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A Comparison of the Neuroprotective and Reactivating Efficacy of a Novel Bispyridinium Oxime K870 with Commonly Used Pralidoxime and the Oxime HI-6 in Tabun-Poisoned Rats
J. Kassa, J. Hatlapatková, J. Žďárová Karasová, V. Hepnarová, F. Caisberger, J. Pejchal
Language English Country Czech Republic
Document type Journal Article
Digital library NLK
Source
NLK
Directory of Open Access Journals
from 1997
Free Medical Journals
from 1997
Open Access Digital Library
from 1997-01-01
Medline Complete (EBSCOhost)
from 2012-06-01
ROAD: Directory of Open Access Scholarly Resources
from 1997
- MeSH
- Acetylcholinesterase MeSH
- Antidotes pharmacology MeSH
- Chemical Warfare Agents * toxicity MeSH
- Cholinesterase Inhibitors pharmacology MeSH
- Poisons * MeSH
- Rats MeSH
- Organophosphates * MeSH
- Oximes * pharmacology MeSH
- Rats, Wistar MeSH
- Pralidoxime Compounds MeSH
- Pyridinium Compounds * pharmacology MeSH
- Cholinesterase Reactivators * pharmacology MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
AIM: The comparison of neuroprotective and central reactivating effects of the oxime K870 in combination with atropine with the efficacy of standard antidotal treatment in tabun-poisoned rats. METHODS: The neuroprotective effects of antidotal treatment were determined in rats poisoned with tabun at a sublethal dose using a functional observational battery 2 h and 24 h after tabun administration, the tabun-induced brain damage was investigated by the histopathological evaluation and central reactivating effects of oximes was evaluated by the determination of acetylcholinesterase activity in the brain using a standard spectrophotometric method. RESULTS: The central reactivating efficacy of a newly developed oxime K870 roughly corresponds to the central reactivating efficacy of pralidoxime while the ability of the oxime HI-6 to reactivate tabun-inhibited acetylcholinesterase in the brain was negligible. The ability of the oxime K870 to decrease tabun-induced acute neurotoxicity was slightly higher than that of pralidoxime and similar to the oxime HI-6. These results roughly correspond to the histopathological evaluation of tabun-induced brain damage. CONCLUSION: The newly synthesized oxime K870 is not a suitable replacement for commonly used oximes in the antidotal treatment of acute tabun poisonings because its neuroprotective efficacy is only slightly higher or similar compared to studied currently used oximes.
References provided by Crossref.org
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