Abstract
Nerve agents are highly toxic organophosphorus (OP) compounds. They inhibit acetylcholinesterase (AChE), an enzyme that hydrolyses acetycholine (ACh) in the nervous system. Pathophysiological changes caused by OP poisonings are primarily the consequence of surplus ACh on cholinergic receptors and in the central nervous system. Standard treatment of OP poisoning includes combined administration of carbamates, atropine, oximes and anticonvulsants. In order to improve therapy, new compounds have been synthesised and tested. Tenocyclidine (TCP) and its adamantane derivative 1-[2-(2-thienyl)-2-adamantyl] morpholine (TAMORF) have shown interesting properties against soman poisoning. In this study, we developed a qualitative GC-MS method to measure elimination of TCP and TAMORF through rat urine in order to learn more about the mechanisms through which TCP protects an organism from OP poisoning and to determine the duration of this protective effect. GC-MS showed that six hours after treatment with TCP, rat urine contained only its metabolite 1-thienylcyclohexene, while urine of rats treated with TAMORF contained both TAMORF and its metabolites.
Highlights
Nerve agents are highly toxic organophosphorus (OP) compounds
For this purpose we developed a gas chromatography - mass spectrometry (GC-MS) method to establish TCP and TAMORF elimination through urine in rats six hours after treatment, as this information speaks about the duration of their antidotal activity
Chloroform phases were put into analytical vials and analysed with GC-MS
Summary
Nerve agents are highly toxic organophosphorus (OP) compounds. They inhibit acetylcholinesterase (AChE), an enzyme that hydrolyses acetycholine (ACh) in the nervous system. The aim of this study was to learn more about the pathways through which TCP and its adamantyl derivatives protect against OP poisoning For this purpose we developed a gas chromatography - mass spectrometry (GC-MS) method to establish TCP and TAMORF elimination through urine in rats six hours after treatment, as this information speaks about the duration of their antidotal activity. Pretreatment with TAMORF protected animals from the lethal effects of soman and eliminated most of the soman-induced signs of toxicity in poisoned rats [2] Both TCP and TAMORF have shown low genotoxicity [2, 17, 18]. TCP and TAMORF showed interesting radioprotective properties [17]
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