Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1996-11-27
pubmed:abstractText
The present work was designed to study the possible implication of apoptosis in ischemic neuronal death, a phenomenon that has been suggested to be involved in neurodegeneration following focal as well as global ischemia. In this study, mouse cortical neurons in primary culture were subjected to oxygen deprivation or oxygen, glucose, and serum deprivation to simulate hypoxia and "ischemia-like" conditions; also, cellular viability as well as DNA degradation were investigated. The results showed that DNA degradation occurred in neurons subjected to oxygen deprivation but not to oxygen and substrate deprivation together. This DNA degradation, resulting in a laddering by agarose gel electrophoresis, could be prevented by cycloheximide and actinomycin-D treatments, although these inhibitors were unable to reduce neuronal death. To investigate if DNA degradation could be elicited by an intracellular free radical generation during reoxygenation, transgenic neurons overexpressing copper-zinc superoxide dismutase were subjected to 9 h of oxygen deprivation and analyzed after 24 h of reoxygenation. The results showed a significant attenuation of DNA degradation in these cells and confirmed a possible relationship between reactive oxygen species and neuronal apoptosis. This study opens the way to further investigations regarding the involvement of an apoptotic process in necrotic neuronal death, and provides some new insights into the mechanisms underlying selective sensitivity of neuronal cells to oxygen and glucose deprivation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0897-7151
pubmed:author
pubmed:issnType
Print
pubmed:volume
13
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
233-44
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:8797173-Animals, pubmed-meshheading:8797173-Apoptosis, pubmed-meshheading:8797173-Cell Hypoxia, pubmed-meshheading:8797173-Cell Survival, pubmed-meshheading:8797173-Cells, Cultured, pubmed-meshheading:8797173-Cerebral Cortex, pubmed-meshheading:8797173-Culture Media, Serum-Free, pubmed-meshheading:8797173-DNA Damage, pubmed-meshheading:8797173-DNA Fragmentation, pubmed-meshheading:8797173-Electrophoresis, Agar Gel, pubmed-meshheading:8797173-Gene Expression Regulation, Enzymologic, pubmed-meshheading:8797173-Glucose, pubmed-meshheading:8797173-Immunohistochemistry, pubmed-meshheading:8797173-Mice, pubmed-meshheading:8797173-Mice, Transgenic, pubmed-meshheading:8797173-Neurofilament Proteins, pubmed-meshheading:8797173-Neurons, pubmed-meshheading:8797173-Nucleic Acid Synthesis Inhibitors, pubmed-meshheading:8797173-Reactive Oxygen Species, pubmed-meshheading:8797173-Superoxide Dismutase
pubmed:year
1996
pubmed:articleTitle
Oxygen deprivation but not a combination of oxygen, glucose, and serum deprivation induces DNA degradation in mouse cortical neurons in vitro: attenuation by transgenic overexpression of CuZn-superoxide dismutase.
pubmed:affiliation
Department of Neurological Surgery, University of California, School of Medicine, San Francisco 94143-0651, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't