Linked Life Data

20711885

Source:http://linkedlifedata.com/resource/pubmed/id/20711885

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2010-8-20
pubmed:abstractText
Epilepsy is considered one of the most common neurological disorders worldwide. The burst firing associated with prolonged epileptic discharges could lead to a large number of changes and cascades of events at the cellular level. From its role as the cellular powerhouse, the mitochondrion is emerging as a key participant in cell death because of its association with an ever-growing list of apoptosis-related proteins. Prolonged seizures may result in the mitochondrial dysfunction and increased production of reactive oxygen species and nitric oxide (NO) precede neuronal cell death and cause subsequent epileptogenesis. Emerging evidences also showed that intrinsic mitochondrial apoptotic pathway may contribute to the neuropathology of human epilepsy, particularly in the hippocampus. Subsequent laboratory studies in the animal model of status epilepticus provide credence to the notion that activation of nuclear factor-?B upregulates NO synthase (NOS) II gene expression with temporal correlation of NOS II derived NO-, superoxide anion- and peroxynitrite-dependent reduction in mitochondrial Complex I activity, leading to apoptotic neuronal cell death in the hippocampus. These results will broaden our understanding on the intimate link between mitochondrial function, oxidative stress and mitochondria-dependent apoptotic signaling triggered by epileptic seizures. It will open a new vista in the development of more effective neuroprotective strategies against seizure-induced brain damage by modification of bioenergetic failure in the mitochondria and in the design of novel treatment perspectives for therapy-resistant forms of epilepsy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1028-768X
pubmed:author
pubmed:issnType
Print
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3-15
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Mitochondrial dysfunction and oxidative stress in seizure-induced neuronal cell death.
pubmed:affiliation
Department of Neurology, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung, Taiwan. ycchuang@adm.cgmh.org.tw
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't