Protein Information

Name Acetylcholinesterase
Synonyms ACHE; ACHE protein; AChE; ARACHE; AcChoEase; Acetylcholine acetylhydrolase; Acetylcholinesterase; Acetylcholinesterase isoform E4 E6 variant…

Compound Information

Name fenthion
CAS

Reference List

PubMed Abstract RScore(About this table)
18344014 Jayasundara VK, Pathiratne A: Effect of repeated application of fenthion as a mosquito larvicide on Nile tilapia (Oreochromis niloticus) inhabiting selected water canals in Sri Lanka. Bull Environ Contam Toxicol. 2008 Apr;80(4):374-7. Epub 2008 Mar 16.

With three spray applications of fenthion to the study sites at weekly intervals at the concentration recommended for mosquito control, condition factor and brain acetylcholinesterase activity of the fish were depressed in a time dependent manner.
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17017223 Cui F, Raymond M, Berthomieu A, Alout H, Weill M, Qiao CL: Recent emergence of insensitive acetylcholinesterase in Chinese populations of the mosquito Culex pipiens (Diptera: Culicidae). J Med Entomol. 2006 Sep;43(5):878-83.

Bioassays performed with a purified G119S strain indicated that this substitution was associated with high levels of resistance to chlorpyrifos, fenitrothion, malathion, and parathion, but low levels of resistance to dichlorvos, trichlorfon, and fenthion.
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11884237 Quistad GB, Sparks SE, Segall Y, Nomura DK, Casida JE: Selective inhibitors of fatty acid amide hydrolase relative to neuropathy target esterase and acetylcholinesterase: toxicological implications. Toxicol Appl Pharmacol. 2002 Feb 15;179(1):57-63.

These FAAH-selective compounds include tribufos and (R)-octylbenzodioxaphosphorin oxide with delayed neurotoxic effects in mice and hens plus several organophosphorus pesticides (e.g., fenthion) implicated as delayed neurotoxicants in humans.
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2147549 Bai CL, Qiao CB, Zhang WD, Chen YL, Qu SX: A study of the pesticide fenthion: toxicity, mutagenicity, and influence on tissue enzymes. Biomed Environ Sci. 1990 Sep;3(3):262-75.

Histochemical changes in enzyme activities (including AChE, ATPase, and AKP) in tissues were observed.
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19479785 Uner N, Sevgiler Y, Piner P: Tissue-specific in vivo inhibition of cholinesterases by the organophosphate fenthion in Oreochromis niloticus. Environ Toxicol. 2009 May 28.

AChE and BChE activities were determined spectrophotometrically.
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985225 Stone BF, Wilson JT, Youlton NJ: Linkage and dominance characteristics of genes for resistance to organophosphorus acaricides and allelic inheritance of decreased brain cholinesterase activity in three strains of the cattle tick, Boophilus microplus. Aust J Biol Sci. 1976 Jul;29(3):251-63.

A very similar mode of inheritance of fenthion resistance in strain B has now been demonstrated with no departure in degree of dominance of resistance from the mean value of +0-57 common to these strains exposed to these chemicals.
F1 adult progeny of B x M and R x M crossings exhibited the incompletely recessive mutant-type decreased brain acetylcholinesterase (AChE) activity common to strains B, M and R, thus satisfying the test for allelism.
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18240518 Rodriguez MM, Bisset JA, Fernandez D: Levels of insecticide resistance and resistance mechanisms in Aedes aegypti from some Latin American countries. J Am Mosq Control Assoc. 2007 Dec;23(4):420-9.

Biochemical tests showed high frequencies of esterase and glutathione-S-transferase activity; however, the frequency of altered acetylcholinesterase mechanism was low.
Eight Latin American strains of Aedes aegypti were evaluated for resistance to 6 organophosphates (temephos, malathion, fenthion, pirimiphos-methyl, fenitrothion, and chlorpirifos) and 4 pyrethroids (deltamethrin, lambdacyhalothrin, betacypermethrin, and cyfluthrin) under laboratory conditions.
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1645823 De Wilde V, Vogelaers D, Colardyn F, Vanderstraeten G, Van den Neucker K, De Bleecker J, De Reuck J, Van den Heede M: Postsynaptic neuromuscular dysfunction in organophosphate induced intermediate syndrome. Klin Wochenschr. 1991 Feb 26;69(4):177-83.

A 65-year-old Caucasian female developed an intermediate syndrome seven days after an acute cholinergic crisis, caused by the ingestion of fenthion.
It is hypothesized that the pathophysiologic process underlying the syndrome is the result of a time-confined phenomenon, which includes both changes in the postsynaptic structures by a desensitization process and a gradually restoring ratio of acetylcholine to acetylcholinesterase.
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8723267 Wirth MC, Georghiou GP: Organophosphate resistance in Culex pipiens from Cyprus. J Am Mosq Control Assoc. 1996 Mar;12(1):112-8.

All population samples generally revealed organophosphate resistance to malathion, temephos, chlorpyrifos, fenthion, dichlorvos, and pirimiphos methyl, in decreasing order of magnitude.
Resistance was associated with the presence of 5 different overproduced esterases (esterases A1, A2, A5, B2, and B5) as well as an insensitive form of acetylcholinesterase.
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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.
We also discuss case reports where neuropathies were not convincingly attributed to fenthion, malathion, omethoate/dimethoate, parathion and merphos.
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11097804 Kim YA, Lee HS, Park YC, Lee YT: A convenient method for oxidation of organophosphorus pesticides in organic solvents. Environ Res. 2000 Nov;84(3):303-9.

All reactions gave the respective oxons as single major product, except that of fenthion, which gave two major products, the respective oxon and another product from further oxidation of the oxon.
The inhibitory power of the pesticides on acetylcholinesterase before and after oxidation was measured and, for all pesticides tested, the power after oxidation was much higher than that before oxidation.
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19444991 Uner N, Sevgiler Y, Durmaz H, Piner P, Cinkiloglu E: N-Acetylcysteine provides dose-dependent protection against fenthion toxicity in the brain of Cyprinus carpio L. Comp Biochem Physiol C Toxicol Pharmacol. 2009 Jul;150(1):33-8.

Enzymes that constitute the first line antioxidant defence, namely SOD and CAT, GSH-related enzymes, GR and GST, together with AChE activities were also determined spectrophotometrically.
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10509433 Tuler SM, Bowen JM: Chronic fenthion toxicity in laying hens. Vet Hum Toxicol. 1999 Oct;41(5):302-7.

Inhibition of serum cholinesterase and brain acetylcholinesterase was greater in the high-dose hens.
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3983971 Misra UK, Nag D, Bhushan V, Ray PK: Clinical and biochemical changes in chronically exposed organophosphate workers. Toxicol Lett. 1985 Feb-Mar;24(2-3):187-93.

Health effects of occupational organophosphate exposure were investigated by subjecting 22 workers chronically exposed to an organophosphate pesticide, fenthion (O,O-dimethyl-O-(4-methylmercapto-3-methylphenyl)-phosphorothioate) to clinical evaluation, estimation of serum cholinesterase, serum alkaline phosphatase (SAP), serum glutamic oxaloacetic transaminase (SGOT) and serum glutamic pyruvic transaminase (SGPT).
Serum acetylcholinesterase and butyrylcholinesterase levels were significantly lower than in controls.
1(0,0,0,1) Details
2612780 Tuler SM, Hazen AA, Bowen JM: Release and metabolism of dopamine in a clonal line of pheochromocytoma (PC12) cells exposed to fenthion. Fundam Appl Toxicol. 1989 Oct;13(3):484-92.

In the first study, cultures were treated with 10 (-5) or 10 (-6) M FEN or 10 (-5) M neostigmine, a non-OP acetylcholinesterase inhibitor.
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8082605 Misra UK, Prasad M, Pandey CM: A study of cognitive functions and event related potentials following organophosphate exposure. Electromyogr Clin Neurophysiol. 1994 Jun;34(4):197-203.

To study the cognitive changes following chronic occupational exposure to organophosphate (OP) pesticides, a clinical and neurophysiological study was performed on 31 workers engaged in spraying fenthion, an OP pesticide.
Serum AChE level was 27% less in the exposed group compared to the controls.
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17110060 Buratti FM, Leoni C, Testai E: Foetal and adult human CYP3A isoforms in the bioactivation of organophosphorothionate insecticides. Toxicol Lett. 2006 Dec 15;167(3):245-55. Epub 2006 Oct 24.


Since OPT-induced neurodevelopmental effects may be due to in situ bioactivation by foetal enzymes, the catalytic activity of the foetal CYP3A7 toward chlorpyrifos (CPF), parathion (PAR), malathion (MAL) and fenthion (FEN) has been assessed by using recombinant enzymes.
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17253727 Gadepalli RS, Rimoldi JM, Fronczek FR, Nillos M, Gan J, Deng X, Rodriguez-Fuentes G, Schlenk D: Synthesis of fenthion sulfoxide and fenoxon sulfoxide enantiomers: effect of sulfur chirality on acetylcholinesterase activity. Chem Res Toxicol. 2007 Feb;20(2):257-62. Epub 2007 Jan 25.
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17024560 Wijeyaratne WM, Pathiratne A: Acetylcholinesterase inhibition and gill lesions in Rasbora caverii, an indigenous fish inhabiting rice field associated waterbodies in Sri Lanka. Ecotoxicology. 2006 Oct;15(7):609-19. Epub 2006 Oct 6.

Laboratory studies showed that prior exposure of R. caverii to Paraquat (2 microg l (-1), 7 days) enhanced the extent of inhibition of brain AChE activity induced by Fenthion (3 microg l (-1)) or a mixture of Fenthion (3 microg l (-1)) and Phenthoate (5 microg l (-1)).
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14976351 Furnes B, Schlenk D: Evaluation of xenobiotic N- and S-oxidation by variant flavin-containing monooxygenase 1 (FMO1) enzymes. Toxicol Sci. 2004 Apr;78(2):196-203. Epub 2004 Feb 19.

Racemic fenthion sulfoxide was a weaker inhibitor of acetylcholinesterase than its parent compound (IC (50) 0.26 and 0.015 mM, respectively).
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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.
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7576821 Senanayake N, Sanmuganathan PS: Extrapyramidal manifestations complicating organophosphorus insecticide poisoning. Hum Exp Toxicol. 1995 Jul;14(7):600-4.

Inhibition of AChE by fenthion, which has ready access to central neurons on account of its lipid solubility, is postulated as the mechanism underlying the extrapyramidal manifestations.
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16243090 Eddleston M, Eyer P, Worek F, Mohamed F, Senarathna L, von Meyer L, Juszczak E, Hittarage A, Azhar S, Dissanayake W, Sheriff MH, Szinicz L, Dawson AH, Buckley NA: Differences between organophosphorus insecticides in human self-poisoning: a prospective cohort study. Lancet. 2005 Oct 22-28;366(9495):1452-9.

Acetylcholinesterase inhibited by fenthion or dimethoate responded poorly to pralidoxime treatment compared with chlorpyrifos-inhibited acetylcholinesterase.
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2773698 Hayakawa S, Hiramoto D, Sekiya H: [Inhibition of acetylcholinesterase at pupil-related central nuclei by organophosphorus pesticide (fenthion)--an experimental study]. Nippon Ganka Gakkai Zasshi. 1989 Feb;93(2):167-73.
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7991222 De Bleecker J, Van den Abeele K, De Reuck J: Electromyography in relation to end-plate acetylcholinesterase in rats poisoned by different organophosphates. Neurotoxicology. 1994 Summer;15(2):331-40.

Paraoxon is acutely toxic, whereas fenthion produces more sustained AChE inhibition.
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2439699 Farage-Elawar M, Francis BM: Acute and delayed effects of fenthion in young chicks. J Toxicol Environ Health. 1987;21(4):455-69.

The effects of desbromoleptophos, fenitrothion, and fenthion on brain acetylcholinesterase (AChE), brain neurotoxic esterase (NTE), and walking were investigated in immature chicks, below the age of organophosphorus ester-induced delayed neurotoxicity (OPIDN).
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2453943 Farage-Elawar M, Francis BM: Effects of fenthion, fenitrothion and desbromoleptophos on gait, acetylcholinesterase, and neurotoxic esterase in young chicks after in ovo exposure. Toxicology. 1988 May;49(2-3):253-61.
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10321902 Barber D, Correll L, Ehrich M: Comparative effectiveness of organophosphorus protoxicant activating systems in neuroblastoma cells and brain homogenates. J Toxicol Environ Health A. 1999 May 14;57(1):63-74.

The ability of bromine and rat liver microsomes (RLM) to convert organophosphorus (OP) protoxicants to esterase inhibitors was determined by measuring acetylcholinesterase (AChE) and neuropathy target esterase (NTE) inhibition.
OP protoxicants examined included tri-o-tolyl phosphate (TOTP), O-ethyl O-p-nitrophenyl phenylphosphonothioate (EPN), leptophos, fenitrothion, fenthion, and malathion.
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2385836 Veronesi B, Jones K, Pope C: The neurotoxicity of subchronic acetylcholinesterase (AChE) inhibition in rat hippocampus. Toxicol Appl Pharmacol. 1990 Jul;104(3):440-56.

The neurotoxic effects of long-term, low-level exposure to the commercially available insecticide, Fenthion, were examined in the present study.
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2449534 Farage-Elawar M, Francis BM: Effects of multiple dosing of fenthion, fenitrothion, and desbromoleptophos in young chicks. J Toxicol Environ Health. 1988;23(2):217-28.

The effects of multiple doses of desbromoleptophos, fenitrothion, and pure fenthion on brain acetylcholinesterase (AChE), brain neurotoxic esterase (NTE), and walking were investigated in immature chicks, below the age of sensitivity to organophosphorus ester-induced delayed neurotoxicity (OPIDN).
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17454383 Somerset VS, Klink MJ, Baker PG, Iwuoha EI: Acetylcholinesterase-polyaniline biosensor investigation of organophosphate pesticides in selected organic solvents. J Environ Sci Health B. 2007 Mar-Apr;42(3):297-304.

Detection limits in the order of 0.147 ppb for diazinon and 0.172 ppb for fenthion in acetone-saline phosphate buffer solution, and 0.180 ppb for diazinon and 0.194 ppb for fenthion in ethanol-saline phosphate buffer solution has been achieved.
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11743808 Pardio VT, Ibarra N, Rodriguez MA, Waliszewski KN: Use of cholinesterase activity in monitoring organophosphate pesticide exposure of cattle produced in tropical areas. J Agric Food Chem. 2001 Dec;49(12):6057-62.

The mean baseline acetylcholinesterase activities of 9.549 +/- 3.619 IU/mL in whole blood, 9.444 +/- 3.006 IU/mL in erythrocytes, and 0.149 +/- 0.063 IU/mL in plasma were estimated for steers from the control group.
Results of multivariate analysis showed that the general responses between the control and experimental groups (in vivo, monitoring and case studies) treated with Coumaphos and Fenthion were statistically different, and the general responses of these experimental groups were statistically different over time as well.
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