| Name | neuropathy target esterase |
|---|---|
| Synonyms | NTE; SWS; Neuropathy target esterase; Neurotoxic esterase; PNPLA 6; patatin like phospholipase domain containing 6; Neuropathy target esterases… |
| Name | methamidophos |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 1781739 | Bertolazzi M, Caroldi S, Moretto A, Lotti M: Interaction of methamidophos with hen and human acetylcholinesterase and neuropathy target esterase. Arch Toxicol. 1991;65(7):580-5. |
82(1,1,1,2) | Details |
| 2170085 | Zheng RY: [Clinical features of delayed polyneuropathy induced by acute methamidophos toxicosis in 74 cases]. Zhonghua Nei Ke Za Zhi. 1990 Feb;29(2):79-82 It is regarded that the pathogenesis of methamidophos-induced delayed polyneuropathy is the toxic effect produced by the "aging" of the phosphoryl-enzyme complex caused by the phosphorylation of a protein neurotoxic esterase (NTE) in the nervous system, and also is the autoimmuno disorder induced by the "aging" of the NTE being probably an immunological basis. |
81(1,1,1,1) | Details |
| 10774823 | Kellner T, Sanborn J, Wilson B: In vitro and in vivo assessment of the effect of impurities and chirality on methamidophos-induced neuropathy target esterase aging. Toxicol Sci. 2000 Apr;54(2):408-15. In vitro and in vivo studies evaluated neuropathy target esterase (NTE) inhibition and aging (i.e., loss of reactivation potential) by analytical and technical grade racemic and resolved L-(-) and D-(+) isomers of methamidophos (O,S-dimethyl phosphoramidothioate). |
37(0,1,2,2) | Details |
| 1660708 | Johnson MK, Vilanova E, Read DJ: Anomalous biochemical responses in tests of the delayed neuropathic potential of methamidophos (O,S-dimethyl phosphorothioamidate), its resolved isomers and of some higher O-alkyl homologues. Toxicology. 1989 Jan;54(1):89-100. The interaction with neural neuropathy target esterase (NTE) and acetylcholinesterase (AChE) in vivo of methamidophos (O,S-dimethyl phosphorothioamidate), its resolved stereoisomers and five higher O-alkyl homologues has been examined along with the ability of these compounds to cause organophosphorus-induced delayed polyneuropathy (OPIDP) in adult hens. |
31(0,1,1,1) | Details |
| 7654138 | Lotti M, Moretto A, Bertolazzi M, Peraica M, Fioroni F: Organophosphate polyneuropathy and neuropathy target esterase: studies with methamidophos and its resolved optical isomers. Arch Toxicol. 1995;69(5):330-6. |
7(0,0,1,2) | Details |
| 9486944 | Sogorb MA, Diaz-Alejo N, Pellin MC, Vilanova E: Inhibition and aging of neuropathy target esterase by the stereoisomers of a phosphoramidate related to methamidophos. Toxicol Lett. 1997 Dec;93(2-3):95-102. |
32(0,1,1,2) | Details |
| 10447555 | McConnell R, Delgado-Tellez E, Cuadra R, Torres E, Keifer M, Almendarez J, Miranda J, El-Fawal HA, Wolff M, Simpson D, Lundberg I: Organophosphate neuropathy due to methamidophos: biochemical and neurophysiological markers. Arch Toxicol. 1999 Aug;73(6):296-300. Neuropathy target esterase (NTE), the putative target enzyme for organophosphate induced delayed polyneuropathy (OPIDP), can be measured in lymphocytes but has rarely been assessed in acute human poisoning. |
1(0,0,0,1) | Details |
| 2284053 | Wilson BW, Henderson JD, Kellner TP, McEuen SF, Griffis LC, Lai JC: Acetylcholinesterase and neuropathy target esterase in chickens treated with acephate. Neurotoxicology. 1990 Fall;11(3):483-91. Reports that near-lethal doses of the pesticide methamidophos (O,S-dimethyl phosphoramidothioate) caused a delayed neurotoxicity (OPIDN) in humans and that another phosphoramidate, isofenphos, caused OPIDN in the hen at high doses, prompted a study of the abilities of acephate (O,S-dimethyl acetylphosphoramidothioate) to inhibit brain acetylcholinesterase (AChE) and neuropathy target esterase (NTE) in vivo. |
32(0,1,1,2) | Details |
| 11696925 | Singh AK: QSAR for the organophosphate-induced inhibition and 'aging' of the enzyme neuropathy target esterase (NTE). SAR QSAR Environ Res. 2001;12(3):275-95. The neuropathy-target-esterase (NTE) inhibition data were either obtained from the literature for a number of OP compounds or were determined experimentally for methamidophos, acephate, coumaphos and EPN. |
31(0,1,1,1) | Details |
| 8211998 | Lotti M, Moretto A, Capodicasa E, Bertolazzi M, Peraica M, Scapellato ML: Interactions between neuropathy target esterase and its inhibitors and the development of polyneuropathy. Toxicol Appl Pharmacol. 1993 Oct;122(2):165-71. In fact, mipafox and methamidophos as well as certain classic protective inhibitors such as and sulfonyl form an inhibited NTE which apparently does not age and yet produces neuropathy. |
2(0,0,0,2) | Details |
| 8568835 | Barril J, Tormo N, Diaz-Alejo N, Vilanova E: Organophosphorus inhibition and heat inactivation kinetics of particulate and soluble forms of peripheral nerve neuropathy target esterase. J Biochem Toxicol. 1995 Aug;10(4):211-8. S-NTE was less sensitive to the inhibition by O,O'-diisopropyl phosphorofluoridate (DFP), hexyl 2,5-dichlorophenyl phosphoramidate (H-DCP), and mipafox than P-NTE and brain NTE, while the opposite was true for O,S-dimethyl phosphoroamidothioate (methamidophos). |
2(0,0,0,2) | Details |
| 2238440 | Blasco R, Moreno E, Sanz P, Repetto M: In vitro modifications of rat NTE and other esterases by chemicals which induce delayed neurotoxicity in vivo. Arch Toxicol. 1991;65(8):618-24. Using rat brain homogenate, a parallel study on the activity of neurotoxic esterase (NTE) and total esterases (TE) compared the action of metamidophos, which is known to induce delayed neurotoxicity, and the synthetic fatty acid anilides, oleylanilide and linoleylanilide. |
1(0,0,0,1) | Details |
| 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. In this article, we mainly discuss OP pesticide poisoning, particularly when caused by chlorpyrifos, dichlorvos, isofenphos, methamidophos, mipafox, trichlorfon, trichlornat, phosphamidon/mevinphos and by certain carbamates. |
1(0,0,0,1) | Details |
| 8492300 | Jokanovic M, Johnson MK: Interactions in vitro of some organophosphoramidates with neuropathy target esterase and acetylcholinesterase of hen brain. J Biochem Toxicol. 1993 Mar;8(1):19-31. However, it has been shown recently that certain N-unsubstituted organophosphoro-monoamidates (analogues of methamidophos) cause delayed neuropathy even though the inhibited NTE appeared not to have aged (Johnson et al. (1991). |
1(0,0,0,1) | Details |
| 2536970 | Johnson MK, Vilanova E, Read DJ: Biochemical and clinical tests of the delayed neuropathic potential of some O-alkyl O-dichlorophenyl phosphoramidate analogues of methamidophos (O,S-dimethyl phosphorothioamidate). Chem Biol Interact. 1993 Jun;87(1-3):369-81. The interaction in vivo of four O-alkyl O-2,5-dichlorophenyl phosphoramidates with neural neuropathy target esterase (NTE) and acetylcholinesterase (AChE) and their ability to cause delayed polyneuropathy in hens has been examined. |
1(0,0,0,1) | Details |
| 1316117 | Moretto A, Bertolazzi M, Capodicasa E, Peraica M, Richardson RJ, Scapellato ML, Lotti M: Phenylmethanesulfonyl elicits and intensifies the clinical expression of neuropathic insults. Arch Toxicol. 1992;66(1):67-72. Chicks are resistant to OPIDP despite high inhibition/aging of neuropathy target esterase (NTE), the putative target of OPIDP initiation. Methamidophos (50 mg/kg p.o. to hens), which produces in vivo a reactivatable form of inhibited NTE, was shown either to protect from or promote OPIDP caused by DBDCVP (0.45 mg/kg s.c.), depending on the sequence of dosing. |
1(0,0,0,1) | Details |
| 2238437 | Sanz P, Moreno E, Blasco R, Repetto M: Study of delayed neurotoxicity caused by fatty acid anilides in hens. Vet Hum Toxicol. 1990 Oct;32(5):422-7. We have compared the modifications produced by each of the 2 treatments on the enzymatic activity of neuropathy target esterase (NTE) measured in nervous tissue homogenates of brain, medulla and sciatic nerve. |
1(0,0,0,1) | Details |
| 8343994 | Vilanova E, Barril J, Carrera V: Biochemical properties and possible toxicological significance of various forms of NTE. 125. NTE (neuropathy target esterase) is considered to be the target for organophosphorus-induced delayed polyneuropathy and is operationally measured by radiolabelling or by determining its esteratic activity as the paraoxon-resistant mipafox-sensitive phosphorylable site (s). The fixed time inhibition curves show that P-NTE is more sensitive to mipafox, DFP and hexyl-DCP than S-NTE, while the reverse is true for methamidophos. |
1(0,0,0,1) | Details |
| 8393746 | Lotti M, Moretto A: The search for the physiological functions of NTE; is NTE a receptor? . Chem Biol Interact. 1993 Jun;87(1-3):407-16. NTE inhibitors have been ranked as full agonists (classic neuropathic inhibitors such as diisopropylfluorophosphate), partial agonists (protective or neuropathic, depending on the dose, such as methamidophos) and antagonists (protective, and neuropathic at the highest doses, such as phenylmethanesulfonyl Neuropathy target esterase (NTE) was identified as the molecular target for organophosphate-induced delayed polyneuropathy several years ago but its physiological functions are still unknown. |
1(0,0,0,1) | Details |
| 15207378 | Battershill JM, Edwards PM, Johnson MK: Toxicological assessment of isomeric pesticides: a strategy for testing of chiral organophosphorus (OP) compounds for delayed polyneuropathy in a regulatory setting. Food Chem Toxicol. 2004 Aug;42(8):1279-85. The combination of differential metabolism of chiral organophosphorus (OP) pesticides and opposing stereoselectivity of inhibition of neuropathy target esterase (NTE) and acetylcholinesterase (AChE) can affect the value of the hen test, performed to OECD guidelines, in predicting the potential to cause organophosphate-induced delayed polyneuropathy (OPIDP) in humans. The experimental data on structural analogues of the pesticide methamidophos and the evidence for stereoselective OPIDP are reviewed and a model is given demonstrating how the properties of a chiral OP can result in the neuropathic potential not being detected by the standard hen test. |
1(0,0,0,1) | Details |
| 11350214 | Quistad GB, Sparks SE, Casida JE: Fatty acid amide hydrolase inhibition by organophosphorus pesticides. Toxicol Appl Pharmacol. 2001 May 15;173(1):48-55. Five OP pesticides inhibit 50% of the brain FAAH activity (ED50) at <30 mg/kg 4 h after ip administration to mice; while inhibition by chlorpyrifos, diazinon, and methamidophos occurs near acutely toxic levels, profenofos and tribufos are effective at asymptomatic doses. |
0(0,0,0,0) | Details |