Activation of mitogen activated protein kinase (MAPK) pathways after soman poisoning in rat cerebellar granule neurons
Language English Country Great Britain, England Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
18041744
DOI
10.1002/jat.1323
Knihovny.cz E-resources
- MeSH
- Enzyme Activation drug effects MeSH
- Chemical Warfare Agents poisoning MeSH
- Cytoplasmic Granules drug effects enzymology MeSH
- Immunohistochemistry MeSH
- Rats MeSH
- p38 Mitogen-Activated Protein Kinases metabolism MeSH
- Mitogen-Activated Protein Kinases metabolism MeSH
- Cerebellum cytology drug effects enzymology MeSH
- Neurons drug effects enzymology MeSH
- Image Processing, Computer-Assisted MeSH
- Rats, Wistar MeSH
- Proto-Oncogene Proteins c-jun metabolism MeSH
- Proto-Oncogene Proteins c-myc metabolism MeSH
- Signal Transduction drug effects MeSH
- Soman poisoning MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Chemical Warfare Agents MeSH
- p38 Mitogen-Activated Protein Kinases MeSH
- Mitogen-Activated Protein Kinases MeSH
- Proto-Oncogene Proteins c-jun MeSH
- Proto-Oncogene Proteins c-myc MeSH
- Soman MeSH
The expression of activated p38 mitogen-activated protein kinase (MAPK) and activated MAPK transcription factors c-jun, c-myc and elk-1 were examined in rat cerebellum after soman poisoning to determine the pathogenetic mechanism of the non-specific long-term effects of nerve agents. Male Wistar rats were poisoned by intramuscular administration of soman at a dose 60 microg kg(-1) (70% LD(50)) and samples were taken 1, 7 and 14 days after poisoning, immunohistochemically stained and p-p38MAPK, p-c-jun, p-c-myc and p-elk-1 expressions were measured using image analysis. Control groups were administered with saline instead of soman. The expression of activated p38MAPK and c-myc increased 14 days after soman poisoning while c-jun and elk-1 expressions remained unchanged 1, 7 and 14 days after soman poisoning. Delayed activation of p38 MAPK and its targets might be involved in the pathogenetic mechanism of the long-term neurophysiological toxic effects of nerve agents.
References provided by Crossref.org
The evaluation of oxidative damage of DNA after poisoning with nerve agents
