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Soman poisoning alters p38 MAPK pathway in rat cerebellar Purkinje cells
J. Pejchal, J. Österreicher, J. Kassa, A. Tichý, S. Mičuda, Z. Šinkorová, L. Zárybnická
Jazyk angličtina Země Velká Británie
Typ dokumentu práce podpořená grantem
- MeSH
- cholinesterasové inhibitory otrava MeSH
- fosforylace MeSH
- imunohistochemie MeSH
- krysa rodu rattus MeSH
- mitogenem aktivované proteinkinasy p38 biosyntéza fyziologie genetika MeSH
- mozeček cytologie patologie účinky léků MeSH
- počítačové zpracování obrazu MeSH
- potkani Wistar MeSH
- proteiny nervové tkáně biosyntéza MeSH
- Purkyňovy buňky patologie účinky léků MeSH
- signální transdukce účinky léků MeSH
- soman otrava MeSH
- transkripční faktory genetika účinky léků MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- práce podpořená grantem MeSH
The aim of the study was to evaluate the expression of phosphorylated p38 mitogen-activated protein kinase (p38 MAPK) and MAPK-activated transcription factors elk-1, c-jun and c-myc in rat cerebellar Purkinje cells after soman poisoning to investigate the pathogenetic mechanism of non-specific long-term adverse effects of nerve agents. Male Wistar rats were poisoned by intramuscular administration of soman at a dose 60 microg kg(-1) (80% LD(50)), while control animals were administered physiological saline. 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 computer image analysis. An increased expression of phosphorylated p38 MAPK and c-myc 14 days after soman poisoning was found, while both activated elk-1 and c-jun expression remained unchanged 1, 7 and 14 days after intoxication. Late activation of p38 MAPK and their targets might be the underlying mechanism of chronic neurophysiological adverse effects.
Citace poskytuje Crossref.org
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