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)

The in vivo effect of dimethoate and deltamethrin on body and organ weights, serum proteins and on plasma acetylcholinesterase (AChE), aromatic esterase and ATPase were examined in growing male rabbits throughout five months period. Both compounds had no significant effect on body weight; however, adrenal, testis & pituitary weights decreased (P less than 0.01); the liver and spleen weights increased (P less than 0.01) in a dose dependent manner. Serum total proteins and globulin decreased (P less than 0.01) in a dose dependent trend, while serum albumin was not greatly affected. AChE activity was increased (P less than 0.01) after 1 month of treatment with the two doses of dimethoate and deltamethrin; thereafter, AChE activity showed 40% inhibition of the control level. The activity of aromatic esterase increased markedly after the first month, then declined gradually until the fifth month. High dose of dimethoate markedly inhibited this enzyme particularly after the 5th month of treatment. Both doses of deltamethrin increased ATPase activity after the first month of treatment, then the ATPase activity was normal. Dimethoate inhibited ATPase particularly at the end of treatment in a dose dependent manner.
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PMID:In vivo chronic effect of dimethoate and deltamethrin on rabbits. 297 91

Dimethoate, an organophosphorus insecticide, was the suspected cause of toxicosis in a group of young cattle grazing on pasture that had been sprayed 6 weeks before the onset of clinical signs. Affected animals had primarily nicotinic signs, such as muscle twitching, stiffness, weakness and paralysis, though muscarinic signs, such as diarrhea, salivation and pollakiuria, were also observed. Whole blood acetylcholinesterase activity was depressed in 3 animals. The atypical clinical syndrome and poor response to treatment with atropine and other anticholinergics may have been due to coexistent hypomagnesemia.
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PMID:Suspected dimethoate toxicity in cattle. 673 94

Technical dimethoate was administered orally to pregnant rats through day 6-20 of gestation at doses 3.75, 7.5, 15 and 30 mg/kg/day. Dose of 30 mg/kg/day produced high mortality rate in dams and was not considered for developmental toxicity evaluation. Dimethoate produced enzymatic changes in liver of dams associated with mild pathomorphological changes in liver and brain. Significant fetotoxic effects were not observed at the tested dose levels as evidenced by total number of implantations, percentage resorption, and live fetuses except reduction in fetal weight. Reduced acetylcholinesterase activity in fetal brain and placenta at higher dose levels indicated possible transmigration of dimethoate from dams to fetuses. The absence of anomalies in fetal gross, visceral morphology and skeleton suggests technical dimethoate as non teratogenic in rat at tested dose levels.
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PMID:Development effect of technical dimethoate in rats: maternal and fetal toxicity evaluation. 869 21

Chronic occupational exposure to organophosphorus and carbamate-type pesticides significantly inhibits acetylcholinesterase activity and causes morbidity. This study on mice was designed to evaluate their amino profile and to identify signs of hepatic dysfunction following their chronic exposure to mixtures of organophosphorus pesticides. Laboratory mice were exposed to a formulated mixture of the six organophosphorus pesticides (Dimethoate, Chlorpyrifos, Profenofos, Pirimiphos methyl, Triazophos and Dimethoate) most commonly used in agriculture in this region of the Middle East. Doses (10% of LD50 of the mixture) were given once a week by gavage in corn oil for 7 weeks; the control group was given only corn oil. At the end of the exposure period, mice were culled and blood samples were collected to determine erythrocyte acetylcholinesterase activity, biochemical markers of liver function and concentrations of serum amino acids. Erythrocyte acetylcholinesterase activity and total serum proteins decreased significantly in the exposed group. Serum concentrations of alanine aminotransferase and aspartate aminotransferase, alanine, glutamic acid, glycine, isoleucine, leucine, methionine, ornithine, proline, serine, threonine and valine were significantly increased in the exposed mice, while serum levels of cystine were decreased significantly. There were also non-significant increases in serum alkaline phosphatase, gama-glutamyl transpeptidase and some of the other amino acids. Chronic exposure to mixtures of organophosphorus pesticides is associated with decreased acetylcholinesterase activity, hepatic dysfunction and disturbance of amino acids profile. Biochemical indices of hepatocellular injury and disturbed amino acid metabolism may be of value as markers of chronic exposure to such pesticides.
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PMID:Hepatic injury and disturbed amino acid metabolism in mice following prolonged exposure to organophosphorus pesticides. 1002 66

Organophosphorus compounds may induce oxidative stress leading to generation of free radicals and alterations in antioxidant and scavengers of oxygen free radicals. The present study demonstrates effect of acute exposure of dimethoate in causation of oxidative stress in male Wistar rats. Dimethoate was administered orally at doses 45, 75 and 90 mg/kg of body weight on the basis of LD(50) for 24 h. After administration of doses, the liver and brain homogenates were analyzed for various parameters of oxidative stress. The results indicated an increase in hepatic cytochrome P450, lipid peroxidation, catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase in liver and brain at 90 and 75 mg/kg doses. There were no significant changes in the levels of glucose-6-phosphate dehydrogenase activity in both liver and brain. Similarly, there were no significant changes in hepatic glutathione and glutathione-S-transferase activities. However, there was a significant increase in glutathione and glutathione-S-transferase in brain at 90 mg/kg dose only. Erythrocyte acetylcholinesterase was inhibited at all doses used. Dose-dependent histopathological changes, observed in both liver and brain, are also described.
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PMID:Effects of acute dimethoate administration on antioxidant status of liver and brain of experimental rats. 1559 Jan 8

Dimethoate, an organophosphate pesticide, is used in controlling the pests of a variety of crops. The study was carried out to understand the role of dimethoate in inducing oxidative stress leading to generation of free radicals and alterations in antioxidant enzymes and scavengers of oxygen free radicals. The effects of subchronic exposure of dimethoate in the production of oxidative stress were evaluated in male Wistar rats in the present study. Dimethoate was administered orally at doses 0.6, 6, and 30 mg/kg for 30 days in these rats. The results indicated an increase in levels of hepatic Cytochrome P450, lipid peroxidation, catalase, superoxide dismutase, glutathione peroxidase and glutathione reductase in liver and brain at doses 6 and 30 mg/kg. There were no significant changes in the level of glucose-6-phosphate dehydrogenase activity except in liver at 30 mg/kg. A decrease in glutathione was observed at 30 and 6 mg/kg in both liver and brain. Glutathione-S-transferase increased at 30 and 6 mg/kg in liver and 30 mg/kg in brain. Erythrocyte acetylcholinesterase was inhibited at 30 and 6 mg/kg doses. Dose-dependent histopathological changes were seen in both liver and brain. This study concludes that oxidative stress due to dimethoate may be ascribed to induction of Cytochrome P450, inhibition of AChE and disturbance in activities of GSH and GST enzymes causing lipid peroxidation and histological and electron microscopic changes in liver and brain.
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PMID:Dimethoate-induced effects on antioxidant status of liver and brain of rats following subchronic exposure. 1611 89

The study was aimed at determining the dimethoate residues in the liver and acetylcholinesterase (AChE) activity in blood of rats exposed to dimethoate (individual intoxication), and dimethoate and pyrantel embonate (simultaneous intoxication). The experiment was carried out in two stages where various doses of preparations and exposure manners were used. In the first stage of the experiment, dimethoate (1/25 LD50) was administered to animals per os for 28 days, and pyrantel embonate (1/2 LD550) twice, i.e. on the day 14th and 28th. In the second stage, dimethoate was administered for 5 days (1/10 LD50), and pyrantel embonate (1/5 LD50) on day 3, 4 and 5 from the beginning of dimethoate intoxication. The short presence of the dimethoate residues in the liver of the animals examined was found until the 2nd day after 28-day intoxication (1/25 LD50) and until 14th day after 5-day intoxication (1/10 LD50), however, a distinct decrease in this insecticide residues in the liver of (analysed groups of) rats occurred between the 3rd hour and the 2nd day after exposure. Dimethoate in both applied doses significantly reduced AChE activity in blood. After application of the higher dose, the inhibition of AChE was more pronounced, and the return of its activity to physiological values lasted considerably longer. Co-administration of pyrantel embonate and dimethoate, slightly influenced changes of the parameters analysed, which have been dependent not only on a dose and manner of pyrantel application but also on time which lapsed from exposure.
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PMID:Residues of dimethoate in the liver and AchE activity in blood of rats after exposure to dimethoate, and dimethoate and pyrantel embonate. 1657 74

The effect of organophosphate insecticide dimethoate at three dosage levels (7, 15, and 28 mg/kg/day) on male reproduction in mice was studied. Dimethoate was given orally by gavage to male mice for 20 days before mating with untreated females. Signs of cholinergic effects were observed in the 15 and 28 mg/kg/day treated groups. Brain and skeletal muscle acetylcholinesterase activities were inhibited in both the middle and high dose groups. Dimethoate was associated with a decreased number of implantations and live fetuses, and an increased number of dead and early resorptions at 28 mg/kg/day treated group. The percent morphologically normal spermatozoa were unaffected in any of dose groups. However, sperm production and percent motile sperm were decreased in the 15 and 28 mg/kg/day treated groups compared to the control. Histological changes in testis were observed in the middle and high treated groups. The current study demonstrated the adverse effects of dimethoate on the reproductive performance of male mice and pregnancy outcomes following mating with untreated female mice at dose levels of 15 and 28 mg/kg/day. The No Observed Effect Level (NOEL) in the present study for reproductive performance was 7 mg/kg/day.
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PMID:Assessment of reproductive toxicity of orally administered technical dimethoate in male mice. 1723 81

Dimethoate is an organophosphorus insecticide and acaricide used for the control of a wide range of insects, including houseflies and mites, on a variety of fruits, vegetables, field and forestry crops. The aim of the current study was to evaluate the subchronic toxicity of orally administered dimethoate in Wistar albino rats, based on the histopathological and biochemical findings in the liver. The animals of the exposed groups were fed with laboratory chow combined with 2, 8 or 20 mg/kg body weight/day dimethoate for 90 consecutive days under controlled laboratory conditions. At the end of the experiment, body weight gain, absolute and relative liver weights, liver cholinesterase activities and total protein levels were determined. Histopathological changes in the liver were also determined using a light microscope. Results showed that there were decreases in relative liver weights of exposed rats. Although liver total protein levels were significantly increased, liver cholinesterase activities were decreased in all exposed groups. Dimethoate caused dose-related histopathological changes such as mononuclear cell infiltration, congestion, an enlargement of the veins and sinusoids, hepatocellular damage, necrotic changes, an increase in the number of Kupffer cells, cytoplasmic vacuolization and degeneration in nuclei in the liver of exposed rats. These effects did not vary between the sexes.
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PMID:Dimethoate-induced biochemical and histopathological changes in the liver of rats. 1786 94

Dimethoate (DIM) is an organophosphorothionate (OPT) pesticide used worldwide as a systemic insecticide and acaricide. It is characterized by low-to-moderate acute mammalian toxicity; similarly to the other OPT pesticides, its mode of action is mediated by the inhibition of acetylcholinesterase (AChE), exerted by its toxic metabolite dimethoate-oxon or omethoate (OME), which is also used as a direct acting pesticide. Human hepatic DIM bioactivation to the toxic metabolite OME has been characterized by using c-DNA expressed human CYPs and human liver microsomes (HLM) also in the presence of CYP-specific chemical inhibitors, with a method based on AChE inhibition. The obtained kinetic parameters and AChE IC(50) have been compared with those previously obtained with other OPTs, indicating a lower efficiency in DIM desulfuration reaction and a lower potency in inhibiting AChE. Results showed that, similarly to the other OPTs tested so far, at low DIM concentration OME formation is mainly catalysed by CYP1A2, while the role of 3A4 is relevant at high DIM levels. Differently from the other OPTs, DIM desulfuration reaction showed an atypical kinetic profile, likely due to CYP3A4 autoactivation. The sigmoidicity degree of the activity curve increased with the level of CYP3A4 in HLM or disappeared in the presence of a CYP3A4 chemical inhibitor. This atypical kinetic behaviour can be considered one of the possible explanations for the recent findings that among patients hospitalized following OPT intoxication, DIM ingestion gave different symptoms and more severe poisoning (23.1% of fatal cases versus total) than chlorpyrifos (8% of deaths), which has a lower LD(50) value. Since DIM-poisoned patients poorly responded to pralidoxime, the possibility to use CYP3A4 inhibitors could be considered as a complementary treatment.
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PMID:Evidences for CYP3A4 autoactivation in the desulfuration of dimethoate by the human liver. 1789 69


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