Please use this identifier to cite or link to this item:
Title: Investigation of mitochondrial involvement in the experimental model of epilepsy induced by pilocarpine
Authors: Nasseh, I. E.
Amado, D.
Cavalheiro, E. A.
Naffah-Mazzacoratti, M. D.
Tengan, C. H.
Universidade Federal de São Paulo (UNIFESP)
Keywords: epilepsy
mitochondrial DNA
cytochrome c oxidase
free radical
Issue Date: 1-Mar-2006
Publisher: Elsevier B.V.
Citation: Epilepsy Research. Amsterdam: Elsevier B.V., v. 68, n. 3, p. 229-239, 2006.
Abstract: Mitochondrial abnormalities have been associated with several aspects of epileptogenesis, such as energy generation, control of cell death, neurotransmitter synthesis, and free radical (FR) production. Increased production of FRs may cause mtDNA damage leading to decreased activities of oxidative phosphorylation complexes containing mtDNA-encoded subunits. in this study, we investigated whether increased generation of FR during status epilepticus would be sufficient to provoke abnormalities in mtDNA and in the expression and activity of cytochrome c oxidase (CCO), complex IV of the respiratory chain, in the chronic phase of the pilocarpine model of temporal lobe epilepsy. DNA analysis revealed low amounts of a 4.8 kb mtDNA deletion but with no differences in frequency or quantity in the control and experimental groups. We did not find abnormalities in the expression and distribution of an mtDNA-encoded subunit of CCO (CCO-I) or a relative decrease in CCO-I when compared with nuclear-encoded subunits (CCO-IV and SDH-fp). No abnormality in CCO activity was observed through histochemistry. Although evidences of mitochondrial abnormalities were found in previously published studies, our results do not suggest that the FRs, generated during the acute phase, determined important abnormalities in mtDNA, in expression of CCO-I, and in CCO activity. (c) 2005 Elsevier B.V. All tights reserved.
ISSN: 0920-1211
Other Identifiers:
Appears in Collections:Em verificação - Geral

Files in This Item:
There are no files associated with this item.

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.