Mitochondrial complex I inhibition in cerebral cortex of immature rats following homocysteic acid-induced seizures
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
17270175
DOI
10.1016/j.expneurol.2006.12.010
PII: S0014-4886(06)00643-1
Knihovny.cz E-zdroje
- MeSH
- akonitáthydratasa metabolismus MeSH
- analýza rozptylu MeSH
- antioxidancia farmakologie MeSH
- citrátsynthasa metabolismus MeSH
- cyklické N-oxidy farmakologie MeSH
- energetický metabolismus účinky léků MeSH
- homocystein analogy a deriváty MeSH
- krysa rodu Rattus MeSH
- lékové interakce MeSH
- metaloporfyriny farmakologie MeSH
- mitochondrie účinky léků MeSH
- mozková kůra enzymologie růst a vývoj ultrastruktura MeSH
- novorozená zvířata MeSH
- peroxidace lipidů účinky léků MeSH
- potkani Wistar MeSH
- respirační komplex I antagonisté a inhibitory metabolismus MeSH
- spinové značení MeSH
- spotřeba kyslíku účinky léků MeSH
- záchvaty chemicky indukované patologie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- 5,10,15,20-tetrakis(4-sulfonatophenyl)porphyrinato iron(III) chloride MeSH Prohlížeč
- akonitáthydratasa MeSH
- antioxidancia MeSH
- citrátsynthasa MeSH
- cyklické N-oxidy MeSH
- homocysteic acid MeSH Prohlížeč
- homocystein MeSH
- metaloporfyriny MeSH
- respirační komplex I MeSH
- spinové značení MeSH
- tempol MeSH Prohlížeč
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.
Citace poskytuje Crossref.org
Epilepsy Research in the Institute of Physiology of the Czech Academy of Sciences in Prague
Sulforaphane Ameliorates Metabolic Changes Associated With Status Epilepticus in Immature Rats
