Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Methidathion applied to cattle as a pour-on insecticide for control of lice (predominantly Linognathus vituli, but also Haematopinus eurysternus and Damalinia bovis) caused a reduction in the lice population of approximately 98% to 99% in laboratory trials at the minimum recommended dose of 4 mg/kg and a 98.8% to 100% efficiency was achieved in field trials. In a comparative efficiency trial in the laboratory methidathion at 3.5 to 5 mg/kg reduced the lice population by 98.8% to 99%, fenthion by 98.5% at 4.5 mg/kg and famphur by 99.7% at 16.5 mg/kg. Methidathion was tolerated by calves aged 15 to 20 weeks at dose rates up to 40 mg/kg indicating an approximate 7 fold safety margin, but 1 of 4 calves treated at 50 mg/kg died following treatment. Treatment with fenthion at 50 mg/kg, 7.4 times the average recommended rate, famphur at 75 mg/kg, 3 times the average rate and chlorpyrifos at 85 mg/kg, 5 times average rate, caused reductions in whole blood cholinesterase activity of 52%, 27% and 47% respectively which were similar to the reductions in cholinesterase activity found in calves treated with methidathion at similar levels above the recommended commercial dose rates. It was found that 2 day old calves were more sensitive to treatment with methidathion than calves 9 or 16 days old. A further 11,900 cattle of varying age, breed and sex were treated with methidathion under field conditions at the recommended rate of 4 to 8 mg/kg, and 534 cattle were treated at 24 mg/kg without any signs of toxicity.
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PMID:Efficiency and safety of methidathion applied as a pour-on systemic insecticide for control of cattle lice. 9 59

The carcinogen potential of methidathion, a dimethoxyorganic phosphorus pesticide and cholinesterase inhibitor, was evaluated by the Health Effects Division of the Office of Pesticide Programs using a consensus peer review process and the EPA's guidelines for risk assessment. Methidathion was categorized as a Group C (possible human) carcinogen based upon evidence of an increased incidence of benign and malignant hepatocellular tumors, alone and in combination, in a single study involving male Chr-CD-1 mice. The compound was not carcinogenic in female Chr-CD-1 mice in the same study or in Sprague-Dawley rats of either sex in a second study. Methidathion was not genotoxic in a variety of in vitro or in vivo tests designed to detect DNA damage, chromosome aberrations, gene mutations, and sister chromatid exchange. Although methidathion was identified as being structurally similar to two other organophosphate insecticides, prothidathion and lythidathion, no toxicological data were available on either of these agents for comparative purposes. The biological information on methidathion was reviewed by the agency's FIFRA Scientific Advisory Panel who agreed with the category C designation for methidathion. The data were not found to be sufficient to quantify human risk to methidathion.
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PMID:Evaluation of the carcinogenic potential of pesticides. 2. Methidathion. 225 53

Methidathion (MD) [ O, O-dimethyl S-(2,3-dihydro-5-methoxy-2-oxo-1,3,4-thiadiazol-3-ylmethyl) phosphorodithioate] is one of the most widely used organophosphate insecticides (OPIs) in agriculture and public health programmes. We have, therefore, examined the in vivo and in vitro effects of MD on the serum activities of cholinesterase (ChE), enzymes concerning liver damage and lipid peroxidation (LPO; only in vivo), and have evaluated the ameliorating effects of a combination of vitamins E and C against MD toxicity. The in vivo experimental groups were: control group, MD-treated group (MD), and a group treated with MD plus vitamin E plus vitamin C (MD+Vit). The MD and MD+Vit groups were treated orally with a single dose of 8 mg MD/kg body weight at 0 h. Vitamin E and vitamin C were injected at doses of 150 mg/kg body weight i.m. and 200 mg/kg body weight i.p., respectively, 30 min after the treatment with MD in the MD+Vit group. Blood samples were taken 24 h after the MD administration. For in vitro study, venous blood samples were obtained from volunteers, and serum recovered. The activities of serum enzymes were determined in each sample and these served as 0 h values. Each sample was divided into four portions, each of which served as one of the experimental groups, as follows: control group, vitamin E plus vitamin C group (Vit), MD-treated group (MD) and MD plus vitamin E plus vitamin C group (MD+Vit). Vitamin E and vitamin C were added at doses of 7.5 and 10 micro g/ml, respectively, into the Vit and MD+Vit groups. MD was added at doses of 0.4 mg/ml into the MD and MD+Vit groups. The activities of serum enzymes were determined in each sample at 24 h. The results of the in vivo experiment demonstrated that thiobarbituric acid reactive substances were increased in the MD group compared with the control group, and decreased in the MD+Vit group compared with MD group. ChE activity was decreased in both MD and MD+Vit groups compared with controls and increased in the MD+Vit group compared with the MD group. The activities of aspartate aminotransferase (AST), alkaline phosphatase (ALP), gamma-glutamyltransferase (GGT) and lactate dehydrogenase (LDH) were increased in both the MD and MD+Vit groups compared with the control group. AST activity was decreased in MD+Vit group compared with the MD group. Alanine aminotransferase (ALT) activity was decreased in both the MD and MD+Vit groups compared with control group. The results of in vitro experiment showed that all enzyme activities remained unchanged in both the control and Vit groups compared with values at 0 h. The activities of ChE, ALT and LDH were decreased in both the MD and MD+Vit groups compared with 0 h values. There was no significant difference between the MD and MD+Vit groups. The activities of AST, ALP and GGT remained unchanged in all groups. From these results, it can be concluded that MD caused liver damage, and LPO may be one of the molecular mechanisms involved in MD-induced toxicity. Single-dose treatment with a combination of vitamins E and C after the administration of MD can reduce LPO caused by MD.
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PMID:The effects of methidathion on lipid peroxidation and some liver enzymes: role of vitamins E and C. 1218 16

Methidathion (MD) phosphorodithioic acid S-[(5-methoxy-2-oxo-1,3,4-thiadiazol-3(2H)-yl)methyl] O,O-dimethyl ester is the organophosphate insecticide (OPI) most commonly used worldwide in the pest control of crops. Subchronic MD exposure was evaluated for its effects on lipid peroxidation, the serum activities of cholinesterase (ChE), and enzymes concerning liver damage, and the protective effects of combination of vitamins E and C in albino rats. Additionally, the histopathological changes in liver tissue were examined. Experimental groups were as follows: control group; a group treated with 5 mg/kg body weight MD (MD group); and a group treated with 5 mg/kg body wight MD plus vitamin E plus vitamin C (MD+AO group). The MD and MD+AO groups were treated orally with MD on five days a week for 4 weeks. The serum activities of cholinesterase (ChE), alanine transferase (ALT), aspartate amiotransferase (AST), lactate dehydrogenase (LDH), gamma-glutamyltransferase (GGT), alkaline phosphatase (ALP), and the concentration of malondialdehyde (MDA) and liver histopathology were studied. In serum samples, MD significantly increased MDA concentration and ALP, AST, GGT, LDH activities but decreased the ALT and ChE activities. In the MD+AO group, MDA level and ALP, AST, LDH activities were significantly decreased and ChE activity was increased compared to the MD group. Histopathological changes found in liver tissue of rats treated with MD included were infiltration with mononuclear cells in all portal areas, sinusoidal dilatation, and focal microvesicular steatosis and hydropic degenerations in parenchymal tissue. The severity of these lesions was reduced by administration of vitamins. From these results, it can be concluded that subchronic MD causes liver damage, and lipid peroxidation may be a molecular mechanism involved in MD-induced toxicity. Furthermore, the combination of vitamins E and C can reduce the toxic effects of MD on liver tissue of rats.
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PMID:The effects of subchronic methidathion toxicity on rat liver: role of antioxidant vitamins C and E. 1658 3