Gholamreza Poorheidari; Alireza Shahriary; Mahdi Mashhadi Akbar Boojar
Volume 23, Issue 2 , 2021
Abstract
Background: It is generally believed that the anticholinesterase effect is induced by the organophosphate insecticide parathion only through its bioactive metabolite (i.e., paraoxon) that is created in the liver.
Objectives: This study aimed to evaluate the intrinsic anticholinesterase ...
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Background: It is generally believed that the anticholinesterase effect is induced by the organophosphate insecticide parathion only through its bioactive metabolite (i.e., paraoxon) that is created in the liver.
Objectives: This study aimed to evaluate the intrinsic anticholinesterase effect of parathion, compared to its main metabolite.
Methods: This study has been conducted to prepare the isolated chick biventer cervicis nerve-muscle using the twitch tension recording method.
Results: According to the results, paraoxon (0.1 µM) induced a highly significant increase (more than 100%) in the twitch height, while higher concentrations (0.3 and 1 µM) induced partial or total contractures. Furthermore, parathion induced almost the same percentage of increase in the twitch height at 1 µM and partial or total contractures at 3 and 10 µM. It should be noted that pralidoxime (2-PAM), at 300 µM, reversed the effects of paraoxon and its parent (i.e., parathion).
Conclusion: These results demonstrate that both parathion and its metabolite inhibit the acetylcholinesterase enzyme which can be reactivated by pralidoxime, whereas parathion is about 10 times less potent, compared to its metabolite. Therefore, the intrinsic toxic effects of parathion, regardless of its metabolite, should be considered in future studies.
