Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Chlorpromazine, an antipsychotic drug is found to inhibit Na+K(+)-ATPase, Ca(2+)-ATPase and acetylcholinesterase activities in the microsomal membranes of rat in vivo, when the drug is injected for certain periods of time. The inhibition seems to be due to the changes in fatty acid composition of lipid and microviscosity of the membranes. However, once the drug has been withdrawn, the enzyme activities are found to return to the normal level in three to five weeks, suggesting that the drug effect is reversible.
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PMID:The in vivo inhibition of transport enzyme activities in different organs of rat by chlorpromazine is reversible. 166 11

Mite infestation in laboratory mice is a common, but troublesome problem in animal facilities. Recommended treatment regimens are frequently ineffective because of the short period of exposure to the control agent. In an effort to develop a time-release approach, we have investigated the use of Dursban granules applied in animal bedding. Initial toxicity studies indicated that this pesticide can be added to shoebox cage litter at levels three times that used for outdoor application (6 g per 27 by 48 cm shoebox cage) without producing clinical signs of toxicity. Metabolism studies demonstrated that although individual mice showed decreased brain acetylcholinesterase activity following treatment, liver cytosolic glutathione-S-transferase, liver microsomal aminopyrine N-demethylase, or aryl hydrocarbon hydroxylase were not induced after 1 week of exposure. Parasitological studies indicated elimination of mites and itching in an experimental infestation, as well as reduction of itching in severely symptomatic, naturally infested mice, following treatment with the granules. These studies demonstrate the nontoxic efficacy of Dursban in the control of Myobia musculi.
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PMID:The efficacy and safety of chlorpyrifos (Dursban) for control of Myobia musculi infestation in mice. 171 72

Previous studies have shown that a single oral pretreatment of rats with the organophosphorus insecticide 2-chloro-1-(2,4-dichlorophenyl)vinyl diethyl phosphate (chlorfenvinphos, CVP) afforded protection against the toxicity of a subsequent challenge with the same compound within 24 hr. This protection may be due to the reduction in brain cholinesterase inhibition caused by the decrease in plasma CVP concentration. The purpose of this study was to investigate the mechanism of the decrease in plasma CVP concentration in relation to metabolic induction. CVP was preferentially metabolized by a liver microsomal fraction with an NADPH-generating system, compared with serum or kidney subcellular fractions. A single oral 24-hr pretreatment with CVP (15 mg/kg) increased the oral LD50 of its next dosage to threefold. The same treatment also increased CVP metabolism (to 178%), cytochrome P450 content (to 130%), cytochrome P450 reductase activity (to 130%), cytochrome b5 content (to 121%), and cytochrome P450-linked activities such as aminopyrine demethylase (to 140%) and aniline hydroxylase (to 127%) in the hepatic microsomal fraction. A single oral 24-hr pretreatment of phenobarbital (50 mg/kg), which is known as an inducer of cytochrome P450, increased the oral LD50 of CVP and all the related metabolic parameters listed above in an order of magnitude similar to that of CVP, although the increments induced by the phenobarbital treatment were greater than those induced by the CVP treatment. These results indicate that the increase in hepatic CVP metabolism may be due to the induction of the hepatic cytochrome P450 system caused by the single oral short-term treatment with CVP. This induction may be one of the reasons for the decrease in plasma CVP concentration which may be responsible for the reduction in toxicity of its next dosage.
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PMID:Metabolic induction of the hepatic cytochrome P450 system by chlorfenvinphos in rats. 176 23

The in vivo and in vitro fate of [14C]carbaryl was compared in adult male and female house flies from an insecticide-susceptible (S) strain and a resistant (R) strain with multiple resistance to different classes of insecticides. Cuticular penetration of topically applied carbaryl (0.01 microgram/insect) was very rapid and rates were essentially the same among males and females of both strains. Rates of penetration were dramatically reduced as the concentration of applied carbaryl was increased over a range of 0.01-5.0 micrograms/insect. In vivo and in vitro tests demonstrated that the R strain had an enhanced capability for the metabolic degradation of carbaryl. In evaluations of topical toxicity and in vitro metabolic degradation, coadministration of the metabolic synergists piperonyl butoxide (a microsomal oxidase inhibitor) and S,S,S-tributyl phosphorothioate (DEF, an esterase inhibitor) with carbaryl provided conclusive evidence that microsomal oxidases were the major factor in enhanced metabolism and that hydrolytic enzymes had only a minor effect. Studies of the in vitro inhibition of acetylcholinesterase (AChE) activity by carbaryl demonstrated that there was no difference between males and females of a given strain and that the R strain AChE was considerably less sensitive to inhibition. These tests also indicated that homogenates of brains from the R strain contained more than one form of AChE with different sensitivities to the inhibitor. This information and results of toxicity tests with other insecticides suggest that the R strain is not homozygous in its resistance to carbaryl.
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PMID:Interactions of carbaryl with susceptible and multiresistant house flies (Diptera: Muscidae). 184 92

The joint neurotoxic action of simultaneous exposure to vapors of n-hexane and methyl iso-butyl ketone (MiBK) and dermally applied O-ethyl O-nitrophenyl phenylphosphonothioate (EPN) was studied in groups of five adult hens. Four groups of hens were concurrently exposed to a dermal 2.5 mg/kg of EPN, 1000 ppm of n-hexane and 100, 250, 500 or 1000 ppm of MiBK. Two groups were each exposed to binary mixtures of a dermal dose of 2.5 mg/kg of EPN and 250 ppm of MiBK or 1000 ppm of n-hexane. Another three groups of hens were exposed to either 250 ppm of MiBK, 1000 ppm of n-hexane or a dermal dose of 2.5 mg/kg of EPN. A Group of hens was kept untreated. All hens were terminated after 30 days of treatment. Hens exposed to MiBK or n-hexane vapor did not exhibit any toxicity signs. In contrast, hens treated with EPN alone or in combination with n-hexane and/or MiBK developed acute cholinergic and delayed neurotoxicity signs. Hen brain acetylcholinesterase and neurotoxic esterase activities were inhibited in hens treated concurrently with EPN, n-hexane and MiBK. MiBK alone or in combination with EPN and n-hexane induced liver microsomal cytochrome P-450 content and phenobarbital-inducible cytochrome P-450 enzyme activities. Microsomes from hens treated with EPN, n-hexane, MiBK or mixtures of EPN, n-hexane and MiBK significantly enhanced the biotransformation of EPN to the more neurotoxic oxidation metabolite O-ethyl O-4-nitrophenyl phenylphosphonate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms of joint neurotoxicity of n-hexane, methyl isobutyl ketone and O-ethyl O-4-nitrophenyl phenylphosphonothioate in hens. 201 92

A number of morphological and functional changes on liver cells were reported during experimental cholestasis. Some specific metabolic pathways catalyzed by "membrane bound" enzymes were described to be altered by lipid microenvironment changes. The purpose of he present study is to establish Bilirubin UDP-Glucuronyltransferase activity--a microsomal integral enzyme responsible for bilirubin conjugation--and microsomal phospholipid profile in cholestatic and normal patients. Surgical liver biopsies were taken fron five patients suffering prolonged extrahepatic cholestasis, and five patients submitted to abdominal surgery excluding hepato-biliary diseases that were considered as controls. The following biochemical parameters were determined in both groups: bilirubin concentration, alkaline phosphatase, gamma-glutamyltranspeptidase, oxalacetic and pyruvic transaminases, and pseudo-cholinesterase activities. Serum cholestatic markers showed significative increments in cholestatic patients (Table 1). Total Bilirubin UDP-Glucuronyltransferase activity was similar comparing normal and cholestatic individuals (1.11 +/- 0.66 and 1.93 +/- 0.82 nmol conjugated bilirubin/mg protein in 10 min. respectively). When final reaction product was analysed, the normal group showed 80% of bilirubin diglucuronide; but resulted undetectable in cholestatic patients yielding 100% of bilirubin monoglucuronide. Microsomal phospholipid analysis showed a decrease in phosphatidylcholine and phosphatidylethanolamine contents in the cholestatic group; probably due to the action of bile acids accumulated into the hepatic cells. Simultaneously we found an increment in phosphatidylserine and sphingomyelin levels in cholestatic patients compared to normals (Figure 1). This fact could be explained by the existence of special sites in the membrane for the latter phospholipids, protected against bile acids detersive action.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Phospholipid composition of the hepatic microsomal membrane and its relationship to bilirubin UDP glucuronyltransferase in human cholestasis]. 213 64

Chlorpromazine, an antipsychotic drug, is found to inhibit Na+,K(+)-ATPase activity in rat brain microsomal membranes in vitro in concentration and time dependent manner but some inconsistency is observed when the effect was studied with respect to different temperatures. Various ligands and/or substrate affect the inhibition by chlorpromazine in different ways. The in vivo study with this drug shows that the activities of Na+,K(+)-ATPase, Ca2(+)-ATPase and acetylcholinesterase in the microsomal membranes of different organs are inhibit with increases in concentration or lengths of time of treatment and then levels off.
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PMID:The chlorpromazine inhibition of transport ATPase and acetylcholinesterase activities in the microsomal membranes of rat in vitro and in vivo. 216 37

1. The inhibition of cholinesterase and carboxylesterase activities in the diisopropyl fluorophosphate (DFP) intoxication, and the inducibility of organophosphate (OP) detoxicating enzymes was studied in rats. 2. In phenobarbital (PB)-, but not in beta-naphthoflavone (NF)-pretreated rats, the activities of DFP-inhibited cholinesterases were 70-120% higher than in non-pretreated rats. Also the inhibition of the microsomal and cytosolic carboxylesterase activity in liver was efficiently antagonized by BP, but not by NF. 3. In vitro the microsomes from PB-treated rats detoxicated DFP probably by O-dealkylation, since no fluoride was released from DFP. Glutathione S-transferase did not detoxicate DFP. 4. 7-Pentoxyresorufin O-dealkylase, a specific enzyme of cytochrome P450IIB subfamily, was induced by PB, flumecinol, isosafrole and NF by 167- 61-, 26- and 1.6-fold, respectively. 7-Ethoxyresorufin O-deethylase, a marker enzyme of cytochrome P450IA subfamily, was induced by those agents 5-, 4-, 31- and 94-fold, given in the same order. Glutathione S-transferase, paraoxonase and DFPase activities were increased 0-72% by the tested inducers. 5. The results suggest that the cytochrome P450IIB subfamily, inducible by PB, participates in DFP detoxication by O-dealkylation. Its induction probably causes the protection against the cholinesterase inhibition by OPs.
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PMID:Inhibition of cholinesterases by DRP and induction of organophosphate-detoxicating enzymes in rats. 216 59

The toxicity of the organophosphorus poison soman (pinacolylmethylphosphonofluoridate) is attributable to its irreversible inhibition of the enzyme acetylcholinesterase. In addition, soman binds irreversibly to a number of noncholinesterase tissue binding sites which appear to be its major means of in vivo detoxification. This study was conducted to determine the hepatic subcellular localization of these sites. Subcellular fractions of liver from male Sprague-Dawley rats (200-250 g) were prepared by differential and isopycnic density gradient centrifugation. The binding of [14C]soman to these subcellular fractions was determined in the presence and absence of cresylbenzodioxaphosphorin oxide (CBDP), a compound that binds irreversibly to the noncholinesterase soman binding sites. Crude fractionation of liver homogenates into nuclear, mitochondrial, microsomal, and soluble fractions revealed that 78% of the total CBDP-sensitive binding activity was localized in the nuclear and microsomal fractions. Further purification of these fractions indicated that all of the homogenate binding activity could be accounted for in the purified microsomal fraction. When purified liver microsomes were solubilized and fractionated on linear sucrose gradients, 90% of the CBDP-sensitive soman binding activity cosedimented with carboxylesterase activity which suggests that these binding sites are carboxylesterase.
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PMID:Hepatic subcellular localization of cresylbenzodioxaphosphorin oxide (CBDP)-sensitive soman binding sites. 224 10

Some biochemical parameters of liver and liver microsomes were studied in albino rats following administration of cobra and viper venoms at dose of 2 mg/kg body weight. The total protein content in cobra venom treated (CVT) animals and DNA and RNA contents of liver and liver microsomes were almost unaltered in both the venom treated animals while total protein content was significantly reduced in viper venom treated (VVT) animals. Alkaline and acid phosphatases activities of whole liver showed significant increase in both the venom treated animals whereas the rise in cholinesterase activity in CVT animals was not significant. Lactic acid content was significantly higher in CVT animals compared to either VVT animals or controls. The glycolytic enzymes viz., aldolase, phosphohexose isomerase and lactate dehydrogenase measured in hepatic microsomal fraction were significantly reduced while alanine and aspartate aminotransferases and gamma-glutamyl transpeptidase activities of liver microsomes were significantly elevated in both the venom treated animals compared to controls.
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PMID:Biochemical studies of liver & liver microsomes in envenomated rats. 227 76


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