| Name | Acetylcholinesterase |
|---|---|
| Synonyms | ACHE; ACHE protein; AChE; ARACHE; AcChoEase; Acetylcholine acetylhydrolase; Acetylcholinesterase; Acetylcholinesterase isoform E4 E6 variant… |
| Name | disulfoton |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 8856746 | Yagle K, Costa LG: Effects of organophosphate exposure on muscarinic acetylcholine receptor subtype mRNA levels in the adult rat. Neurotoxicology. 1996 Summer;17(2):523-30. Adult male Sprague-Dawley rats were orally administered disulfoton (2 mg/kg/day) for 14 days, and a subset of exposed animals was allowed to recover for 28 days. This treatment caused a 28% and 81% decrease, respectively, in [3H]-QNB binding and acetylcholinesterase activity in the cortex, similar to that observed in previous studies; after recovery, these levels had returned to 99% and 90%, respectively, of controls. |
1(0,0,0,1) | Details |
| 4764536 | Foley DJ, Stitzel RE, McPhillips JJ: The relationship between inhibition of acetylcholinesterase and sensitivity of the rat ileum to carbachol. Pharmacology. 1973;10(5):298-305. |
1(0,0,0,1) | Details |
| 15294458 | Henderson MC, Krueger SK, Siddens LK, Stevens JF, Williams DE: S-oxygenation of the thioether organophosphate insecticides phorate and disulfoton by human lung flavin-containing monooxygenase 2. Biochem Pharmacol. 2004 Sep 1;68(5):959-67. As the sulfoxide of phorate is a markedly less effective acetylcholinesterase inhibitor than the cytochrome P450 metabolites (oxon, oxon sulfoxide or oxon sulfone), humans possessing the FMO2*1 allele may be more resistant to organophosphate-mediated toxicity when pulmonary metabolism is an important route of exposure or disposition. |
1(0,0,0,1) | Details |
| 4764290 | Foley DJ, McPhillips JJ: Response of the rat ileum, uterus and vas deferens to carbachol and following repeated daily administration of a cholinesterase inhibitor. Br J Pharmacol. 1973 Jul;48(3):418-25. Daily i.p. administration, for eight days, of the cholinesterase inhibitor disulfoton to rats produced mild to moderate signs of intoxication (tremors, incontinence and diarrhoea) but no deaths.2. Acetylcholinesterase activity was 60-70% inhibited in all three tissues. |
1(0,0,0,1) | Details |
| 8793319 | Arnold H, Pluta HJ, Braunbeck T: Sublethal effects of prolonged exposure to disulfoton in rainbow trout (Oncorhynchus mykiss): cytological alterations in the liver by a potent acetylcholine esterase inhibitor. Ecotoxicol Environ Saf. 1996 Jun;34(1):43-55. Mature male rainbow trout (Oncorhynchus mykiss) were exposed for 28 days to 0, 1, 5, and 20 micrograms/liter disulfoton, i.e., to concentrations well below any macroscopically visible effect due to the primary acute toxic mechanism of acetylcholine esterase inhibition. |
112(1,2,2,2) | Details |
| 7150362 | Costa LG, Schwab BW, Murphy SD: Differential alterations of cholinergic muscarinic receptors during chronic and acute tolerance to organophosphorus insecticides. Biochem Pharmacol. 1982 Nov 1;31(21):3407-13. A single injection of disulfoton produced 74, 65 and 27% inhibition of AChE activity after 4, 48 and 96 hr respectively. |
82(1,1,1,2) | Details |
| 8449387 | Llorens J, Crofton KM, Tilson HA, Ali SF, Mundy WR: Characterization of disulfoton-induced behavioral and neurochemical effects following repeated exposure. Fundam Appl Toxicol. 1993 Feb;20(2):163-9. Repeated exposure to disulfoton decreased brain AChE activity and the number of [3H] quinuclidinyl benzilate binding sites. |
32(0,1,1,2) | Details |
| 6875853 | Costa LG, Murphy SD: [3H] binding in rat brain: alteration after chronic acetylcholinesterase inhibition. J Pharmacol Exp Ther. 1983 Aug;226(2):392-7. Chronic treatment with the acetylcholinesterase inhibitor disulfoton (2 mg/kg/day for 10 days) decreased the number of cholinergic muscarinic and nicotinic binding sites in rat brain. |
32(0,1,1,2) | Details |
| 8392202 | Mundy WR, Ward TR, Dulchinos VF, Tilson HA: Effect of repeated organophosphate administration on carbachol-stimulated phosphoinositide hydrolysis in the rat brain. Pharmacol Biochem Behav. 1993 Jun;45(2):309-14. Similar to DFP, repeated disulfoton exposure decreased acetylcholinesterase activity, receptor density, and carbachol-stimulated IP accumulation. |
32(0,1,1,2) | Details |
| 3341049 | McDonald BE, Costa LG, Murphy SD: Spatial memory impairment and central muscarinic receptor loss following prolonged treatment with organophosphates. Toxicol Lett. 1988 Jan;40(1):47-56. Acetylcholinesterase activity was inhibited 71-77% in the cortex, hippocampus, and striatum of rats treated with DFP, and 73-74% in those treated with disulfoton. |
32(0,1,1,2) | Details |
| 2303319 | Costa LG, Kaylor G, Murphy SD: In vitro and in vivo modulation of cholinergic muscarinic receptors in rat lymphocytes and brain by cholinergic agents. Int J Immunopharmacol. 1990;12(1):67-75. Repeated administrations of the organophosphorus insecticide disulfoton (2 mg/kg/day for 14 days, i.p.) caused significant reductions (59-88%) of acetylcholinesterase activity in brain, lymphocytes, plasma and red blood cells, as well as a 23-39% decrease of 3H-QNB binding in brain areas and circulating lymphocytes.(ABSTRACT TRUNCATED AT 250 WORDS) |
31(0,1,1,1) | Details |
| 6609006 | Costa LG, Shao M, Basker K, Murphy SD: Chronic administration of an organophosphorus insecticide to rats alters cholinergic muscarinic receptors in the pancreas. Chem Biol Interact. 1984 Mar;48(3):261-9. Male rats were treated for 10 days with the organophosphorus insecticide, acetylcholinesterase inhibitor, O,O-diethyl S-[2-(ethylthio) ethyl] phosphorodithioate (disulfoton, 2 mg/kg/day by gavage). |
31(0,1,1,1) | Details |
| 7200580 | Schwab BW, Hand H, Costa LG, Murphy SD: Reduced muscarinic receptor binding in tissues of rats tolerant to the insecticide disulfoton. Neurotoxicology. 1981 Dec;2(4):635-47. Tolerance to the toxic effects of exposure to the organophosphate acetylcholinesterase inhibitor, disulfoton, was induced by giving multiple, sublethal doses of the compound to male rats. |
31(0,1,1,1) | Details |
| 6636179 | Schwab BW, Costa LG, Murphy SD: Muscarinic receptor alterations as a mechanism of anticholinesterase tolerance. Toxicol Appl Pharmacol. 1983 Oct;71(1):14-23. Tolerance to the toxic signs of the organophosphorus ester acetylcholinesterase inhibitor, O,O-diethyl S-[2-(ethylthio) ethyl] phosphorodithioate (disulfoton), was induced in rats by giving 10 doses of 2.0 mg/kg/day. |
31(0,1,1,1) | Details |
| 12935443 | Matsuda H, Seo Y, Kakizaki E, Takahama K: Changes in mRNA expression levels of synaptic- and target tissue-specific proteins after organophosphate exposure. Leg Med. 2000 Aug;2(2):55-63. We treated rats with a single dose of Disulfoton (O,O-diethyl S-2-ethylthioethyl phosphorodithioate) and used quantitative reverse transcription-polymerase chain reaction (RT-PCR) to measure the time course of changes in the levels of mRNAs encoding acetylcholinesterase (AChE), nicotinic acetylcholine receptor (nAChR), beta-enolase (MSE), and gamma-enolase (NSE) in soleus muscles and sciatic nerves. |
8(0,0,1,3) | Details |
| 7328703 | Schwab BW, Murphy SD: Induction of anticholinesterase tolerance in rats with doses of disulfoton that produce no cholinergic signs. J Toxicol Environ Health. 1981 Jul-Aug;8(1-2):199-204. Thus the organophosphorus ester insecticide disulfoton, fed to rats in a dietary concentration that depressed acetylcholinesterase but was insufficient to cause cholinergic signs, induced tolerance to the lethal effects of carbachol. |
6(0,0,1,1) | Details |
| 8212012 | Ward TR, Ferris DJ, Tilson HA, Mundy WR: Correlation of the anticholinesterase activity of a series of organophosphates with their ability to compete with agonist binding to muscarinic receptors. Toxicol Appl Pharmacol. 1993 Oct;122(2):300-7. Some compounds that inhibit acetylcholinesterase (AChE) activity compete directly with quinuclidinyl benzilate (QNB) binding, a muscarinic antagonist which binds to all subtypes equally, and with cis-methyldioxolane (CD), an agonist that binds with high affinity to the M2 subtype of muscarinic receptors. Echothiophate and DFP were potent inhibitors of [3H] CD binding, as were the active "oxon" forms of parathion, malathion, and disulfoton. |
5(0,0,0,5) | Details |
| 16962835 | Poyot T, Nachon F, Froment MT, Loiodice M, Wieseler S, Schopfer LM, Lockridge O, Masson P: Mutant of Bungarus fasciatus acetylcholinesterase with low affinity and low hydrolase activity toward organophosphorus esters. Biochim Biophys Acta. 2006 Sep;1764(9):1470-8. Epub 2006 Aug 4. |
4(0,0,0,4) | Details |
| 11052723 | Gao JR, Zhu KY: Comparative toxicity of selected organophosphate insecticides against resistant and susceptible clones of the greenbug, Schizaphis graminum (Homoptera: aphididae). J Agric Food Chem. 2000 Oct;48(10):4717-22. The OR-1 clone showed lower levels of resistance to phenyl (parathion and parathion-methyl) and heterocyclic (chlorpyrifos) OPs than to aliphatic OPs (dimethoate, omethoate, disulfoton, and demeton-S-methyl), whereas the OR-2 clone showed a rather broad spectrum of resistance to nearly all OP insecticides examined. In vitro inhibition of acetylcholinesterase (AChE) using six selected OP oxon analogues showed that alterations of AChE were involved in resistance to all OP compounds examined in both the OR-1 and OR-2 clones. |
3(0,0,0,3) | Details |
| 3020234 | Costa LG, Kaylor G, Murphy SD: Carbachol- and -stimulated phosphoinositide metabolism in rat brain: effect of chronic cholinesterase inhibition. J Pharmacol Exp Ther. 1986 Oct;239(1):32-7. In this study we have investigated whether repeated administration of the organophosphorus insecticide disulfoton, known to cause the development of tolerance to this compound, would affect phosphoinositide metabolism in rat brain. Acetylcholinesterase was inhibited by 85%. |
2(0,0,0,2) | Details |
| 8449393 | Fitzgerald BB, Costa LG: Modulation of muscarinic receptors and acetylcholinesterase activity in lymphocytes and in brain areas following repeated organophosphate exposure in rats. Fundam Appl Toxicol. 1993 Feb;20(2):210-6. Using the mAChR antagonist [3H] quinuclidinyl benzilate (QNB) to label mAChRs, we found that exposure to disulfoton for 14 days (2 mg/kg/day by gavage) caused a significant decrease (25-35%) in muscarinic receptors density in the cerebral cortex, hippocampus, and striatum, as well as in circulating lymphocytes. |
2(0,0,0,2) | Details |
| 7726573 | Lai K, Stolowich NJ, Wild JR: Characterization of P-S bond hydrolysis in organophosphorothioate pesticides by organophosphorus hydrolase. Arch Biochem Biophys. 1995 Apr 1;318(1):59-64. The extensive use of organophosphorothioate insecticides in agriculture has resulted in the risk of environmental contamination with a variety of broadly based neurotoxins that inhibit the acetylcholinesterases of many different animal species. |
2(0,0,0,2) | Details |
| 15342957 | Smulders CJ, Bueters TJ, Vailati S, van Kleef RG, Vijverberg HP: Block of neuronal nicotinic acetylcholine receptors by organophosphate insecticides. Toxicol Sci. 2004 Dec;82(2):545-54. Epub 2004 Sep 1. Chronic and acute exposure to organophosphate (OP) pesticides may lead to persistent neurological and neurobehavioral effects, which cannot be explained by acetylcholinesterase (AChE) inhibition alone. Several OP pesticides, e.g., parathion-ethyl, chlorpyrifos and disulfoton, inhibited the -induced ion current with potencies in the micromolar range. |
2(0,0,0,2) | Details |
| 4781488 | Brzezinski J, Ludwicki K: The interrelationship of the changes of acetylcholine esterase and catecholamines blood and urine levels in rats poisoned with disyston. Pol J Pharmacol Pharm. 1973 May-Jun;25(3):313-6. |
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