Autor: |
Bajgar J; Purkyne Military Medical Academy, Department of Toxicology, Hradec Králové, Czech Republic. bajgar@pmfgk.cz, Sevelová L, Krejcová G, Fusek J, Vachek J, Kassa J, Herink J, de Jong LP, Benschop HP |
Jazyk: |
angličtina |
Zdroj: |
Inhalation toxicology [Inhal Toxicol] 2004 Jul; Vol. 16 (8), pp. 497-507. |
DOI: |
10.1080/08958370490442430 |
Abstrakt: |
Soman belongs to the most dangerous nerve agents because of the low effectiveness of the presently available antidotes. Soman acts by inhibiting acetylcholinesterase (AChE) both peripherally and centrally, with a subsequent accumulation of neuromediator acetylcholine and other metabolic changes. From the data published in literature it can be concluded that exposure to nerve agents leading to acute effects or chronic exposure to nerve agents may lead to delayed and persistent adverse effects. The aim of this study was to demonstrate changes in AChE and butyrylcholinesterase (BuChE) activities, stressogenic markers (i.e., tyrosine aminotransferase [TAT] activity, and plasma corticosterone level), and neuroexcitability and behavior 24 h and 4 wk following a single soman inhalation exposure at low level. AChE activity in erythrocytes and BuChE activity in plasma was decreased (dependent on the dose of soman) 24 h and 4 wk after the exposure. A similar decrease in AChE activity in different brain parts was observed. One of the stressogenic parameters, TAT, was changed 24 h after exposure only. Behavior of experimental animals was changed 24 h after the exposure, and 4 behavioral parameters persisted 4 wk after the exposure. Neuroexcitability was increased at 24 h after the exposure and had become about normal 4 wk after the exposure. Summarizing, long-term effects (4 wk) were observed after inhalation exposure of guinea pigs to sublethal concentrations of soman. |
Databáze: |
MEDLINE |
Externí odkaz: |
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