Anticholinesterase action of methyl parathion, parathion and azinphosmethyl in mice and fish: Onset and recovery of inhibition

Benke, G.M.; Murphy, Sheldon D.

doi:10.1007/bf01713037

Cited by 60 publications

(20 citation statements)

References 9 publications

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“…Time-dependent changes in cholinesterase activity in blood and other tissues following administration of methyl parathion to adult female rats by different routes noted here are consistent with those noted in previous studies [2,11,40] after administration of an organophosphorus insecticide. For example, oral administration of 7.5 mg/kg methyl parathion to female rats caused maximal inhibition of red blood cell acetylcholinesterase within 30 min with full recovery in vivo occurring over the next 96-120 h [40].…”

Section: Discussionsupporting

confidence: 91%

“…For example, oral administration of 7.5 mg/kg methyl parathion to female rats caused maximal inhibition of red blood cell acetylcholinesterase within 30 min with full recovery in vivo occurring over the next 96-120 h [40]. Intraperitoneal injection of methyl parathion (8-10 mg/kg) to rats or mice also caused rapid (F1 h) inhibition of cholinesterase in brain which was followed by a prolonged period (1-7 days) of recovery in vivo [2,11].…”

Section: Discussionmentioning

confidence: 99%

“…Influences on the pharmacokinetics of methyl paraoxon and the activity of acetylcholinesterase follow in turn. Yet, there are only limited data related to methyl parathion with which to predict the potential long-term health risks resulting from a pattern of exposure that occurred with its use in domestic settings [2,7,8,14,16,20,22,36,40]. Also, methyl parathion and other organophosphorus insecticides exhibit a broad range of toxicities and abilities to inhibit acetylcholinesterase [10,11,18,19], making inferences between agents and across species speculative at best.…”

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confidence: 99%

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A Comparison of Cholinesterase Activity after Intravenous, Oral or Dermal Administration of Methyl Parathion

Krämer¹,

Wellman²,

Zhu³

et al. 2002

J Biomed Sci

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Time-dependent changes in blood cholinesterase activity caused by single intravenous, oral or dermal administration of methyl parathion to adult female rats were defined. Intravenous and oral administration of 2.5 mg/kg methyl parathion resulted in rapid (<60 min) decreases in cholinesterase activity which recovered fully in vivo within 30–48 h. In contrast, spontaneous reactivation of cholinesterase in vitro was complete within 6 h at 37°C. Dermal administration of methyl parathion caused dose-dependent inhibition of cholinesterase activity which developed slowly (≧6 h) and was prolonged (≧48 h). Time- and route-dependent effects of methyl parathion on cholinesterase activity in brain and other tissues generally paralleled its effects on activity in blood. In conclusion, pharmacodynamics of methyl parathion differ substantially with route of exposure. Recovery of cholinesterase in vivo after intravenous or oral exposure may partially reflect spontaneous reactivation and suggests a rapid clearance of methyl parathion or its active metabolite methyl paraoxon. The more gradual and prolonged inhibition of cholinesterase caused by dermal administration is consistent with disposition of methyl parathion at a site from which it or methyl paraoxon is only slowly distributed. Thus, dermal exposure to methyl parathion may pose the greatest risk for long-term adverse effects.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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A Comparison of Cholinesterase Activity after Intravenous, Oral or Dermal Administration of Methyl Parathion

Krämer¹,

Wellman²,

Zhu³

et al. 2002

J Biomed Sci

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“…However, the rapidity of the initial recovery and the point of inflection of the recovery curve appeared to depend on the anti-ChE compound administered. Brain ChE activity of fish (Benke and Murphy, 1974) and ducks exposed to some OPs (W.J. Fleming, unpublished data) also exhibits an apparent decrease in the slope of ChE recovery at about 50-60% of normal ChE activity.…”

Section: Discussionmentioning

confidence: 94%

Recovery of cholinesterase activity in mallard ducklings administered organophosphorus pesticides

1981

Journal of Toxicology and Environmental Health

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Oral doses of the organophosphorus pesticides acephate, dicrotophos, fensuifothion, fonofos, malathion, and parathion were administered to mallard ducklings (Anas platyrhynchos), and brain and plasma cholinesterase (ChE) activities were determined for up to 17 d after dosing. In vivo recovery of brain ChE activity to within 2 standard deviations of the mean activity of undosed birds occurred within 8 d, after being depressed an average of 25-58% at 24 h after dosing. In vivo recovery of plasma ChE appeared as fast as or faster than that of brain, but the pattern of recovery was more erratic and therefore statistical comparison with brain ChE recovery was not attempted. In vitro tests indicated that the potential for dephosphorylation to contribute to in vivo recovery of inhibited brain ChE differed among chemical treatments. Some ducklings died as a result of organophosphate dosing. In an experiment in which ducklings within each treatment group received the same dose (mg/kg), the brain ChE activity in birds that died was less than that in birds that survived. Brain ChE activities in ducklings that died were significantly different among pesticide treatments: fensuifothion > parathion > acephate > malathion (p < 0.05). RightsWorks produced by employees of the U.S. Government as part of their official duties are not copyrighted within the U.S. The content of this document is not copyrighted. PLEASE SCROLL DOWN FOR ARTICLETaylor & Francis makes every effort to ensure the accuracy of all the information (the "Content") contained in the publications on our platform. However, Taylor & Francis, our agents, and our licensors make no representations or warranties whatsoever as to the accuracy, completeness, or suitability for any purpose of the Content. Any opinions and views expressed in this publication are the opinions and views of the authors, and are not the views of or endorsed by Taylor & Francis. The accuracy of the Content should not be relied upon and should be independently verified with primary sources of information. Taylor and Francis shall not be liable for any losses, actions, claims, proceedings, demands, costs, expenses, damages, and other liabilities whatsoever or howsoever caused arising directly or indirectly in connection with, in relation to or arising out of the use of the Content. This article may be used for research, teaching, and private study purposes. Any substantial or systematic reproduction, redistribution, reselling, loan, sub-licensing, systematic supply, or distribution in any form to anyone is expressly forbidden. Terms & Conditions of access and use can be found at http:// www.tandfonline.com/page/terms-and-conditions

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“…However, studies of the effects of other organophosphates on fish indicate that AChE activity is depressed or inhibited following exposure. Benke and Murphy (1974) have shown that the onset of AChE inhibition in fish by some organophosphate insecticides occurs within 24 hr. Recovery requires an extended period of time (about 4 weeks) to approach normal activity again.…”

Section: )mentioning

confidence: 99%

The Effect of Ultra Low Volume Aerial Dispersal of Naled on an Aquatic Habitat. Robins AFB, Georgia

Livingston¹,

Goodwin²

1974

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Anticholinesterase action of methyl parathion, parathion and azinphosmethyl in mice and fish: Onset and recovery of inhibition

Cited by 60 publications

References 9 publications

A Comparison of Cholinesterase Activity after Intravenous, Oral or Dermal Administration of Methyl Parathion

A Comparison of Cholinesterase Activity after Intravenous, Oral or Dermal Administration of Methyl Parathion

Recovery of cholinesterase activity in mallard ducklings administered organophosphorus pesticides

The Effect of Ultra Low Volume Aerial Dispersal of Naled on an Aquatic Habitat. Robins AFB, Georgia

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