Abstract
1. To study the influence of antidotes on tabun-induced neurotoxicity, the rats were injected intramuscularly with organophosphate tabun (LD50). The efficacy of choice antidotal treatment consisting of acetylcholinesterase reactivator obidoxime and one of four anticholinergic drugs (atropine, benactyzine, biperiden, scopolamine) was compared. 2. Testing of tabun-induced neurotoxicity progress was carried out using the method Functional observational battery. The experimental animals as well as controls were observed at 24 hours and 7 days following tabun or saline administration. 3. The results were compared to the condition of animals without anticholinergic drug (oxime alone) and control rats that received physiological solution instead of tabun and treatment. Antidotal treatment involving centrally acting anticholinergic drugs (benactyzine, biperiden, scopolamine) showed significantly higher neuroprotective efficacy compared to antidotal treatment containing atropine.
Highlights
The inhibition of acetylcholinesterase (AChE, EC 3.1.1.7) by organophosphorus compounds (OPs) causes acute toxicity or death of the intoxicated animals because of endogenic increase in acetylcholine (ACh) level in the cholinergic nervous system, that leads to muscle fasciculations, respiratory distress and epileptic fits
Testing of tabun-induced neurotoxicity progress was carried out using the method Functional observational battery
The results were compared to the condition of animals without anticholinergic drug and control rats that received physiological solution instead of tabun and treatment
Summary
The inhibition of acetylcholinesterase (AChE, EC 3.1.1.7) by organophosphorus compounds (OPs) causes acute toxicity or death of the intoxicated animals because of endogenic increase in acetylcholine (ACh) level in the cholinergic nervous system, that leads to muscle fasciculations, respiratory distress and epileptic fits. Pathogenesis probably involves a combination of hypoxia and cholinergically mediated excitotoxicity with secondary recruitment of glutamatergic excitotoxicity [14]. One group of these compounds, called nerve agents, pose an increasing threat in the world due to their possible use in the battlefield or terrorist acts. Antidotes containing oxime compounds to reactivate the inhibited enzyme AChE are highly valued for the treatment of OP poisonings [7]. Apart from oximes, the current antidotal treatment of nerve agent-induced acute poisoning includes anticholinergic drugs to antagonize the effects of ACh excess at cholinergic receptor sites [15]
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