Linked Life Data

21505893

Source:http://linkedlifedata.com/resource/pubmed/id/21505893

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2011-6-29
pubmed:abstractText
In this study, we describe the presence of apoptosis, associated with a mitochondrial dysfunction in the hippocampus of animals in an experimental model defined as minimal hepatic encephalopathy (MHE). This experimental model was studied after 10 days of induced portal vein calibrated stricture, leading to portal hypertension and to a moderate hyperammonemia, without the presence of other evident central nervous system changes. The molecular mechanisms here proposed indicate the presence of apoptotic intrinsic pathways that point to hippocampal mitochondria as an important mediator of apoptosis in this experimental model. In this model of MHE, the presence of DNA fragmentation is documented by 2.3-times increased number of TUNEL-positive cells. These findings together with a higher ratio of the Bcl-2 family members Bax/Bcl-xL in the outer mitochondrial membrane of the MHE animals together with 11% of cytochrome c release indicate the presence of apoptosis in this experimental model. A detailed analysis of the hippocampal mitochondrial physiology was performed after mitochondrial isolation. The determination of the respiratory rate in the presence of malate plus glutamate and ADP showed a 45% decrease in respiratory control in MHE animals as compared with the sham group. A marked decrease of cytochrome oxidase (complex IV of the electron transport chain) was also observed, showing 46% less activity in hippocampal mitochondria from MHE animals. In addition, mitochondria from these animals showed less ability to maintain membrane potential (?? (m)) which was 13% lower than the sham group. Light scattering experiments showed that mitochondria from MHE animals were more sensitive to swell in the presence of increased calcium concentrations as compared with the sham group. In addition, in vitro studies performed in mitochondria from sham animals showed that mitochondrial permeability transition (MPT) could be a mitochondrial mediator of the apoptotic signaling in the presence of NH(4) (+) and calcium.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1573-4919
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
354
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
231-40
pubmed:meshHeading
pubmed-meshheading:21505893-Ammonium Chloride, pubmed-meshheading:21505893-Animals, pubmed-meshheading:21505893-Apoptosis, pubmed-meshheading:21505893-Apoptosis Regulatory Proteins, pubmed-meshheading:21505893-Calcium, pubmed-meshheading:21505893-Constriction, Pathologic, pubmed-meshheading:21505893-DNA Fragmentation, pubmed-meshheading:21505893-Disease Models, Animal, pubmed-meshheading:21505893-Electron Transport Complex I, pubmed-meshheading:21505893-Electron Transport Complex II, pubmed-meshheading:21505893-Electron Transport Complex III, pubmed-meshheading:21505893-Electron Transport Complex IV, pubmed-meshheading:21505893-Hepatic Encephalopathy, pubmed-meshheading:21505893-Hippocampus, pubmed-meshheading:21505893-Hyperammonemia, pubmed-meshheading:21505893-Male, pubmed-meshheading:21505893-Membrane Potential, Mitochondrial, pubmed-meshheading:21505893-Mitochondria, pubmed-meshheading:21505893-Mitochondrial Swelling, pubmed-meshheading:21505893-Oxygen Consumption, pubmed-meshheading:21505893-Permeability, pubmed-meshheading:21505893-Portal Vein, pubmed-meshheading:21505893-Rats, pubmed-meshheading:21505893-Rats, Inbred WKY
pubmed:year
2011
pubmed:articleTitle
Mitochondrial dysfunction as a mediator of hippocampal apoptosis in a model of hepatic encephalopathy.
pubmed:affiliation
Laboratory of Free Radical Biology, School of Pharmacy and Biochemistry, University of Buenos Aires, Junin 956, C1113AAD Buenos Aires, Argentina. juanitab@ffyb.uba.ar
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't