| Name | Acetylcholinesterase |
|---|---|
| Synonyms | ACHE; ACHE protein; AChE; ARACHE; AcChoEase; Acetylcholine acetylhydrolase; Acetylcholinesterase; Acetylcholinesterase isoform E4 E6 variant… |
| Name | acephate |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 2097819 | Singh AK: Molecular properties and inhibition kinetics of acetylcholinesterase obtained from rat brain and cockroach ganglion. Toxicol Ind Health. 1990 Dec;6(6):551-70. Acephate was a potent inhibitor of cockroach AChE, but a poor inhibitor of rat AChE. |
521(6,7,7,11) | Details |
| 1670382 | Singh AK: Molecular properties and inhibition kinetics of acetylcholinesterase obtained from rat brain and cockroach ganglion. Toxicol Ind Health. 1990 Dec;6(6):551-70. Acephate was a potent inhibitor of cockroach AChE, but a poor inhibitor of rat AChE. |
521(6,7,7,11) | Details |
| 3798464 | Singh AK: Kinetic analysis of acetylcholinesterase inhibition by combinations of acephate and methamidophos. Toxicology. 1986 Dec 15;42(2-3):143-56. |
436(5,6,6,6) | 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. |
281(3,4,5,6) | Details |
| 14694584 | Zhou L, Zhang Y, Shi N: [Comparison of the toxic effect of methamidophos and acephate on acetylcholinesterase]. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2002 Dec;20(6):405-8. RESULTS: Acephate and methamidophos could directly inhibit AChE activities in human erythrocyte membrane and rat brain synatosomal membrane in dose- and time-dependent manners in vitro, and this effect was irreversible. |
202(2,3,4,7) | Details |
| 9074804 | Mahajna M, Quistad GB, Casida JE: Acephate insecticide toxicity: safety conferred by inhibition of the bioactivating carboxyamidase by the metabolite methamidophos. Chem Res Toxicol. 1997 Jan;10(1):64-9. These relationships are established by finding that 4 h pretreatment of mice with methamidophos i.p. at 5 mg/kg has the following effects on acephate action: reduces methamidophos and acephate levels in liver by 30-60% in the first 2 h after i.p. acephate dosage; inhibits the liver carboxyamidase cleaving [14CH3S] acephate to [14CH3S] methamidiphos with 50% block at approximately 1 mg/kg; strongly inhibits 14CO2 liberation from [CH3 (14) C (O)] acephate in vivo; markedly alters the pattern of urinary metabolites of acephate by increasing O- and S-demethylation products retaining the carboxyamide moiety; greatly reduces the brain AChE inhibition following acephate treatment; doubles the LD50 of i.p.-administered acephate from 540 to 1140 mg/kg. |
112(1,2,2,2) | Details |
| 10681099 | Lesser J, Blodgett D, Ehrich M: Comparison of oxime-initiated reactivation of organophosphorous-inhibited acetylcholinesterase in brains of avian embryos. J Toxicol Environ Health A. 2000 Jan 14;59(1):57-66. Doses of chlorpyrifos, parathion, acephate, and trichlorfon that inhibited AChE > 70% were administered to the embryos. |
117(1,2,2,7) | Details |
| 4060156 | Singh AK: Kinetic analysis of inhibition of brain and red blood cell acetylcholinesterase and plasma cholinesterase by acephate or methamidophos. Toxicol Appl Pharmacol. 1985 Nov;81(2):302-9. |
96(0,3,3,6) | Details |
| 15180375 | Printes LB, Callaghan A: A comparative study on the relationship between acetylcholinesterase activity and acute toxicity in Daphnia magna exposed to anticholinesterase insecticides. Environ Toxicol Chem. 2004 May;23(5):1241-7. Binding sites other than AChE possibly are involved in acephate toxicity to D. magna. |
93(1,1,2,8) | Details |
| 11328714 | Spassova DP, Singh AK: QSAR for acetylcholinesterase inhibition and toxicity of two classes of phosphoramidothioates. SAR QSAR Environ Res. 2001 Feb;11(5-6):453-71. Acephate (Ace), like Met, is a poor inhibitor of AChE in vitro and has a comparable to Met insect toxicity in vivo. |
88(1,1,1,8) | Details |
| 3975930 | Rattner BA, Michael SD: Organophosphorus insecticide induced decrease in plasma luteinizing hormone concentration in white-footed mice. Toxicol Lett. 1985 Jan;24(1):65-9. Oral intubation of 50 and 100 mg/kg acephate inhibited brain acetylcholinesterase (AChE) activity by 45% and 56%, and reduced basal luteinizing hormone (LH) concentration by 29% and 25% after 4 h in white-footed mice (Peromyscus leucopus noveboracensis). |
81(1,1,1,1) | Details |
| 16563591 | Caldas ED, Boon PE, Tressou J: Probabilistic assessment of the cumulative acute exposure to organophosphorus and insecticides in the Brazilian diet. Toxicology. 2006 May 1;222(1-2):132-42. Epub 2006 Mar 6. Relative potency factors (RPF) were calculated with methamidophos or acephate as index compounds (IC), using BMD (10) or NOAEL for AChE inhibition, mostly in rat brain, obtained from national and international pesticide evaluations. |
64(0,2,2,4) | Details |
| 3608937 | Singh AK, Drewes LR: effects of low-level chronic acephate exposure in rats. Environ Res. 1987 Aug;43(2):342-9. Similar changes occurred in rats exposed to 10 mg of acephate/kg.day; however, plasma cholinesterase and RBC acetylcholinesterase activities were inhibited. |
38(0,1,2,3) | Details |
| 11048668 | Spassova D, White T, Singh AK: Acute effects of acephate and methamidophos on acetylcholinesterase activity, endocrine system and amino acid concentrations in rats. Comp Biochem Physiol C Toxicol Pharmacol. 2000 May;126(1):79-89. |
14(0,0,2,4) | Details |
| 2241237 | Maroni M, Catenacci G, Galli D, Cavallo D, Ravazzani G: Biological monitoring of human exposure to acephate. . Arch Environ Contam Toxicol. 1990 Sep-Oct;19(5):782-8. Before, during, and after exposure, the workers were monitored for the urine content of acephate and methamidophos, and for erythrocyte (AChE) and plasma (PChE) cholinesterase levels. |
12(0,0,2,2) | Details |
| 20021020 | Das GP, Jamil K, Rahman MF: Effect of four organophosphorus compounds on human blood acetylcholinesterase: in vitro studies. Toxicol Mech Methods. 2006;16(8):455-9. The IC50 values for RBC-AChE were 0.12 muM, 0.25 muM, 0.35 muM, and 4.0 muM for chlorpyrifos, monocrotophos, profenofos, and acephate, respectively. |
10(0,0,1,5) | Details |
| 18569613 | Rajini PS, Melstrom P, Williams PL: A comparative study on the relationship between various toxicological endpoints in Caenorhabditis elegans exposed to organophosphorus insecticides. J Toxicol Environ Health A. 2008;71(15):1043-50. The toxicity of 10 organophophorus (OP) insecticides-acephate, dimethoate, dichlorvos, dicrotophos, monocrotophos, methamidophos, phosphamidon, omethoate, phosdrin, and trichlorfon-was evaluated in Caenorhabditis elegans using lethality, movement, and acetylcholinesterase (AChE) activity as the endpoints after a 4-hr- exposure period. |
9(0,0,1,4) | Details |
| 10530896 | Singh AK: Quantitative structure-activity relationships for phosphoramidothioate toxicity in housefly. Comp Biochem Physiol C Pharmacol Toxicol Endocrinol. 1999 Jul;123(3):241-55. Ace II- and Ace IV-induced inhibition of fly-head AChE was influenced by the spatial configuration of the inhibitor. |
5(0,0,0,5) | Details |
| 18206231 | Printes LB, Fellowes MD, Callaghan A: Clonal variation in acetylcholinesterase biomarkers and life history traits following OP exposure in Daphnia magna. Ecotoxicol Environ Saf. 2008 Oct;71(2):519-26. Epub 2008 Feb 21. Two clones of Daphnia magna (Standard and Ruth) were exposed for 7 days to sub-lethal concentrations of acephate (5.0 and 10.0 mg/L). |
4(0,0,0,4) | Details |
| 9568380 | Singh AK, White T, Spassova D, Jiang Y: Physicochemical, molecular-orbital and electronic properties of acephate and methamidophos. Comp Biochem Physiol C Pharmacol Toxicol Endocrinol. 1998 Jan;119(1):107-17. Me is a potent inhibitor, while Ac is a poor inhibitor of mammalian AChE (mAChE). |
3(0,0,0,3) | 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 |
| 12355557 | Singh AK, Jiang Y: Immunotoxicity of acute acephate exposure in control or IL-1-challenged rats: correlation between the immune cell composition and corticosteroid concentration in blood. J Appl Toxicol. 2002 Sep-Oct;22(5):279-91. Ace, in a dose- and time-dependent manner, inhibited blood and brain acetylcholinesterase (AChE) activities, increased blood concentrations, suppressed blood CD4, CD8, B cell and monocyte contents and increased blood neutrophil counts. |
2(0,0,0,2) | Details |
| 10048144 | Poovala VS, Kanji VK, Tachikawa H, Salahudeen AK: Role of oxidant stress and antioxidant protection in acephate-induced renal tubular cytotoxicity. Toxicol Sci. 1998 Dec;46(2):403-9. Although the toxicity of OP compounds is primarily through blockade of neural transmission via inhibition of acetylcholinesterase, studies have revealed histopathological alterations in the renal proximal tubules, suggesting a role for additional mechanisms in renal toxicity. |
1(0,0,0,1) | Details |
| 17549541 | Venkateswara Rao J, Kavitha P, Jakka NM, Sridhar V, Usman PK: Toxicity of organophosphates on morphology and locomotor behavior in brine shrimp, Artemia salina. Arch Environ Contam Toxicol. 2007 Aug;53(2):227-32. Epub 2007 Jun 1. The acute toxicity and hatching success of four organophosphorus insecticides--acephate (ACEP), chlorpyrifos (CPP), monocrotophos (MCP), and profenofos (PF)--was studied in a short-term bioassay using brine shrimp, Artemia salina. The in vivo effect of these insecticides on acetylcholinesterase (Enzyme commission number (EC 3.1.1.7) activity was also determined in LC (50)-exposed nauplii after 24 hours. |
1(0,0,0,1) | 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. Log10I50 for AChE that determined the OP concentration causing 50% inhibition in AChE activity, correlated with EBOND and Charge-1 (Eq. (3)). |
1(0,0,0,1) | Details |
| 11681666 | Maklakov A, Ishaaya I, Freidberg A, Yawetz A, Horowitz AR, Yarom I: Toxicological studies of organophosphate and pyrethroid insecticides for controlling the fruit fly Dacus ciliatus (Diptera: Tephritidae). J Econ Entomol. 2001 Oct;94(5):1059-66. This was supported by the insignificant decrease of head acetylcholinesterase activity. |
1(0,0,0,1) | Details |
| 11020656 | Farag AT, Eweidah MH, El-Okazy AM: Reproductive toxicology of acephate in male mice. Reprod Toxicol. 2000 Sep-Oct;14(5):457-62. Brain and skeletal muscle acetylcholinesterase activity was inhibited only in this group. |
1(0,0,0,1) | Details |
| 12039681 | Singh AK: Acute effects of acephate and methamidophos and interleukin-1 on corticotropin-releasing factor (CRF) synthesis in and release from the hypothalamus in vitro. Comp Biochem Physiol C Toxicol Pharmacol. 2002 May;132(1):9-24. Acute effects of Ace, Meth and IL-1 on AChE activity, and CRF mRNA levels in, and CRF-release from the hypothalamus were studied in vitro. |
1(0,0,0,1) | Details |
| 16004201 | Fujikawa Y, Satoh T, Suganuma A, Suzuki S, Niikura Y, Yui S, Yamaura Y: Extremely sensitive biomarker of acute organophosphorus insecticide exposure. Hum Exp Toxicol. 2005 Jun;24(6):333-6. Thus, the single administration of EPN (O-ethyl O-p-nitrophenylphenylphosphonothioate), acephate and chlorpyrifos increased plasma BG activity in approximately 100-fold the control level in rats. The increase in plasma BG activity after OP exposure is a much more sensitive biomarker of acute OP exposure than acetylcholinesterase (AChE) inhibition. |
1(0,0,0,1) | Details |
| 9325279 | Watkins LM, Mahoney HJ, McCulloch JK, Raushel FM: Augmented hydrolysis of diisopropyl fluorophosphate in engineered mutants of phosphotriesterase. J Biol Chem. 1997 Oct 10;272(41):25596-601. The phosphotriesterase from Pseudomonas diminuta hydrolyzes a wide variety of organophosphate insecticides and acetylcholinesterase inhibitors. Kinetic constants were measured for all of the mutants with the substrates paraoxon, diethylphenylphosphate, acephate, and diisopropylfluorophosphate. |
1(0,0,0,1) | Details |
| 10333576 | Rufingier C, Pasteur N, Lagnel J, Martin C, Navajas M: Mechanisms of insecticide resistance in the aphid Nasonovia ribisnigri (Mosley) (Homoptera: Aphididae) from France. Insect Biochem Mol Biol. 1999 Apr;29(4):385-91. Resistance to pirimicarb was shown to be mainly due to a decreased sensitivity of the target acetylcholinesterase; this modification conferred also, resistance to propoxur but not to methomyl and the two tested organophosphates (acephate and paraoxon). |
0(0,0,0,0) | Details |