A Comparison between Neuromuscular Effects of Parathion and Paraoxon on Chick Biventer Cervicis Nerve-Muscle and the Reversal of their Effects by Pralidoxime

被引:2
作者
Poorheidari, Gholamreza [1 ,2 ]
Shahriary, Alireza [2 ]
Boojar, Mahdi Mashhadi Akbar [1 ,2 ]
机构
[1] Baqiyatallah Univ Med Sci, Dept Pharmacol & Toxicol, Fac Pharm, Tehran, Iran
[2] Baqiyatallah Univ Med Sci, Chem Injuries Res Ctr, Tehran, Iran
关键词
Chick biventer cervicis nerve-muscle; Organophosphate; Paraoxon; Parathion; Pralidoxime; ORGANOPHOSPHORUS; REACTIVATION;
D O I
10.32592/ircmj.2021.23.2.28
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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 mu M) induced a highly significant increase (more than 100%) in the twitch height, while higher concentrations (0.3 and 1 mu M) induced partial or total contractures. Furthermore, parathion induced almost the same percentage of increase in the twitch height at 1 mu M and partial or total contractures at 3 and 10 mu M. It should be noted that pralidoxime (2-PAM), at 300 mu M, 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.
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页数:4
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共 27 条
  • [1] A comprehensive review on experimental and clinical findings in intermediate syndrome caused by organophosphate poisoning
    Abdollahi, Mohammad
    Karami-Mohajeri, Somayyeh
    [J]. TOXICOLOGY AND APPLIED PHARMACOLOGY, 2012, 258 (03) : 309 - 314
  • [2] Ai P, 2017, COCHRANE DB SYST REV, V8, DOI [10.1002/14651858.CD006253.pub2, DOI 10.1002/14651858.CD006253.PUB2]
  • [3] Bueno LGF, 2007, J VENOM ANIM TOXINS, V13, P479, DOI 10.1590/S1678-91992007000200007
  • [4] Species Differences in Paraoxonase Mediated Hydrolysis of Several Organophosphorus Insecticide Metabolites
    Carr, Russell L.
    Dail, Mary Beth
    Chambers, Howard W.
    Chambers, Janice E.
    [J]. JOURNAL OF TOXICOLOGY, 2015, 2015
  • [5] Protective action of the serine protease inhibitor N-tosyl-L-lysine chloromethyl ketone (TLCK) against acute soman poisoning
    Cowan, FM
    Broomfield, CA
    Lenz, DE
    Shih, TM
    [J]. JOURNAL OF APPLIED TOXICOLOGY, 2001, 21 (04) : 293 - 296
  • [6] Pharmacological treatment of organophosphorus insecticide poisoning: the old and the (possible) new
    Eddleston, Michael
    Chowdhury, Fazle Rabbi
    [J]. BRITISH JOURNAL OF CLINICAL PHARMACOLOGY, 2016, 81 (03) : 462 - 470
  • [7] Eyer Florian, 2003, Toxicological Reviews, V22, P143, DOI 10.2165/00139709-200322030-00003
  • [8] Foroutan A, 2007, PERSPECTIVE MED HIST
  • [9] Foroutan A., 2002, MED REV IRAQI CHEM W
  • [10] Gupta R. C., 2006, CLASSIFICATION USES, DOI DOI 10.1016/B978-012088523-7/50003-X