Inhibition of acetylcholinesterase and butyrylcholinesterase by the organophosphorus insecticide methylparathion in the central nervous system of the golden hamster (Mesocricetus auratus)

Hahn, Tom; Ruhnke, Martin; Luppa, H

doi:10.1016/s0065-1281(11)80284-9

Cited by 10 publications

(6 citation statements)

References 22 publications

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“…Changes in the contributions of reactivation and replacement may explain the biphasic recovery of cholinesterase activity following oral or intravenous administration of methyl parathion ( fig. 1) or other organophosphorus insecticides [2,11,22]. Spontaneous reactivation may be more important during the initial, faster phase of recovery, whereas synthesis of new enzyme assumes a greater role during the later, slower phase.…”

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: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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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“…11,12,24 Chambers and Carr 20 reported a rapid inhibition of rat brain AChE following methyl parathion administration. Furthermore, Hahn et al 25 detected maximum inhibition of AChE and BuChE activity in the hamster nervous system 45 min after oral administration of methyl parathion. A similar effect has been detected after 30-60 min of intravenous injection of methyl parathion in male rats.…”

Section: Discussionmentioning

confidence: 99%

Inhibition and recovery of maternal and fetal cholinesterase enzyme activity following a single cutaneous dose of methyl parathion and diazinon, alone and in combination, in pregnant rats

Abu-Qare

Abou‐Donia

2001

J of Applied Toxicology

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Pregnant Sprague-Dawley rats (14-18 days of gestation) were treated with a single cutaneous subclinical dose(s) of 10 mg kg(-1) (15% of LD(50)) of methyl parathion (O,O-dimethyl O-4-nitrophenyl phosphorothioate) and 65 mg kg(-1) (15% of LD(50)) of diazinon (O,O)-diethyl O-2-isopropyl-6-methylpyrimidinyl phosphorothioate, and their combination. Animals were sacrificed at 1, 2, 4, 12, 24, 48, 72, and 96 h after dosing. Inhibition of maternal and fetal cholinesterase enzyme activity has been determined. Methyl parathion significantly inhibited maternal and fetal brain acetylcholinesterase (AChE) and plasma butyrylcholinesterase (BuChE) activity within 24 h after dosing. Diazinon and a mixture of methyl parathion and diazinon caused lesser inhibition compared with methyl parathion alone. Recovery of maternal and fetal brain AChE activity was in the order of diazinon > combination of diazinon and methyl parathion > methyl parathion 96 h after dosing. Although fetal plasma BuChE activity recovered to 100% of control within 96 h of application, maternal BuChE activity remained inhibited to 55% and 32% of control 96 h after application of methyl parathion and a mixture of methyl parathion and diazinon, respectively. Following a single dermal dose of methyl parathion, the activity of maternal liver BuChE was 63% of control 2 h after dosing, whereas inhibition of placental AChE or BuChE activity occurred 12 and 1 h following a single dose of methyl parathion, corresponding to activities of 63% and 54% of control, respectively. Diazinon, alone or in combination with methyl parathion, did not inhibit significantly the maternal liver BuChE or placental AChE and BuChE activity. The results suggest that dermal application of a single dose of methyl parathion and diazinon, alone or in combination, has an easy access into maternal and fetal tissues, resulting in inhibition of cholinesterase enzymes. The lower inhibitory effect of the combination of methyl parathion and diazinon might be due to competition of diazinon with methyl parathion for cytochrome P-450 enzymes, resulting in formation of the potent cholinesterase inhibitor methyl paraoxon. The faster recovery of fetal cholinesterase enzymes is attributed to the rapid de novo synthesis of cholinesterase fetal tissues compared with the mother.

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“…The fast inhibition of the enzyme is related to the rapid distribution of methyl parathion in maternal and fetal tissues , and to rapid oxidation into methyl paraoxon, which is a more potent inhibitor of AChE activity Chambers & Carr, 1993;. Chambers and Carr (1993) reported rapid inhibition of rat brain AChE following methyl parathion administration, and Hahn et al (1991) detected maximum inhibition of AChE and BuChE activity in the hamster nervous system 45 min after oral administration of methyl parathion. Similar effects have been detected 30-60 min following intravenous injection of methyl parathion in male rats (Gupta & Kadel, 1990).…”

Section: Effects Of Dermal Exposure To Chlorpyrifos and Methyl Parathionmentioning

confidence: 99%

Inhibition of Cholinesterase Enzymes Following a Single Dermal Dose of Chlorpyrifos and Methyl Parathion, Alone and in Combination, in Pregnant Rats

Abu-Qare¹,

Abdel-Rahman²,

Brownie³

et al. 2001

Journal of Toxicology and Environmental Health, Part A

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Pregnant Sprague-Dawley rats (14-18 d of gestation) were treated with either a single dermal subclinical dose of 30 mg/kg (15% of dermal LD50) chlorpyrifos (O,O-diethyl-O-[3,5,6-trichloro-2-pyridinyl] phosphorothioate) or a single dermal subclinical dose of 10 mg/kg (15% of dermal LD50) methyl parathion (O,O-dimethyl O-4-nitrophenyl phosphorothioate) or the two in combination. Chlorpyrifos inhibited maternal and fetal brain acetylcholinesterase (AChE) activity within 24 h of dosing, (48% and 67% of control activity, respectively). Following application of methyl parathion, peak inhibition of maternal and fetal brain AChE activity occurred at 48 h and 24 h after dosing (17% and 48% of control activity, respectively). A combination of chlorpyrifos and methyl parathion produced peak inhibition of maternal and fetal brain AChE activity at 24 h postdosing (35% and 73% of control activity, respectively). Maternal and fetal brain AChE activity recovered to various degrees of percentage of control 96 h after dosing. Application of methyl parathion or chlorpyrifos alone or in combination significantly inhibited maternal plasma butyrylcholinesterase (BuChE) activity. No significant inhibition of fetal plasma BuChE activity was detected. Peak inhibition of maternal liver BuChE occurred 24 h after application of methyl parathion or chlorpyrifos alone or in combination (64%, 80%, and 61% of control activity, respectively). Significant inhibition of placental AChE occurred within 24 h after application of methyl parathion or chlorpyrifos alone or in combination. The results suggest that methyl parathion and chlorpyrifos, alone or in combination, were rapidly distributed in maternal and fetal tissues, resulting in rapid inhibition of cholinesterase enzyme activities. The lower inhibitory effect of the combination could be due to competition between chlorpyrifos and methyl parathion for cytochrome P-450 enzymes, resulting in inhibition of the formation of the potent cholinesterase inhibitor oxon forms. The faster recovery of fetal plasma BuChE is attributed to the de novo synthesis of cholinesterase by fetal tissues compared to maternal tissues.

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Inhibition of acetylcholinesterase and butyrylcholinesterase by the organophosphorus insecticide methylparathion in the central nervous system of the golden hamster (Mesocricetus auratus)

Cited by 10 publications

References 22 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

Inhibition and recovery of maternal and fetal cholinesterase enzyme activity following a single cutaneous dose of methyl parathion and diazinon, alone and in combination, in pregnant rats

Inhibition of Cholinesterase Enzymes Following a Single Dermal Dose of Chlorpyrifos and Methyl Parathion, Alone and in Combination, in Pregnant Rats

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