| Name | Acetylcholinesterase |
|---|---|
| Synonyms | ACHE; ACHE protein; AChE; ARACHE; AcChoEase; Acetylcholine acetylhydrolase; Acetylcholinesterase; Acetylcholinesterase isoform E4 E6 variant… |
| Name | mipafox |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 4092885 | Gupta RC, Patterson GT, Dettbarn WD: Mechanisms involved in the development of tolerance to DFP toxicity. Fundam Appl Toxicol. 1985 Dec;5(6 Pt 2):S17-28. Rats treated daily with diisopropylfluorophosphate (DFP) (0.5 mg/kg, sc), an inhibitor of acetylcholinesterase (AChE) activity, exhibited the symptoms of cholinergic hyperactivity between Days 3 and 5 similar to those observed 15 min after a single acute dosage (1.5 mg/kg, sc). DFP toxicity was potentiated in rats that were pretreated with BuChE inhibitors, such as iso-OMPA (3 mg/kg, sc) or mipafox (0.05 mg/kg, sc), 30 min prior to DFP (0.5 mg/kg, sc). |
4(0,0,0,4) | Details |
| 17323978 | Kropp TJ, Richardson RJ: Mechanism of aging of mipafox-inhibited butyrylcholinesterase. . Chem Res Toxicol. 2007 Mar;20(3):504-10. Epub 2007 Feb 27. However, recent evidence has shown that acetylcholinesterase (AChE) and the catalytic domain of human neuropathy target esterase (NEST) undergo aging by alternative mechanisms following their inhibition with N,N'-diisopropylphosphorodiamidofluoridate (mipafox, MIP). |
3(0,0,0,3) | Details |
| 833008 | Lindvall O: Combined visualization of central catecholamine- and acetylcholinesterase-containing neurons: application of the and thiocholine histochemical methods to the same Vibratome section. Histochemistry. 1977 Jan 24;50(3):191-6. The unmounted sections are examined and photographed in the fluorescence microscope, and then stained for acetylcholinesterse according to Holmstedt's modification of the Koelle thiocholine method (incubation for 4-6 h with acetylthiocholine as substrate and Mipafox as inhibitor of non-specific cholinesterases). the sections are then examined in the light microscope, rephotographed, and the picture compared with that following the GA reaction. |
3(0,0,0,3) | Details |
| 9515941 | Ehrich M, Correll L: Inhibition of carboxylesterases in SH-SY5Y human and NB41A3 mouse neuroblastoma cells by organophosphorus esters. J Toxicol Environ Health A. 1998 Mar 13;53(5):385-99. CbxE are thought to protect the critical enzyme acetylcholinesterase (AChE) from OP inhibition in animals. Therefore, this study examined concentration-related OP-induced inhibition of CbxE in human SH-SY5Y and mouse NB41A3 neuroblastoma cells with 11 active esterase inhibitors: paraoxon, malaoxon, chlorpyrifos-oxon, tolyl saligenin (TSP), phenyl saligenin (PSP), diisopropyl phosphorofluoridate (DFP), mipafox, dichlorvos, trichlorfon, dibutyryl dichlorovinyl (DBVP), and dioctyl dichlorovinyl (DOVP). |
3(0,0,0,3) | Details |
| 7909676 | Husain K: Phenyl and ester hydrolases in the platelets of human, hen, rat and mouse. Hum Exp Toxicol. 1994 Mar;13(3):157-9. The activities of total phenyl hydrolase (PVase), paraoxon insensitive phenyl hydrolase (PI-PVase), paraoxon and mipafox resistant esterase (PMRE) and propionyl-cholinesterase (PChE) were maximal in hen followed by mouse, rat and human. 3. Neurotoxic esterase (NTE) and acetylcholinesterase (AChE) activities were concentrated in the platelets of hens followed by humans, rats and mice in order. 4. |
1(0,0,0,1) | Details |
| 1540236 | Chemnitius JM, Chemnitius GC, Haselmeyer KH, Kreuzer H, Zech R: Cholinesterases of heart muscle. Biochem Pharmacol. 1992 Feb 18;43(4):823-9. Cholinesterases of porcine left ventricular heart muscle were characterized with respect to substrate specificity and inhibition kinetics with organophosphorus inhibitors N,N'-di-isopropyl-phosphorodiamidic (Mipafox), di-isopropylphosphorofluoridate (DFP), and diethyl p-nitro-phenyl (Paraoxon). One ester-hydrolysing enzyme was identified as acetylcholinesterase (EC 3.1.1.7), and one as butyrylcholinesterase (EC 3.1.1.8). |
1(0,0,0,1) | Details |
| 6865914 | Chemnitius JM, Zech R: Inhibition of brain carboxylesterases by and nonneurotoxic organophosphorus compounds. Mol Pharmacol. 1983 May;23(3):717-23. By iterative elimination of exponential inhibition curves and by sequential inhibition experiments using a combination of two organophosphorus inhibitors, 11 different carboxylesterases of chicken brain were characterized with respect to their phenyl -hydrolyzing activity (milliunits per gram of brain) and their inhibition by O,O-diethyl O- (Paraoxon), O,O-diisopropylphosphorofluoridate, and N,N'-diisopropylphosphorodiamidic (Mipafox). The corresponding data for acetylcholinesterase (EC 3.1.1.7) in chicken brain were determined. |
1(0,0,0,1) | Details |
| 8685903 | Wu SY, Casida JE: Subacute neurotoxicity induced in mice by potent organophosphorus neuropathy target esterase inhibitors. Toxicol Appl Pharmacol. 1996 Jul;139(1):195-202. Acetylcholinesterase and butyrylcholinesterase are much less sensitive than NTE to inhibition by OBDPO and EOPF both in vitro and in vivo. |
1(0,0,0,1) | Details |
| 10421494 | Makhaeva GF, Malygin VV: A stable preparation of hen brain neuropathy target esterase for rapid biochemical assessment of potential of organophosphates. Chem Biol Interact. 1999 May 14;119-120:551-7. This enzyme has proved to be an excellent tool for the assessment of neuropathic potential of organophosphates (OP), in particular by comparison of an OP inhibitory activity in vitro against NTE and acetylcholinesterase. To obtain a stable NTE preparation the influence of intensive freezing and subsequent lyophilization of paraoxon-preinhibited (P2 + P3) hen brain membrane fraction on NTE properties has been studied using two neuropathic OP: mipafox and O,O-dipropyldichlorovinyl (PrDChVP). |
1(0,0,0,1) | Details |
| 6651578 | Alonso JL, Atalla A, Cavaliere MJ, Gagioti SM, Lorenti MA: [Polyneuropathy caused by parathion: clinical, electrophysiologic and histologic studies of a case]. Arq Neuropsiquiatr. 1983 Sep;41(3):292-308. Electromyography (EMG) in the first observation showed neuromuscular transmission blocking characterized by deficiency or absence of voluntary activity, unexcitability of fibular nerves, with fibrillations and positive peaks as described previously with Mipafox (another organophosphorus agent). One year later, the concentration of erythrocyte acetylcholinesterase was found to be low and plasma cholinesterase was normal, suggesting that the patient was carrier of a congenital deficiency of acetylcholinesterase. |
1(0,0,0,1) | Details |
| 20000741 | Vyas NK, Nickitenko A, Rastogi VK, Shah SS, Quiocho FA: Structural insights into the dual activities of the nerve agent degrading organophosphate anhydrolase/prolidase. Biochemistry. 2010 Jan 26;49(3):547-59. The organophosphate acid anhydrolase (OPAA) is a member of a class of bimetalloenzymes that hydrolyze a variety of toxic acetylcholinesterase-inhibiting organophosphorus compounds, including -containing chemical nerve agents. Here we report the X-ray structure determination of the native OPAA (58 kDa mass) from Alteromonas sp. strain JD6.5 and its cocrystal with the inhibitor mipafox [N,N'-diisopropyldiamidofluorophosphate (DDFP)], a close analogue of the nerve agent organophosphate substrate diisopropyl fluorophosphate (DFP). |
1(0,0,0,1) | Details |
| 6870909 | Chemnitius JM, Haselmeyer KH, Zech R: Brain cholinesterases. Biochem Pharmacol. 1983 Jun 1;32(11):1693-9. Three organophosphorus inhibitors were used: diethyl p-nitrophenyl (Paraoxon, E 600), di-isopropylphosphorofluoridate (DFP), and N,N'-di-isopropylphosphorodiamidic (Mipafox). Six cholinesterases were shown to hydrolyse esters in hen brain, one was identified as acetylcholinesterase (EC 3.1.1.7) and one as cholinesterase (EC 3.1.1.8). |
1(0,0,0,1) | Details |
| 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. All three compounds significantly inhibited acetylcholinesterase (AChE) activity in the platelets. |
1(0,0,0,1) | Details |
| 8525498 | Mutch E, Kelly SS, Blain PG, Williams FM: Comparative studies of two organophosphorus compounds in the mouse. Toxicol Lett. 1995 Nov;81(1):45-53. Mipafox (110 mumol/kg, s.c.) inhibited brain acetylcholinesterase (AChE), neuropathy target esterase (NTE) and phenylvalerate hydrolases by 58, 64 and 65%, while diaphragm AChE and phenylvalerate hydrolases were inhibited by 66 and 80%, respectively. |
163(2,2,2,3) | Details |
| 7713347 | Ehrich M, Jortner BS, Padilla S: Comparison of the relative inhibition of acetylcholinesterase and neuropathy target esterase in rats and hens given cholinesterase inhibitors. Fundam Appl Toxicol. 1995 Jan;24(1):94-101. Rat NTE/AChE inhibition ratios were 0.9 after TOTP, 2.6 after PSP, 1.0 after mipafox, 0.62 after DFP, 1.3 after dichlorvos, 2.2 after malathion, and 1.1 after carbaryl. |
145(1,3,3,5) | Details |
| 16042503 | Lotti M, Moretto A: Organophosphate-induced delayed polyneuropathy. . Toxicol Rev. 2005;24(1):37-49. The ratio of inhibitory powers for acetylcholinesterase and NTE represents the crucial guideline for the aetiological attribution of OP-induced peripheral neuropathy. 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 |
| 16485911 | Kropp TJ, Richardson RJ: Aging of mipafox-inhibited human acetylcholinesterase proceeds by displacement of both isopropylamine groups to yield a adduct. Chem Res Toxicol. 2006 Feb;19(2):334-9. |
89(1,1,1,9) | Details |
| 9051410 | Williams FM, Charlton C, de Blaquiere GE, Mutch E, Kelly SS, Blain PG: The effects of multiple low doses of organophosphates on target enzymes in brain and diaphragm in the mouse. Hum Exp Toxicol. 1997 Feb;16(2):67-71. Multiple low doses of the direct acting organophosphates, ecothiopate, paraoxon and mipafox produced persistent and additive inhibition of diaphragm acetylcholinesterase. |
87(1,1,2,2) | Details |
| 7991223 | De Bleecker J, Lison D, Van Den Abeele K, Willems J, De Reuck J: Acute and subacute organophosphate poisoning in the rat. Neurotoxicology. 1994 Summer;15(2):341-8. Marked differences are noted in the duration of cholinergic symptoms and of AChE inhibition after either paraoxon and mipafox, or fenthion poisoning. |
84(1,1,1,4) | Details |
| 7979963 | Kelly SS, Mutch E, Williams FM, Blain PG: Electrophysiological and biochemical effects following single doses of organophosphates in the mouse. Arch Toxicol. 1994;68(7):459-66. Mipafox inhibited brain and diaphragm acetylcholinesterase and brain neuropathy target esterase. |
83(1,1,1,3) | Details |
| 9586870 | Sarin S, Gill KD: Biochemical and behavioral deficits in adult rat following chronic dichlorvos exposure. Pharmacol Biochem Behav. 1998 Apr;59(4):1081-6. Dichlorvos administration significantly decreased the activities of neuropathy target esterase and other carboxylesterase viz., paraoxon resistant and mipafox and paraoxon resistant esterases. The acetylcholinesterase activity was also appreciably decreased following dichlorvos exposure. |
1(0,0,0,1) | Details |
| 14635269 | Petroianu G, Arafat K, Kosanovic M, Saleh A, Camasamudram V, Hasan MY: In vitro protection of red blood cell acetylcholinesterase by metoclopramide from inhibition by organophosphates (paraoxon and mipafox). J Appl Toxicol. 2003 Nov-Dec;23(6):447-51. |
83(1,1,1,3) | Details |
| 9051411 | Kelly SS, de Blaquiere GE, Williams FM, Blain PG: Effects of multiple doses of organophosphates on evoked potentials in mouse diaphragm. Hum Exp Toxicol. 1997 Feb;16(2):72-8. Single doses of mipafox (20 mg/kg), ecothiopate (0.192 mg/kg) or paraoxon (0.415 mg/kg) in the mouse produced ca. 70% inhibition of diaphragm acetylcholinesterase at 3 h after dosing. |
83(1,1,1,3) | Details |
| 9653066 | de Blaquiere GE, Williams FM, Blain PG, Kelly SS: A comparison of the electrophysiological effects of two organophosphates, mipafox and ecothiopate, on mouse limb muscles. Toxicol Appl Pharmacol. 1998 Jun;150(2):350-60. Acetylcholinesterase activity was inhibited by mipafox (65% in the soleus; 76% in the EDL) and ecothiopate (59% in the soleus; 42% in the EDL). |
82(1,1,1,2) | Details |
| 12825237 | Tang Y, Donnelly KC, Tiffany-Castiglioni E, Mumtaz MM: Neurotoxicity of polycyclic aromatic hydrocarbons and simple chemical mixtures. J Toxicol Environ Health A. 2003 May 23;66(10):919-40. In addition, PCP appeared to increase the inhibition of acetylcholinesterase by mipafox. |
81(1,1,1,1) | Details |
| 9268605 | Ehrich M, Correll L, Veronesi B: Acetylcholinesterase and neuropathy target esterase inhibitions in neuroblastoma cells to distinguish organophosphorus compounds causing acute and delayed neurotoxicity. Fundam Appl Toxicol. 1997 Jul;38(1):55-63. For example, apparent IC50 values for NTE inhibition were less than 9.6-fold the apparent IC50 values for AChE inhibition when cells were exposed to the neuropathy-inducing OPs diisopropyl phosphorofluoridate, cyclic tolyl saligenin phenyl saligenin mipafox, dibutyl dichlorovinyl and di-octyl-dichlorovinyl |
37(0,1,1,7) | Details |
| 9147026 | Chemnitius JM, Haselmeyer KH, Gonska BD, Kreuzer H, Zech R: Mipafox differential inhibition assay for heart muscle cholinesterases: substrate specificity and inhibition of three isoenzymes by physostigmine and quinidine. Gen Pharmacol. 1997 Apr;28(4):567-75. With acetylthiocholine (ASCh) as substrate (1.25 mM), hydrolytic activities (A) of cholinesterase isoenzymes were determined after preincubation (60 min, 25 degrees C) of heart muscle samples with either saline (total activity, A tau), 7 microM mipafox (AM1), or 0.8 mM mipafox (AM2): (BChE) = A tau-AM1, (AChE) = AM1-AM2, (Atypical ChE) = AM2. 3. |
35(0,1,1,5) | Details |
| 4347708 | Heffron PF: Actions of the selective inhibitor of cholinesterase tetramonoisopropyl pyrophosphortetramide on the rat phrenic nerve-diaphragm preparation. Br J Pharmacol. 1972 Dec;46(4):714-24. Amongst anticholinesterases, octamethyl pyrophosphortetramide and tetraethylpyrophosphate also enhanced the amplitude of the tetanic response, but paraoxon, dyflos, and mipafox did not.4. A concentration of 3 muM produced near complete inhibition of cholinesterase, and a concentration of 300 muM also inhibited acetylcholinesterase marginally.2. |
1(0,0,0,1) | Details |
| 2851472 | Chettur G, DeFrank JJ, Gallo BJ, Hoskin FC, Mainer S, Robbins FM, Steinmann KE, Walker JE: Soman-hydrolyzing and -detoxifying properties of an enzyme from a thermophilic bacterium. Fundam Appl Toxicol. 1988 Oct;11(3):373-80. Like the squid enzyme, it is not inhibited by mipafox (N,N'-diisopropylphosphordiamidofluoridate), is not inactivated by ammonium and does hydrolyze the acetylcholinesterase-inhibitory pair of diastereoisomers of soman as well as the relatively noninhibitory pair, thus detoxifying soman. |
0(0,0,0,0) | Details |
| 12791540 | Kropp TJ, Richardson RJ: Relative inhibitory potencies of chlorpyrifos oxon, chlorpyrifos methyl oxon, and mipafox for acetylcholinesterase versus neuropathy target esterase. J Toxicol Environ Health A. 2003 Jun 27;66(12):1145-57. |
34(0,1,1,4) | Details |
| 8343998 | Milatovic D, Johnson MK: Reactivation of phosphorodiamidated acetylcholinesterase and neuropathy target esterase by treatment of inhibited enzyme with Chem Biol Interact. 1993 Jun;87(1-3):425-30. We have found that both acetylcholinesterase (AChE) and neuropathy target esterase (NTE) which had been inhibited with either mipafox or with a di-n-butylphosphorodiamidate could be reactivated by prolonged treatment with aqueous (KF): the reaction proceeded with first-order kinetics. |
32(0,1,1,2) | Details |
| 9788582 | Li W, Casida JE: Organophosphorus neuropathy target esterase inhibitors selectively block outgrowth of neurite-like and cell processes in cultured cells. Toxicol Lett. 1998 Sep 15;98(3):139-46. This study compares two direct-acting neuropathy target esterase (NTE) inhibitors (mipafox and 2-octyl-4H-1,3,2-benzodioxophosphorin 2-oxide (OBDPO)), a metabolic precursor to an NTE inhibitor (tri-o-cresyl or TOCP) and a potent acetylcholinesterase inhibitor (chlorpyrifos oxon or CPO) for their effects on outgrowth of neurite-like and cell processes and on viability in differentiated cultured cells (rat adrenal pheochromocytoma (PC-12) and brain glial tumor (C6)). |
31(0,1,1,1) | Details |
| 10421452 | Chemnitius JM, Sadowski R, Winkel H, Zech R: Organophosphate inhibition of human heart muscle cholinesterase isoenzymes. Chem Biol Interact. 1999 May 14;119-120:183-92. Final classification of heart muscle cholinesterases was achieved according to substrate hydrolysis patterns (nmol/min per g wet weight) and to second-order organophosphate inhibition rate constants k2 (1/mol per min); one ester hydrolyzing enzyme was identified as acetylcholinesterase (AChE; k2/mipafox = 6.1 (+/- 0.8) x 10 (2)), and one as butyrylcholinesterase (BChE; k2/mipafox = 5.3 (+/- 1.1) x 10 (3)). |
31(0,1,1,1) | Details |
| 16963094 | Read DJ, Langford L, Barbour HR, Forshaw PJ, Glynn P: Phospholipase B activity and organophosphorus compound toxicity in cultured neural cells. Toxicol Appl Pharmacol. 2007 Mar;219(2-3):190-5. Epub 2006 Aug 8. Organophosphorus compounds (OP) such as phenyl saligenin (PSP) and mipafox (MPX) which cause delayed neuropathy, inhibit neuropathy target esterase (NTE), while OPs such as paraoxon (PXN) react more readily with acetylcholinesterase. |
31(0,1,1,1) | Details |
| 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 -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. |
19(0,0,3,4) | Details |
| 9745921 | Makhaeva GF, Filonenko IV, Yankovskaya VL, Fomicheva SB, Malygin VV: Comparative studies of O,O-dialkyl-O-chloromethylchloroformimino phosphates: interaction with neuropathy target esterase and acetylcholinesterase. Neurotoxicology. 1998 Aug-Oct;19(4-5):623-8. |
6(0,0,0,6) | Details |