Linked Life Data

15698621

Source:http://linkedlifedata.com/resource/pubmed/id/15698621

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-2-8
pubmed:abstractText
Mitochondrial function is a key determinant of both excitability and viability of neurons. Present studies were carried out to decipher cerebral mitochondrial oxidative energy metabolism and membrane function in the chronic condition of generalized seizures induced by picrotoxin (PTX) in rats. PTX-induced convulsions resulted in decreased respiration rates (14-41%) with glutamate, pyruvate + malate, and succinate as substrate. The ADP phosphorylation rates were drastically reduced by 44-65%. An opposite trend was observed with ascorbate + N,N,N',N'-tetramethyl-p-phenylenediamine [corrected] (TMPD) as substrate. In general, uncoupling of the mitochondrial electron transport was observed after PTX treatment. Malate dehydrogenase (MDH) and succinate dehydrogenase (SDH) activities were decreased by 20-80%; also, there was significant reduction in cytochrome b content after PTX treatment, while the F(o)F(1) ATPase (complex V) activity increased in basal and 2,4-dinitrophenol (DNP)-stimulated condition, indicating increased membrane fragility. The substrate kinetics analysis had shown that K(m) and V(max) of the higher affinity kinetic component of ATPase increased significantly by 1.2- to 1.4-fold in epileptic condition. Temperature kinetic analysis revealed 1.2-fold increase in energies of activation with decreased transition temperature. The total phospholipid (TPL) and cholesterol (CHL) contents decreased significantly with lowering of diphosphatidylglycerol (DPG), phosphatidylethanolamine (PE), phosphatidylinositol (PI), and phosphatidylserine (PS), while lysophospholipid (lyso), sphingomyelin (SPM), and phosphatidylcholine components were found to be elevated. Brain mitochondrial membrane was somewhat more fluidized in epileptic animals. Possible consequences of mitochondrial respiratory chain (MRC) dysfunction are discussed. In conclusion, impairment of MRC function along with structural alterations suggests novel pathophysiological mechanisms important for chronic epileptic condition.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0014-4886
pubmed:author
pubmed:issnType
Print
pubmed:volume
192
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
79-88
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15698621-Animals, pubmed-meshheading:15698621-Brain, pubmed-meshheading:15698621-Cell Death, pubmed-meshheading:15698621-Cell Respiration, pubmed-meshheading:15698621-Convulsants, pubmed-meshheading:15698621-Cytochromes, pubmed-meshheading:15698621-Disease Models, Animal, pubmed-meshheading:15698621-Electron Transport Chain Complex Proteins, pubmed-meshheading:15698621-Energy Metabolism, pubmed-meshheading:15698621-Epilepsy, pubmed-meshheading:15698621-Intracellular Membranes, pubmed-meshheading:15698621-Male, pubmed-meshheading:15698621-Membrane Fluidity, pubmed-meshheading:15698621-Membrane Lipids, pubmed-meshheading:15698621-Membrane Potentials, pubmed-meshheading:15698621-Mitochondria, pubmed-meshheading:15698621-Mitochondrial Proton-Translocating ATPases, pubmed-meshheading:15698621-Nerve Degeneration, pubmed-meshheading:15698621-Oxidative Phosphorylation, pubmed-meshheading:15698621-Picrotoxin, pubmed-meshheading:15698621-Rats
pubmed:year
2005
pubmed:articleTitle
Structural and functional alterations in mitochondrial membrane in picrotoxin-induced epileptic rat brain.
pubmed:affiliation
Department of Biochemistry, Faculty of Science, M.S. University of Baroda, Vadodara 390 002, Gujarat, India. munjalres@yahoo.com
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't