Name | anticholinesterase |
---|---|
Synonyms | Acylcholine acylhydrolase; BCHE; BCHE protein; Butyrylcholine esterase; Butyrylcholinesterase; CHE1; Choline esterase II; Cholinesterase… |
Name | mipafox |
---|---|
CAS |
PubMed | Abstract | RScore(About this table) | |
---|---|---|---|
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. |
277(3,4,4,7) | 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. We characterized cholinesterases of human left ventricular heart muscle with respect to both substrate specificity and irreversible inhibition kinetics with the organophosphorus inhibitor N,N'-di-isopropylphosphorodiamidic (mipafox). |
94(0,3,3,4) | Details |
15052610 | Petroianu G, Kuhn F, Arafat K, Zuleger K, Missler A: In vitro protection of plasma cholinesterases by metoclopramide from inhibition by mipafox. J Appl Toxicol. 2004 Mar-Apr;24(2):143-6. |
86(1,1,1,6) | 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. |
82(1,1,1,2) | 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). |
65(0,2,2,5) | Details |
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. 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). |
34(0,1,1,4) | 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 |
486506 | Axenfors B, Andersson I, Augustinsson KB: Isolation and characterization of a butyrylesterase from human erythrocytes. Biochim Biophys Acta. 1979 Sep 12;570(1):74-87. The enzyme is inhibited by low concentrations of Hg2+, Cd2+, Zn2+ and the organophosphorus compound Mipafox, but is insensitive to eserine. The properties of this butyrylesterase, including its ability to hydrolyze thiocholine esters at a relatively rapid rate (albeit with a high Km), are a mixture of those expected for an arylesterase and a cholinesterase. |
1(0,0,0,1) | Details |
56273 | Freed VH, Matin MA, Fang SC, Kar PP: Role of striatal Mipafox administered to rats daily for 35 days produced ataxia and a reduction in the level of in the corpus striatum. The cholinesterase activity of corpus striatum was inhibited by all the compounds. |
in delayed effects of organophosphorus compounds. Eur J Pharmacol. 1976 Jan;35(1):229-32.1(0,0,0,1) | Details |
14081661 | BROWNLEE G, JOHNSON ES: THE SITE OF THE 5-HYDROXYTRYPTAMINE RECEPTOR ON THE INTRAMURAL NERVOUS PLEXUS OF THE GUINEA-PIG ISOLATED ILEUM. Br J Pharmacol Chemother. 1963 Oct;21:306-22. The anticholinesterase N,N'-diisopropylphosphorodiamidic (mipafox) potentiated all the agonists except |
32(0,1,1,2) | Details |
14110755 | JOHNSON ES: THE ORIGIN OF THE When the guinea-pig isolated ileum had been previously treated with the anticholinesterase, NN-diisopropylphosphodiamidic (mipafox), and attached to an isotonic lever loaded with 0.5 g, it released into Krebs solution gassed with a mixture of 95% and 5% |
RELEASED SPONTANEOUSLY FROM THE GUINEA-PIG ISOLATED ILEUM. Br J Pharmacol Chemother. 1963 Dec;21:555-68.31(0,1,1,1) | 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. Inhibition of neuropathy target esterase (NTE, neurotoxic esterase) and acetylcholinesterase (AChE) activities was compared in brain and spinal cords of adult While Leghorn hens and adult male Long Evan rats 4-48 hr after administration of triortho-tolyl (TOTP po, 50-500 mg/kg to hens; 300-1000 mg/kg to rats), phenyl saligenin (PSP im 0.1-2.5 mg/kg to hens; 5-24 mg/kg to rats), mipafox (3-30 mg/kg ip to hens and rats), diisopropyl phosphorofluoridate (DFP sc, 0.25-1.0 mg/kg to hens; 1-3 mg/kg to rats), dichlorvos (5-60 mg/kg ip to hens; 600-2000 mg/kg to rats), and carbaryl (300-560 mg/kg ip to hens; 30-170 mg/kg to rats). |
1(0,0,0,1) | 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. 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. |
1(0,0,0,1) | Details |
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). |
1(0,0,0,1) | 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. It has been thought that the -enzyme bond in inhibited esterases inhibited by such agents as mipafox (N,N'-di-iso-propylphosphorodiamidate) was refractory to reactivating agents either because an 'aging' reaction occurs soon after inhibition or because the bond was intrinsically very strong. Di-isopropylphosphoro-butyrylcholinesterase could be fully reactivated by this treatment but after 18 h to allow aging the monoisopropyl phosphoro-enzyme was totally refractory to KF. |
1(0,0,0,1) | Details |
14066138 | CARLYLE RF: THE MODE OF ACTION OF NEOSTIGMINE AND PHYSOSTIGMINE ON THE GUINEA-PIG TRACHEALIS MUSCLE. Br J Pharmacol Chemother. 1963 Aug;21:137-49. The anticholinesterase diisopropylphosphodiamidic (mipafox) itself caused no contractile response even in concentrations of 100 mug/ml., yet neostigmine or physostigmine still caused contractions after treatment with mipafox. |
0(0,0,0,0) | Details |
16292756 | Lamango NS: Liver prenylated methylated protein methyl esterase is an organophosphate-sensitive enzyme. J Biochem Mol Toxicol. 2005;19(5):347-57. Only about 25% of the brain enzyme was inhibited by 0.5-1 mM solutions of mipafox, while 0.1 and 1 mM paraoxon inhibited over 50% and 95% of the enzyme, respectively. |
0(0,0,0,0) | Details |
14110754 | BROWNLEE G, HARRY J: SOME PHARMACOLOGICAL PROPERTIES OF THE CIRCULAR AND LONGITUDINAL MUSCLE STRIPS FROM THE GUINEA-PIG ISOLATED ILEUM. Br J Pharmacol Chemother. 1963 Dec;21:544-54. Incubation of the preparations with the anticholinesterase, mipafox (NN-diisopropylphosphodiamidic sensitized both preparations to the action of potentiation of the contraction of the longitudinal muscle was 16-times; that of the circular one 4,000-times. |
7(0,0,1,2) | Details |
7909676 | Husain K: Phenyl 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. |
and ester hydrolases in the 7(0,0,1,2) | Details |
13953023 | HARRY J: The action of drugs on the circular muscle strip from the guinea-pig isolated ileum. Br J Pharmacol Chemother. 1963 Jun;20:399-417. This behaviour necessitated the treatment of each strip with the anticholinesterase NN-diisopropylphosphodiamidic (mipafox) before each experiment. |
7(0,0,1,2) | Details |
13904922 | HARRY J: Effect of cooling, local anaesthetic compounds and botulinum toxin on the responses of and the ileum. Br J Pharmacol Chemother. 1962 Aug;19:42-55. In the presence of the anticholinesterase NN-diisopropylphosphodiamidic (Mipafox), was detected in the fluid passing through the lumen and also in the fluid in the organ bath. |
output from the electrically transmurally stimulated isolated guinea-pig 6(0,0,1,1) | Details |
14126042 | CARLYLE RF: THE RESPONSES OF THE GUINEA-PIG ISOLATED INTACT TRACHEA TO TRANSMURAL STIMULATION AND THE RELEASE OF AN -LIKE SUBSTANCE UNDER CONDITIONS OF REST AND STIMULATION. Br J Pharmacol Chemother. 1964 Feb;22:126-36. The contraction is enhanced by treatment of the trachea with the anticholinesterase NN-diisopropylphosphodiamidic (mipafox), and is thus probably due to stimulation of intrinsic cholinergic nerves. |
6(0,0,1,1) | 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). |
6(0,0,0,6) | Details |
8343980 | Chemnitius JM, Dewald K, Kreuzer H, Zech R: Computerized analysis of covalent inhibition kinetics for identification of heart muscle cholinesterase and brain carboxylesterase isoenzymes. Chem Biol Interact. 1993 Jun;87(1-3):239-44. |
3(0,0,0,3) | 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. |
3(0,0,0,3) | 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). Low concentrations of blood cholinesterases confirmed the etiology. |
2(0,0,0,2) | 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. In addition, MCP is a reversible inhibitor of cholinesterases from the human central nervous system and blood, and may have a red blood cell (RBC) acetylcholinesterase (AChE) protective effect against inhibition by organophosphates. |
2(0,0,0,2) | Details |
13882799 | CUTHBERT AW: Actions of some anticholinesterases on the smooth muscle of the chick amnion. Br J Pharmacol Chemother. 1962 Jun;18:550-62. The actions of both reversible and irreversible anticholinesterase drugs on the nerve-free smooth muscle of the chick amnion are described. The tertiary compound physostigmine and the irreversible inhibitor diisopropylfluorophosphonate were found to be active in causing contractions, whereas the quaternary compound neostigmine and the irreversible inhibitor Mipafox were only slightly active in this respect. |
2(0,0,0,2) | Details |
2859406 | Matin MA, Hussain K: Striatal neurochemical changes and motor dysfunction in mipafox-treated animals. Methods Find Exp Clin Pharmacol. 1985 Feb;7(2):79-81. The animals developed motor dysfunction-muscle twitchings, fasciculations and slight ataxia towards the end of the experimental period; the motor dysfunction was accompanied by neurochemical changes in the corpus striatum which included significantly reduced levels of cholinesterase, neurotoxicesterase, and |
1(0,0,0,1) | Details |