It was selective for complex I since activities of complex II and IV and citrate synthase remained unaffected. Inhibition of complex I activity was not associated with changes in complex I content. Based on enhanced lipoperoxidation and decreased aconitase activity, it can be postulated that oxidative modification is most likely responsible for the observed inhibition. Mitochondrial respiration, as well as cortical ATP levels remained in the control range, apparently due to excess capacity of the complex I documented by energy thresholds. On the other hand, the enhanced production of reactive oxygen species by inhibited complex I was observed in mitochondria from HCA-treated animals. The decrease of complex I activity was substantially attenuated when animals were treated with substances providing an anticonvulsant effect and also with selected free radical scavengers. We can assume that inhibition of complex I may elicit enhanced formation of reactive oxygen species and contribute thus to neuronal injury demonstrated in this model. |
| doi_str_mv | 10.1016/j.expneurol.2006.12.010 |
| format | Article |
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dl-homocysteic acid (600 nmol/side). This decrease was already evident during the acute phase of seizures (60–90 min after infusion) and persisted for at least 20 h after the seizures. It was selective for complex I since activities of complex II and IV and citrate synthase remained unaffected. Inhibition of complex I activity was not associated with changes in complex I content. Based on enhanced lipoperoxidation and decreased aconitase activity, it can be postulated that oxidative modification is most likely responsible for the observed inhibition. Mitochondrial respiration, as well as cortical ATP levels remained in the control range, apparently due to excess capacity of the complex I documented by energy thresholds. On the other hand, the enhanced production of reactive oxygen species by inhibited complex I was observed in mitochondria from HCA-treated animals. The decrease of complex I activity was substantially attenuated when animals were treated with substances providing an anticonvulsant effect and also with selected free radical scavengers. We can assume that inhibition of complex I may elicit enhanced formation of reactive oxygen species and contribute thus to neuronal injury demonstrated in this model.</description><identifier>ISSN: 0014-4886</identifier><identifier>EISSN: 1090-2430</identifier><identifier>DOI: 10.1016/j.expneurol.2006.12.010</identifier><identifier>PMID: 17270175</identifier><identifier>CODEN: EXNEAC</identifier><language>eng</language><publisher>Amsterdam: Elsevier Inc</publisher><subject>Aconitate Hydratase - metabolism ; Analysis of Variance ; Animals ; Animals, Newborn ; Antioxidants - pharmacology ; Biological and medical sciences ; Cerebral Cortex - enzymology ; Cerebral Cortex - growth & development ; Cerebral Cortex - ultrastructure ; Citrate (si)-Synthase - metabolism ; Complex I inhibition ; Cyclic N-Oxides - pharmacology ; dl-Homocysteic acid-induced seizures ; Drug Interactions ; Electron Transport Complex I - antagonists & inhibitors ; Electron Transport Complex I - metabolism ; Energy Metabolism - drug effects ; Energy metabolites ; Free radicals ; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy ; Homocysteine - analogs & derivatives ; Immature rats ; Injuries of the nervous system and the skull. Diseases due to physical agents ; Lipid Peroxidation - drug effects ; Male ; Medical sciences ; Metalloporphyrins - pharmacology ; Mitochondria - drug effects ; Mitochondrial respiratory chain ; Nervous system (semeiology, syndromes) ; Neurology ; Oxygen Consumption - drug effects ; Protection ; Rats ; Rats, Wistar ; Respiration ; Seizures - chemically induced ; Seizures - pathology ; Spin Labels ; Traumas. Diseases due to physical agents</subject><ispartof>Experimental neurology, 2007-04, Vol.204 (2), p.597-609</ispartof><rights>2006 Elsevier Inc.</rights><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c546t-7d0b6c1a16cca8d634f8c902b321b8e7f76e883f14c0dd96259bd8478d523c8e3</citedby><cites>FETCH-LOGICAL-c546t-7d0b6c1a16cca8d634f8c902b321b8e7f76e883f14c0dd96259bd8478d523c8e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0014488606006431$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18688006$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17270175$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Folbergrová, Jaroslava</creatorcontrib><creatorcontrib>Ješina, Pavel</creatorcontrib><creatorcontrib>Drahota, Zdeněk</creatorcontrib><creatorcontrib>Lisý, Václav</creatorcontrib><creatorcontrib>Haugvicová, Renata</creatorcontrib><creatorcontrib>Vojtíšková, Alena</creatorcontrib><creatorcontrib>Houštěk, Josef</creatorcontrib><title>Mitochondrial complex I inhibition in cerebral cortex of immature rats following homocysteic acid-induced seizures</title><title>Experimental neurology</title><addtitle>Exp Neurol</addtitle><description>The major finding of the present study concerns the marked decrease of respiratory chain complex I activity in the cerebral cortex of immature rats following seizures induced by bilateral intracerebroventricular infusion of
dl-homocysteic acid (600 nmol/side). This decrease was already evident during the acute phase of seizures (60–90 min after infusion) and persisted for at least 20 h after the seizures. It was selective for complex I since activities of complex II and IV and citrate synthase remained unaffected. Inhibition of complex I activity was not associated with changes in complex I content. Based on enhanced lipoperoxidation and decreased aconitase activity, it can be postulated that oxidative modification is most likely responsible for the observed inhibition. Mitochondrial respiration, as well as cortical ATP levels remained in the control range, apparently due to excess capacity of the complex I documented by energy thresholds. On the other hand, the enhanced production of reactive oxygen species by inhibited complex I was observed in mitochondria from HCA-treated animals. The decrease of complex I activity was substantially attenuated when animals were treated with substances providing an anticonvulsant effect and also with selected free radical scavengers. We can assume that inhibition of complex I may elicit enhanced formation of reactive oxygen species and contribute thus to neuronal injury demonstrated in this model.</description><subject>Aconitate Hydratase - metabolism</subject><subject>Analysis of Variance</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Antioxidants - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Cerebral Cortex - enzymology</subject><subject>Cerebral Cortex - growth & development</subject><subject>Cerebral Cortex - ultrastructure</subject><subject>Citrate (si)-Synthase - metabolism</subject><subject>Complex I inhibition</subject><subject>Cyclic N-Oxides - pharmacology</subject><subject>dl-Homocysteic acid-induced seizures</subject><subject>Drug Interactions</subject><subject>Electron Transport Complex I - antagonists & inhibitors</subject><subject>Electron Transport Complex I - metabolism</subject><subject>Energy Metabolism - drug effects</subject><subject>Energy metabolites</subject><subject>Free radicals</subject><subject>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</subject><subject>Homocysteine - analogs & derivatives</subject><subject>Immature rats</subject><subject>Injuries of the nervous system and the skull. Diseases due to physical agents</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metalloporphyrins - pharmacology</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondrial respiratory chain</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Neurology</subject><subject>Oxygen Consumption - drug effects</subject><subject>Protection</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Respiration</subject><subject>Seizures - chemically induced</subject><subject>Seizures - pathology</subject><subject>Spin Labels</subject><subject>Traumas. Diseases due to physical agents</subject><issn>0014-4886</issn><issn>1090-2430</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMFu1DAQhi1ERZfCK4AviFNS20kc51hVLa1UxAXOljOesLNK4sVOaMvT43ZX9MhpRprvnxl9jH2UopRC6vNdiQ_7GdcYxlIJoUupSiHFK7aRohOFqivxmm2EkHVRG6NP2duUdkKIrlbtG3YqW9UK2TYbFr_SEmAbZh_JjRzCtB_xgd9ymrfU00Jhzi0HjNjHZyAueR4GTtPkljUij25JfAjjGO5p_sm3YQrwmBYk4A7IFzT7FdDzhPQn8-kdOxncmPD9sZ6xH9dX3y9virtvX24vL-4KaGq9FK0XvQbppAZwxuuqHgx0QvWVkr3Bdmg1GlMNsgbhfadV0_Xe1K3xjarAYHXGPh_27mP4tWJa7EQJcBzdjGFN1jRVdlOpLpPtgYQYUoo42H2kycVHK4V98m139p9v--TbSmWz75z8cLyx9hP6l9xRcAY-HQGXwI1DdDNQeuGMNibvy9zFgcNs5DdhtAkI5-yNIsJifaD_PvMXCRelkg</recordid><startdate>20070401</startdate><enddate>20070401</enddate><creator>Folbergrová, Jaroslava</creator><creator>Ješina, Pavel</creator><creator>Drahota, Zdeněk</creator><creator>Lisý, Václav</creator><creator>Haugvicová, Renata</creator><creator>Vojtíšková, Alena</creator><creator>Houštěk, Josef</creator><general>Elsevier Inc</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>20070401</creationdate><title>Mitochondrial complex I inhibition in cerebral cortex of immature rats following homocysteic acid-induced seizures</title><author>Folbergrová, Jaroslava ; Ješina, Pavel ; Drahota, Zdeněk ; Lisý, Václav ; Haugvicová, Renata ; Vojtíšková, Alena ; Houštěk, Josef</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c546t-7d0b6c1a16cca8d634f8c902b321b8e7f76e883f14c0dd96259bd8478d523c8e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Aconitate Hydratase - metabolism</topic><topic>Analysis of Variance</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Antioxidants - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Cerebral Cortex - enzymology</topic><topic>Cerebral Cortex - growth & development</topic><topic>Cerebral Cortex - ultrastructure</topic><topic>Citrate (si)-Synthase - metabolism</topic><topic>Complex I inhibition</topic><topic>Cyclic N-Oxides - pharmacology</topic><topic>dl-Homocysteic acid-induced seizures</topic><topic>Drug Interactions</topic><topic>Electron Transport Complex I - antagonists & inhibitors</topic><topic>Electron Transport Complex I - metabolism</topic><topic>Energy Metabolism - drug effects</topic><topic>Energy metabolites</topic><topic>Free radicals</topic><topic>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</topic><topic>Homocysteine - analogs & derivatives</topic><topic>Immature rats</topic><topic>Injuries of the nervous system and the skull. Diseases due to physical agents</topic><topic>Lipid Peroxidation - drug effects</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metalloporphyrins - pharmacology</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondrial respiratory chain</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Neurology</topic><topic>Oxygen Consumption - drug effects</topic><topic>Protection</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Respiration</topic><topic>Seizures - chemically induced</topic><topic>Seizures - pathology</topic><topic>Spin Labels</topic><topic>Traumas. Diseases due to physical agents</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Folbergrová, Jaroslava</creatorcontrib><creatorcontrib>Ješina, Pavel</creatorcontrib><creatorcontrib>Drahota, Zdeněk</creatorcontrib><creatorcontrib>Lisý, Václav</creatorcontrib><creatorcontrib>Haugvicová, Renata</creatorcontrib><creatorcontrib>Vojtíšková, Alena</creatorcontrib><creatorcontrib>Houštěk, Josef</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>Experimental neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Folbergrová, Jaroslava</au><au>Ješina, Pavel</au><au>Drahota, Zdeněk</au><au>Lisý, Václav</au><au>Haugvicová, Renata</au><au>Vojtíšková, Alena</au><au>Houštěk, Josef</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mitochondrial complex I inhibition in cerebral cortex of immature rats following homocysteic acid-induced seizures</atitle><jtitle>Experimental neurology</jtitle><addtitle>Exp Neurol</addtitle><date>2007-04-01</date><risdate>2007</risdate><volume>204</volume><issue>2</issue><spage>597</spage><epage>609</epage><pages>597-609</pages><issn>0014-4886</issn><eissn>1090-2430</eissn><coden>EXNEAC</coden><abstract>The major finding of the present study concerns the marked decrease of respiratory chain complex I activity in the cerebral cortex of immature rats following seizures induced by bilateral intracerebroventricular infusion of
dl-homocysteic acid (600 nmol/side). This decrease was already evident during the acute phase of seizures (60–90 min after infusion) and persisted for at least 20 h after the seizures. It was selective for complex I since activities of complex II and IV and citrate synthase remained unaffected. Inhibition of complex I activity was not associated with changes in complex I content. Based on enhanced lipoperoxidation and decreased aconitase activity, it can be postulated that oxidative modification is most likely responsible for the observed inhibition. Mitochondrial respiration, as well as cortical ATP levels remained in the control range, apparently due to excess capacity of the complex I documented by energy thresholds. On the other hand, the enhanced production of reactive oxygen species by inhibited complex I was observed in mitochondria from HCA-treated animals. The decrease of complex I activity was substantially attenuated when animals were treated with substances providing an anticonvulsant effect and also with selected free radical scavengers. We can assume that inhibition of complex I may elicit enhanced formation of reactive oxygen species and contribute thus to neuronal injury demonstrated in this model.</abstract><cop>Amsterdam</cop><pub>Elsevier Inc</pub><pmid>17270175</pmid><doi>10.1016/j.expneurol.2006.12.010</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aconitate Hydratase - metabolism Analysis of Variance Animals Animals, Newborn Antioxidants - pharmacology Biological and medical sciences Cerebral Cortex - enzymology Cerebral Cortex - growth & development Cerebral Cortex - ultrastructure Citrate (si)-Synthase - metabolism Complex I inhibition Cyclic N-Oxides - pharmacology dl-Homocysteic acid-induced seizures Drug Interactions Electron Transport Complex I - antagonists & inhibitors Electron Transport Complex I - metabolism Energy Metabolism - drug effects Energy metabolites Free radicals Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy Homocysteine - analogs & derivatives Immature rats Injuries of the nervous system and the skull. Diseases due to physical agents Lipid Peroxidation - drug effects Male Medical sciences Metalloporphyrins - pharmacology Mitochondria - drug effects Mitochondrial respiratory chain Nervous system (semeiology, syndromes) Neurology Oxygen Consumption - drug effects Protection Rats Rats, Wistar Respiration Seizures - chemically induced Seizures - pathology Spin Labels Traumas. Diseases due to physical agents |
| title | Mitochondrial complex I inhibition in cerebral cortex of immature rats following homocysteic acid-induced seizures |
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