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:3.1.1.8 (cholinesterase)
12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Growing male rats that weighed 120 +/- 5 g were kept for 30 days on the following synthetic diets: high protein diet (HPD), 59% casein; high fat diet (HFD), 50% saturated fat; and normal diet (ND), 19% casein, 10% saturated fat, and 60% sucrose. Other essential dietary ingredients were included in all the diets. All animals were injected at the end of the 30-day period with parathion [10 mg/kg intraperitoneal (ip) injection as a single dose] or dichlorvos (30 mg/kg ip as a single dose) to compare the effect of dietary pretreatments on mortality from parathion and dichlorvos. A lower dose of parathion (7.5 mg/kg) and dichlorvos (20 mg/kg) was employed in another set of experiments to compare the spontaneous regeneration of plasma and red blood cell (RBC) cholinesterase (ChE) activity at 2 hr, 1 day, 3 days, and 5 days after administration of parathion or dichlorvos. The effect of these diets on hepatic microsomal oxidases was also determined. Results showed that diets per se did not affect initial plasma and RBC ChE activity. The HPD and HFD significantly protected against mortality from parathion but not from dichlorvos. Hepatic microsomal cytochrome P-450 and aminopyrine demethylase activity were unchanged, but aniline hydroxylase activity was increased significantly by HPD and HFD. Parathion oxidase in hepatic microsomes was significantly increased in rats fed HFD only. For the HPD, spontaneous regeneration of ChE diminished in RBCs in parathion-intoxicated rats and in plasma and RBCs of dichlorvos-intoxicated rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of high-fat and high-protein diets on toxicity of parathion and dichlorvos. 652 63

Chickens housed for 4.5 months in an environment of either low social stress or high social stress were administered triorthotolyl phosphate (TOTP) 180 mg/kg po. Clinical signs of delayed neuropathy were less in the low social stress group, unless moved to a high stress environment 24 hr before TOTP administration. Neurotoxic esterase activity was less than 20% of control values in all treatment groups. Birds from the low social stress group moved 24 hr prior to TOTP were more susceptible to inhibition of brain and liver cholinesterase activities following organophosphate administration. Liver microsomal enzyme activities (O-demethylase and aniline hydroxylase) were lowest in unmoved low social stress birds after TOTP, possibly protecting these birds from delayed neuropathy by reducing conversion of this organophosphate to its active metabolite.
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PMID:Modification of triorthotolyl phosphate toxicity in chickens by stress. 662 67

Previous studies have shown that subchronic treatment of mice with the organophosphate insecticide, disulfoton, or the carbamate insecticide, propoxur, leads to the development of tolerance to their toxicity. Tolerance to disulfoton was due to a decrease in the number of muscarinic cholinergic receptors, while tolerance to propoxur appeared to be due to an induction of hepatic microsomal enzymes. In the present study we investigated if cross-tolerance between disulfoton and propoxur would occur. Cross-tolerance was evaluated by measuring acute toxicities, cholinesterase and carboxylesterase inhibition and hypothermic and antinociceptive effects. Mice tolerant to propoxur were cross-tolerant to the hypothermic and anticholinesterase effects of disulfoton. Similarly, when mice were pretreated with the microsomal enzyme inducer, phenobarbital, the toxicity of disulfoton was decreased. Mice made tolerant to disulfoton were cross-tolerant to the organophosphate chlorpyrifos, but were more sensitive than controls to the toxicity of propoxur. The acute toxicity of the organophosphate malathion was also increased in disulfoton-tolerant mice. Propoxur is metabolized by mixed function oxidases and possibly by a carboxylesterase. While hepatic microsomal enzymes appeared to be unchanged in disulfoton-tolerant mice, brain and liver carboxylesterase activities were significantly inhibited. Pretreatment of mice with the specific carboxylesterase inhibitor triorthotolylphosphate is known to greatly potentiate the toxicity of malathion and also potentiated, to a lesser extent, the toxicity of propoxur.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Unidirectional cross-tolerance between the carbamate insecticide propoxur and the organophosphate disulfoton in mice. 664 6

The differential effects of oral and dermal administration of single doses of 100 to 1000 mg/kg S,S,S-tri-n-butyl phosphorotrithioate (DEF) on nonspecific esterases and liver metabolism enzymes were investigated one day following administration. O,O-Diethyl O-(4-nitrophenyl) phosphorothioate (parathion) and tri-o-cresyl phosphate (TOCP) were used as negative and positive controls for organophosphorus-induced delayed neurotoxicity (OPIDN). Brain acetylcholinesterase was significantly inhibited with topical doses of 500 and 1,000 mg/kg of DEF and with orally and dermally applied parathion. Plasma cholinesterase and liver microsomal carboxylesterase activities were significantly reduced from control in all treatment groups. Neurotoxic esterase (NTE) was significantly decreased from control with topical dosing of 200, 500, and 1000 mg/kg DEF and with TOCP treatments. Oral doses of DEF increased cytochrome P-450 content by 70 to 200% while dermal application caused a 200 to 325% increase over control. p-Chloro-N-methylaniline demethylase was also increased by DEF treatments but to a lesser extent than that of aniline hydroxylase or cytochrome P-450 content. TOCP and parathion had no significant effect on liver microsomal oxidative enzymes. Liver microsomal proteins from hens treated with phenobarbital (PB), 3-methylcholanthrene (3MC), or DEF were analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. A striking increase in a 49K protein band in microsomes from PB and DEF (616 and 338%, respectively) treated hens was seen, while the 55K protein band showed an 861% increase in microsomes from 3MC-treated hens. In conclusion, dermally applied DEF was more effective in inhibiting esterases and inducing cytochrome P-450 than orally administered DEF; toxicity was directly related to the dose and route of administration.
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PMID:Induction of hepatic microsomal cytochrome P-450 and inhibition of brain, liver, and plasma esterases by an acute dose of S,S,S-tri-n-butyl phosphorotrithioate (DEF) in the adult hen. 671 May 30

We measured several biochemical effects of 10 days of intragastric administration of phosphatidylcholine (10 mmoles/kg) to rats because of the expanding clinical use of chronic phosphatidylcholine treatment for disorders involving impaired cholinergic neurotransmission. The plasma and erythrocyte choline concentrations were increased 3.5-fold, which was the same percent increase as found after an acute treatment with phosphatidylcholine. The lipid and fatty acid compositions of the plasma were also altered; free and total cholesterol levels increased, triglycerides increased, the monoene fatty acids generally decreased, and the diene and tetraene fatty acids generally increased. We found no effect of this treatment on the hepatic microsomal cytochrome P-450 activity or on the N-demethylation of benzphetamine or methamphetamine. Ten days of phosphatidylcholine treatment increased the concentration of choline in the brain but had no effect on the concentration of acetylcholine, the activity of choline acetyltransferase, cholinesterase activity, the apparent KD or Bmax of muscarinic receptors, or the fatty acid composition of rat brain lipids. These findings indicate that the largest effect caused by this treatment was an increase in the choline levels. No indication of altered cholinergic metabolism was observed. Further studies of the effects of chronic phosphatidylcholine treatment are required to clarify its therapeutic mechanism of action.
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PMID:Biochemical effects of phosphatidylcholine treatment in rats. 671 9

Serum pseudocholinesterase in accordance with indicators revealing the lipid metabolism and liver function was studied in rats exposed to phenobarbital, bis-p-nitrophenylphosphate and disulfiram in vivo. Phenobarbital markedly induced the hepatic microsomal drug-metabolizing enzymes and tended to decrease the triglyceride content in serum. Serum lipids remained almost unaffected after the treatment of bis-p-nitrophenylphosphate. However, serum gamma-glutamyltransferase activity showed a marked decrease to this organophosphorus compound. Disulfiram activated the microsomal UDP-glucuronosyltransferase (p-nitrophenol) activity, and caused an enhancement of serum total cholesterol, which suggests that this drug might be atherogenic.
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PMID:Serum lipids and hepatic microsomal enzymes with special reference to serum cholinesterase in Wistar rats. 671 39

Rats were treated, during 8 weeks, with different doses of edifenphos (0, 5, 10, 20, 40 mg/kg/day) incorporated in the food. Treatments with 20 and 40 mg/kg increased the relative liver weight and hepatic concentrations of phospholipids, microsomal proteins and cytochrome P450. Aminopyrine N-demethylase and aniline hydroxylase activities were increased at the same doses. Hepatic lipids and blood triacylglycerols remained unchanged by the treatment, but blood cholesterol increased significantly (33%) at 40 mg/kg. Plasma cholinesterase activity was slightly depressed in rats treated with the two higher doses. Under these experimental conditions, the dose of edifenphos, inducing no significant difference was 10 mg/kg/day.
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PMID:Biochemical changes in liver and plasma of rats after oral administration of edifenphos. 683 11

The effect of adrenalectomy (Adx), SKF 525-A, phenobarbital (PB), and diethyl maleate (DEM) on the acute toxicity of fenitrothion was investigated in male rats by assessing the degree of plasma cholinesterase activity. PB, 60 mg/kg/day for 3 days, exerted no protective effect on the toxicity of fenitrothion (100 mg/kg, p.o.) given 24 h after the last injection. In adrenalectomized and SKF 525-A-pretreated rats, the toxicity of fenitrothion was lower than that of the controls. Fenitrothion toxicity was increased by administration of DEM (1 ml/kg), which depletes hepatic glutathione (GSH) levels. In vitro, the rates of fenitrothion decomposition and fenitrooxon formation by microsomes were markedly affected by PB, SKF 525-A and Adx. The decomposition of fenitrooxon by the microsomal fraction and GSH-dependent decomposition of fenitrooxon by the soluble fraction were not affected by PB, SKF 525-A and Adx pretreatment. The GSH-dependent decomposition of fenitrothion and fenitrooxon was increased by addition of GSH to the incubation mixture. The present results indicate that the GSH-dependent metabolic pathway plays an important role in the detoxication of fenitrothion.
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PMID:Effect of adrenalectomy, pretreatment with SKF 525-A, phenobarbital and diethyl maleate on the acute toxicity of fenitrothion in male rats. 686 Jan 45

Rats were pretreated with phenobarbitol [PB (75 mg/kg, IP)] for 3 days and subsequently injected with parathion, an organophosphorous insecticide, which requires microsomal activation for its anticholinesterase effect or with dichlorovos, a cholinesterase (ChE) inhibitor as such. The difference in the mortality and spontaneous regeneration of inhibited plasma ChE by IP administration of the two insecticides was compared. A single dose of 10 mg/kg parathion caused 100% mortality in PB-untreated rats, but effected no mortality in PB-pretreated rats. A lower dose (7.5 mg/kg) of parathion resulted in plasma ChE levels which were 5, 5, 17, and 93% of initial values in PB-untreated rats and 85, 97, and 92% of initial values in PB-pretreated rats at 2-hr, 1-3-, and 5-day periods, respectively. Mortality resulting from single dose of 30 mg/kg dichlorovos was 30% in PB-pretreated, as well as untreated rats. A lower dose of dichlorovs (20 mg/kg) resulted in plasma ChE activity which was 48, 82, 90, and 97% of initial levels in PB-untreated rats, and 60, 100, 100, and 130% in PB-pretreated rats at 2 hr, 1, 3, and 5 day's, respectively. Administration of 2 mg/kg parathion for 3 days did not affect cytochrome P-450 levels in liver microsomes, but administration of 6 mg/kg dichlorovos for 3 days caused greatly lowered levels of liver microsomal cytochrome P-450, resulting from its inactivation to cytochrome P-420. Phenobarbital caused accelerated in vitro ChE regeneration in the case of dichlorovos-inhibited enzyme in the plasma, but not in the case of parathion-inhibited enzyme.
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PMID:Effect of phenobarbitol pretreatment on regeneration of plasma cholinesterase activity inhibited by parathion or dichlorovos. 705 32

The effects of fenitrothion and methylparathion on the activities of cholinesterase and hepatic microsomal monooxygenases were investigated and compared following a single or repeated oral administration of an equimolar and low dose of the insecticides. The activities of cholinesterase in brain and plasma were inhibited equally by the repetitive administration of both insecticides. Aminopyrine N-demethylase activity and cyt.P-450 content were not affected under the same experimental conditions. However, methylparathion, when given repeatedly, inhibited the dearylation and desulfuration of it own. The results may indicate that low dose continuous exposure to methylparathion could cause the depression of its own metabolism in rat.
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PMID:Comparison of the effect of an equimolar and low dose of fenitrothion and methylparathion on their own metabolism in rat liver. 709 8


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