Some possibilities of protection against acetylcholinesterase inhibition by organophosphates in vivo.
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Biomedical subjects
Publications and source records attributed to J Bajgar.
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Acetylcholinesterase activity in rat blood was continuously monitored following O-ethyl-S-(2-dimethylaminoethyl)-methylphosphonothioate intoxication (p.o.) alone and in combination with atropine and the reactivators trimedoxime, obidoxime and methoxime. Decrease of acetylcholinesterase activity was not influenced by atropine alone but following treatment with a combination of atropine with the reactivators mentioned, an increase (reactivation) of the blood enzyme was demonstrated. This increase was highest for the combination atropine-trimedoxime and the lowest for the combination atropine-obidoxime.
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Acetylcholinesterase (AChE) activity and its molecular forms in the rectal tissue in Hirsprung's disease were studied. Total AChE activity was increased in Hirsprung's disease; the activity was separated by polyacrylamide gel electrophoresis into two molecular forms. The AChE form with higher electrophoretic mobility was not observed in healthy children, and it might be of diagnostic importance in this disease.
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In vivo inhibition of blood acetylcholinesterase activity by 9-amino-1, 2, 3, 4-tetrahydroacridine, its 7-methoxy derivative and physostigmine was studied in rats. Changes of enzyme activity in the blood were continually registered using an automatic colorimeter Auto Analyzer system. The dependence of % enzyme inhibition upon time in semilogarithmic transformation was characterized by a two phase curve. The first phase reflected the increase in the concentration of inhibitors in the blood during their resorption; this was followed by a slow second phase of inhibition. The inhibitory effect decreased in the order: physostigmine greater than tacrine greater than 7-methoxytacrine. The relationship between the anticholinesterase and antipsychotomimetic action of the examined substances is discussed.
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