Acute dermal toxicities of various organophosphate insecticides in mice

Skinner, Clint S.; Kilgore, Wendell W.

doi:10.1080/15287398209530180

Cited by 15 publications

(4 citation statements)

References 16 publications

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“…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.…”

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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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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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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“…This is in agreement with Marinovich et al 44 that a mixture of diazinon, dimethoate and azinophos was more toxic to protein synthesis than any of the single compounds alone, whereas it was equal to a maximum toxic compound as relates to inhibition of AChE activity. Furthermore, the toxicity of diazinon compared with methyl parathion is related to the animal species, thus the dermal toxicity of methyl parathion was higher than diazinon in mice, 35 whereas in another study, diazinon was more toxic than methyl parathion in Anquilla anquilla. 45 Furthermore, exposure of rainbow trout fish to a mixture of diazinon and malathion significantly decreased cholinesterase activity and differed significantly among exposure durations, 46 whereas Cha et al 8 showed that pretreatment of mice with diazinon completely blocked the serum esterase activity and enhanced ethyl carbamate toxicity.…”

Section: Discussionmentioning

confidence: 97%

“…This may be due to the low level of plasma BuChE during pregnancy. 21 Skinner and Kilgore 35 reported that diazinon was much more inhibitory on blood than the nervous system tissue cholinesterase in mice. Also, exposure of Anquilla anquilla to diazinon inhibited plasma BuChE activity by >90% of control.…”

Section: Discussionmentioning

confidence: 98%

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 LD 50 value for methyl parathion dissolved in xylene and applied to the backs of male and female rats was reported to be 67 mg/kg [Gaines 1960]. In another study, the LD 50 value for methyl parathion dissolved in acetone and applied to the hind foot of mice was 1200 mg/ kg [Skinner and Kilgore 1982a]. The reported acute dermal LD 50 value for methyl parathion in rats is lower than the critical dermal LD 50 value of 200 mg/kg that identifies chemical substances that are potentially fatal at relatively low doses following dermal exposure [NIOSH 2009].…”

Section: Overview Of Sk Assignmentmentioning

confidence: 97%

NIOSH skin notation (SK) profile: methyl parathion [CAS No. 298-00-0].

Hudson¹,

Dotson²

2015

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Acute dermal toxicities of various organophosphate insecticides in mice

Cited by 15 publications

References 16 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

NIOSH skin notation (SK) profile: methyl parathion [CAS No. 298-00-0].

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