Protein Information

Name neurotoxic esterase
Synonyms NTE; SWS; Neuropathy target esterase; Neurotoxic esterase; PNPLA 6; patatin like phospholipase domain containing 6; Neuropathy target esterases…

Compound Information

Name parathion
CAS

Reference List

PubMed Abstract RScore(About this table)
2432215 Soliman SA, Curley A, Farmer J, Novak R: In vivo inhibition of chicken brain acetylcholinesterase and neurotoxic esterase in relation to the delayed neurotoxicity of leptophos and cyanofenphos. J Environ Pathol Toxicol Oncol. 1986 Sep-Dec;7(1-2):211-24.

Parathion and TOCP at 2 and 1000 mg/kg of chicken body weight were tested in the same manner as negative and positive neurotoxicants, respectively.
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7077681 Soliman SA, Linder R, Farmer J, Curley A: Species susceptibility to delayed toxic neuropathy in relation to in vivo inhibition of neurotoxic esterase by neurotoxic organophosphorus esters. J Toxicol Environ Health. 1982 Feb;9(2):189-97.

Parathion [O,O-diethyl O-(4-nitrophenyl) phosphorothioate], at 2 or 6.75 mg/kg . d for 15 or 30 d, did not induce neuropathy in either chicken or mice and produced no significant in vivo inhibition of brain NTE activity at the end of the dosing regimen.
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8511793 Veronesi B, Ehrich M: Differential cytotoxic sensitivity in mouse and human cell lines exposed to organophosphate insecticides. Toxicol Appl Pharmacol. 1993 Jun;120(2):240-6.

Baseline activities of the major target esterases, i.e., cholinesterase, carboxylesterase, and neurotoxic esterase, were assayed in mouse and several human neural candidate cell lines.
IC50 data indicated that the tested mouse cell line was consistently more sensitive than the human cell line to equimolar doses of various OP compounds (e.g., mipafox, parathion, paraoxon, DFP, leptophos oxon, fenthion, and fenitrothion).
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16042503 Lotti M, Moretto A: Organophosphate-induced delayed polyneuropathy. . Toxicol Rev. 2005;24(1):37-49.

Neuropathy target esterase (NTE) is thought to be the target of OPIDP initiation.
We also discuss case reports where neuropathies were not convincingly attributed to fenthion, malathion, omethoate/dimethoate, parathion and merphos.
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16766477 Cho TM, Wild JR, Donnelly KC, Tiffany-Castiglioni E: Degradation of organophosphorus neurotoxicity in SY5Y neuroblastoma cells by organophosphorus hydrolase (OPH). J Toxicol Environ Health A. 2006 Aug;69(15):1413-29.

Short-term effects of four OPH-treated OPs on acetylcholinesterase (AChE) and neuropathy target esterase (NTE) activities were measured in retinoic acid-differentiated or undifferentiated cells, and delayed effects of OPH-treated paraoxon or mipafox on levels of neuronal cytoskeletal proteins in nerve growth factor (NGF)-differentiated cells.
Anti-AChE activities of mipafox, methyl parathion, and demeton-S were partially ameliorated, depending on OP concentration.
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3617103 Somkuti SG, Lapadula DM, Chapin RE, Lamb JC 4th, Abou-Donia MB: Testicular toxicity following oral administration of tri-o-cresyl phosphate (TOCP) in roosters. Toxicol Lett. 1987 Aug;37(3):279-90.

Parathion (O,O-diethyl-O-4-nitrophenyl phosphorothioate, 0.1 mg/kg/day, p.o., n = 3) was used as a positive control for AChE inhibition and a negative control for inducing OPIDN.
Analysis at termination revealed significant inhibition of neurotoxic esterase activity (NTE) in both brain and testis.
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6710530 Lapadula DM, Carrington CD, Abou-Donia MB: Induction of hepatic microsomal cytochrome P-450 and inhibition of brain, liver, and plasma esterases by an acute dose of S,S,S-tri-n-butyl phosphorotrithioate (DEF) in the adult hen. Toxicol Appl Pharmacol. 1984 Apr;73(2):300-10.

O,O-Diethyl O-(4-nitrophenyl) phosphorothioate (parathion) and tri-o-cresyl phosphate (TOCP) were used as negative and positive controls for organophosphorus-induced delayed neurotoxicity (OPIDN).
Neurotoxic esterase (NTE) was significantly decreased from control with topical dosing of 200, 500, and 1000 mg/kg DEF and with TOCP treatments.
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7705869 Husain K, Pant SC, Raza SK, Singh R, Das Gupta S: A comparative study of delayed neurotoxicity in hens following repeated administration of organophosphorus compounds. Indian J Physiol Pharmacol. 1995 Jan;39(1):47-50.


Hens treated with Mipafox (10 mg/kg, sc), sarin (50 micrograms/kg, sc) or parathion (1 mg/kg, sc) daily for 10 days exhibited severe, moderate and no ataxia respectively on 14th day after the start of exposure.
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11690566 Barber DS, Ehrich M: Esterase inhibition in SH-SY5Y human neuroblastoma cells following exposure to organophosphorus compounds for 28 days. In Vitr Mol Toxicol. 2001 Summer;14(2):129-35.


To examine metabolic activation in these exposures, pairs of pro- and active toxicants were studied, including chlorpyrifos and its oxon, parathion and paraoxon, and tri-ortho-tolyl phosphate and phenyl saligenin phospahte.
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7123563 Soliman SA, Farmer J, Curley A: Is delayed neurotoxicity a property of all organophosphorus compounds? A study with a model compound: parathion. Toxicology. 1982;23(4):267-79.

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