Activation of mitogen activated protein kinase (MAPK) pathways after soman poisoning in rat cerebellar granule neurons

• Published in: Journal of applied toxicology Vol. 28; no. 5; pp. 689 - 693
• Main Authors: Pejchal, J., Österreicher, J., Kassa, J., Tichý, A., Mokrý, J.
• Format: Journal Article
• Language: English
• Published: Chichester, UK John Wiley & Sons, Ltd 01.07.2008; Wiley
• Subjects: Animals; Biological and medical sciences; C-jun; C-myc; cerebellum; Cerebellum - cytology; Cerebellum - drug effects; Cerebellum - enzymology; Chemical and industrial products toxicology. Toxic occupational diseases; Chemical Warfare Agents - poisoning; Cytoplasmic Granules - drug effects; Cytoplasmic Granules - enzymology; Elk-1; Enzyme Activation - drug effects; Gas, fumes; Image Processing, Computer-Assisted; Immunohistochemistry; Male; Medical sciences; Mitogen-Activated Protein Kinases - metabolism; Neurons - drug effects; Neurons - enzymology; p38; p38 Mitogen-Activated Protein Kinases - metabolism; Proto-Oncogene Proteins c-jun - metabolism; Proto-Oncogene Proteins c-myc - metabolism; Rats; Rats, Wistar; Signal Transduction - drug effects; soman; Soman - poisoning; Toxicology; Cerebellum; Rat; Central nervous system; Encephalon; Chemical warfare agent; p38; Elk-1; Anticholinesterase agent; Soman; Protooncogene; Toxic gas; Granule neuron; Transcription factor Elk1; Enzyme; Transferases; Rodentia; Mitogen-activated protein kinase; C-myc; Vertebrata; Mammalia; Animal; C-Onc gene; myc Gene; Organophosphorus compounds; Poisoning; C-jun
• ISSN: 0260-437X; 1099-1263
• DOI: 10.1002/jat.1323

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 µg kg−1 (70% LD50) 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. Copyright © 2007 John Wiley & Sons, Ltd.