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
Jazyk angličtina Země Česko Médium print
Typ dokumentu časopisecké články
PubMed
34779379
DOI
10.14712/18059694.2021.25
PII: am_2021064030145
Knihovny.cz E-zdroje
- Klíčová slova
- acetylcholinesterase, functional observational battery, histopathology, neurotoxicity, oximes, rats, tabun,
- MeSH
- acetylcholinesterasa MeSH
- antidota farmakologie MeSH
- chemické bojové látky * toxicita MeSH
- cholinesterasové inhibitory farmakologie MeSH
- jedy * MeSH
- krysa rodu Rattus MeSH
- organofosfáty * MeSH
- oximy * farmakologie MeSH
- potkani Wistar MeSH
- pralidoximové sloučeniny MeSH
- pyridinové sloučeniny * farmakologie MeSH
- reaktivátory cholinesterasy * farmakologie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- acetylcholinesterasa MeSH
- antidota MeSH
- asoxime chloride MeSH Prohlížeč
- chemické bojové látky * MeSH
- cholinesterasové inhibitory MeSH
- jedy * MeSH
- organofosfáty * MeSH
- oximy * MeSH
- pralidoxime MeSH Prohlížeč
- pralidoximové sloučeniny MeSH
- pyridinové sloučeniny * MeSH
- reaktivátory cholinesterasy * MeSH
- tabun MeSH Prohlížeč
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.
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