| Name | Acetylcholinesterase |
|---|---|
| Synonyms | ACHE; ACHE protein; AChE; ARACHE; AcChoEase; Acetylcholine acetylhydrolase; Acetylcholinesterase; Acetylcholinesterase isoform E4 E6 variant… |
| Name | mevinphos |
|---|---|
| CAS | methyl 3-[(dimethoxyphosphinyl)oxy]-2-butenoate |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 8783813 | Worek F, Kirchner T, Backer M, Szinicz L: Reactivation by various oximes of human erythrocyte acetylcholinesterase inhibited by different organophosphorus compounds. Arch Toxicol. 1996;70(8):497-503. For this purpose human erythrocyte AChE (EC 3.1.1.7) was inhibited (30 min) by chlorfenvinphos, dichlorvos, dicrotophos, heptenophos, mevinphos, monocrotophos, paraoxon, phosphamidon, trichlorfon, malaoxon, omethoate, oxydemeton-methyl or methamidophos by 85-98% of control. |
84(1,1,1,4) | Details |
| 938396 | Revzin AM: Effects of mevinphos (Phosdrin) on unit discharge patterns in avian hippocampus. Aviat Space Environ Med. 1976 Jun;47(6):608-11. Low doses of the acetylcholinesterase inhibitors, mevinphos and physostigmine, reduce hippocampal inhibitory phenomena, measured in terms of the duration of the poststimulus inhibitory pause seen in individual hippocampal neurones in the pigeon. |
31(0,1,1,1) | Details |
| 10022307 | Ray DE: Chronic effects of low level exposure to anticholinesterases--a mechanistic review. Toxicol Lett. 1998 Dec 28;102-103:527-33. A single dose of sarin or repeated doses of metrifonate or mevinphos, have produced only transient adverse effects at doses causing substantial acetylcholinesterase inhibition. |
31(0,1,1,1) | Details |
| 10916212 | Kassa J: [Importance of reactivation of fosdrin-inhibited acetylcholinesterase in the brain and diaphragm for the in vivo therapeutic effect of oximes in rats poisoned with fosdrin]. Cas Lek Cesk. 2000 Apr 26;139(8):237-9. |
3(0,0,0,3) | Details |
| 10953441 | Kassa J: [The effect of panpal prophylaxis on acetylcholinesterase activity in the blood, diaphragm and various parts of the brain in rats during treated and untreated poisoning with the organophosphorus insecticide phosdrine]]. Ceska Slov Farm. 2000 Jan;49(1):37-40. |
3(0,0,0,3) | Details |
| 10376416 | Kassa J: [Comparison of the effects of BI-6, a new asymmetric bipyridine oxime, with HI-6 oxime and obidoxime in combination with atropine on soman and fosdrine toxicity in mice]. Ceska Slov Farm. 1999 Jan;48(1):44-7. At the equi-effective level which respects the toxicity of the oxime and is therefore more important for practical use, it is a therapeutically weaker reactivator of acetylcholinesterase than HI-6. |
1(0,0,0,1) | Details |
| 6138014 | Michalek H, Nemesio R, Meneguz A, Bisso GM: Interactions between anticholinesterase agents and neuroleptics in terms of cholinesterase inhibition in brain and other tissues of rats. Arch Toxicol Suppl. 1983;6:386-90. The enhanced inhibition of total ChE due to CPZ depended in most peripheral organs on the effect on pseudoChE (as measured by a spectrophotometric method), except in the case of skeletal muscle in which potentiation of PhS effect was observed on true acetylcholinesterase (AcChE). CPZ was found to potentiate slightly the effects of Mevinphos but did not interact with Carbaryl, Diazinon or Azinphos. |
1(0,0,0,1) | Details |
| 7097799 | Skinner CS, Kilgore WW: Acute dermal toxicities of various organophosphate insecticides in mice. J Toxicol Environ Health. 1982 Mar;9(3):491-7. Values were simultaneously generated for the ED50 (milligrams per kilogram) for both cholinesterase and acetylcholinesterase. Lethality was greatest with mevinphos, followed by parathion, methyl parathion, diazinon, and azinphosmethyl. |
1(0,0,0,1) | 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 |
| 16984802 | Chan JY, Chan SH, Dai KY, Cheng HL, Chou JL, Chang AY: Cholinergic-receptor-independent dysfunction of mitochondrial respiratory chain enzymes, reduced mitochondrial transmembrane potential and ATP depletion underlie necrotic cell death induced by the organophosphate poison mevinphos. Neuropharmacology. 2006 Dec;51(7-8):1109-19. Epub 2006 Sep 18. Taking advantage of the absence in an in vitro system of acetylcholinesterase, the pharmacological target of organophosphate compounds, the present study evaluated the hypothesis that the repertoire of cholinergic receptor-independent cellular events that underlie fatal organophosphate poisoning entails induction of mitochondrial dysfunction, followed by bioenergetic failure that leads to necrotic cell death because of ATP depletion. |
1(0,0,0,1) | Details |
| 17438462 | Tsai CY, Wu CH, Chan SH, Chang AY: Muscarinic receptor-independent activation of cyclic -dependent protein kinase in rostral ventrolateral medulla underlies the sympathoexcitatory phase of cardiovascular responses during mevinphos intoxication in the rat. Shock. 2007 May;27(5):559-64. As inhibitors of acetylcholinesterase, clinical presentations of poisoning from organophosphate compounds are generally believed to entail overstimulation by the accumulated on muscarinic receptors at peripheral and central synapses. |
1(0,0,0,1) | Details |