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)

Male Sprague-Dawley rats were treated with a solution of ethanol (20% v/v) as the only source of fluid for 28 weeks while controls received tap water. Profound reductions of acetylcholine content, the activities of choline acetyltransferase and acetylcholinesterase and choline uptake were observed in the cortex, hippocampus, substantia innominata and striatum four weeks after withdrawal from ethanol. These changes in cholinergic markers were accompanied by an impaired performance in a spontaneous alternation task tested at long acquisition-retention intervals. This ethanol induced behavioural deficiency, which most likely represents a memory impairment, could be reversed by application of physostigmine (0.45 g/kg; i.p) whereas neostigmine did not show any behavioural effect. The results suggest that ethanol-induced memory impairment can be ameliorated by pharmacological manipulation of central cholinergic function.
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PMID:The cholinergic system and memory: amelioration of ethanol-induced memory deficiency by physostigmine in rat. 213 Jun 47

The effects of a reversible (physostigmine) and an irreversible (soman) acetylcholinesterase inhibitor were compared in terms of nociception using the rat tail flick (TF), and hot plate (HP) tests. The conditioned taste aversion (CTA) procedure was employed to evaluate the stimulus properties of these drugs. In all procedures physostigmine salicylate was administered at doses of 0.20, 0.32, 0.45, or 0.65 mg/kg, IM. Soman was administered at doses ranging from 40 to 80 microgram/kg, IM. Using either TF or HP, physostigmine and soman were evaluated at 40 min following injection. Both physostigmine and soman produced dose-related effects on each measure of nociception. The median effective dose of physostigmine was 0.27 mg/kg on TF and 0.55 mg/kg on HP. For soman, the median effective dose was 54 micrograms/kg on TF and 52 micrograms/kg on HP. In the CTA procedure, a novel, saccharin sweetened solution was paired with either physostigmine or soman. Three days later rats were offered a choice of saccharin or tap water. Both soman and physostigmine produced dose-related CTAs over the range of doses studied. Whereas the ED50 for soman was 59 micrograms/kg with significant effects at doses of 60 micrograms/kg or more, physostigmine produced effects at doses of 0.45 mg/kg or greater (ED50 = 0.05 mg/kg) with no additional changes in saccharin preference beyond 0.45 mg/kg. The data suggest that these experimental procedures, TF, HP, and conditioned taste aversion may be employed to evaluate the behavioral toxicity of physostigmine and soman.
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PMID:A comparison of physostigmine and soman using taste aversion and nociception. 403 65

Male white rats were given with drinking water detergents: sodium alkylbenzenosulphonate /ABSNa/S/ and Rokamid MRZ 17, Group I/control/received tap water. Groups II, III and IV were given ABSNa/S in doses of 2, 6 or 18 mg/l of water, and groups V, VI and VII were given Rokamid MRZ 17 in the same concentrations. After 10 months of exposure to these detergents haematological tests were done: haemoglobin level, haematocrit value and clotting time; biochemical investigations included blood cholinesterase activity, bilirubin and cholesterol levels in plasma. Then memory potential was tested by teaching the rats differentiation and memorizing of visual stimuli in a cage specially adapted for that purpose. On the ground of the obtained results it can be said that in the groups receiving Rokamid MRZ 17 in 18 mg/l concentration and ABSNa/S 6 and 18 mg/l the median survival was decreased by over ten per cent, and blood clotting time was prolonged in relation to the control group. The results of conditioning tests showed that the highest concentration of Rokamid MRZ 17 produced memory impairment in this group.
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PMID:[Chronic toxic effects of surface-active substances varying in chemical structure]. 906 37

We have shown that acetylcholine (ACh) is present in the blood of various species of mammals using a specific, sensitive radioimmunoassay. In the present study, the effect on blood and plasma ACh levels of feeding after overnight fasting was studied in one male and five female 4- to 7-year-old chimpanzees. The mean basal ACh concentrations of the blood and plasma were 3143 +/- 380 and 184 +/- 10 pg/ml (+/-SEM, n = 6), respectively. Feeding each chimpanzee 500 g boiled sweet potatoes as breakfast at 1000 h and tap water given ad libitum did not affect the ACh content of the blood and plasma, and constant values of the blood and plasma ACh contents were observed for 4 h after the feeding. Hematocrit and plasma acetylcholinesterase (AChE) activity were also insensitive to feeding. No correlation was observed between plasma AChE activity and either blood or plasma ACh content. The results of the present study indicate that the blood ACh of chimpanzees is distributed mainly in the blood cell fraction, and that the blood ACh content is not regulated directly by cholinergic nerve activity or by plasma AChE activity.
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PMID:Maintenance of constant blood acetylcholine content before and after feeding in young chimpanzees. 917 49

Excessive dietary intake of sugars could alter various biotransformation processes and the pharmacological and toxicological properties of numerous xenobiotics. In the present study, the effects of glucose supplementation were examined on the neurotoxicity of the organophosphorus (OP) pesticide parathion (PS) and its active metabolite, paraoxon (PO), a potent inhibitor of acetylcholinesterase (AChE). Rats (n = 6-12/treatment group) were given free access to tap water or 15% glucose (w/v) in tap water beginning 7 d prior to OP toxicant exposure. Food, caloric intake, and body weight were measured daily. Animals were challenged with either PS (4.5, 9, or 18 mg/kg, sc) or PO (0.3 0.5, or 0.7 mg/kg, sc) and clinical signs of neurotoxicity (i.e., autonomic dysfunction, involuntary movements) were recorded daily for the following 13 d. Glucose feeding was associated with a dramatic drop (approximately 50%) in feed intake and an increase (approximately 20% in total caloric consumption over the 7 d prior to OP exposure. Functional toxicity associated with PS exposure was increased in glucose-fed (GF) rats, but the glucose diet had no apparent effect on clinical signs of toxicity following PO treatment. Glucose feeding increased the magnitude of AChE inhibition in the frontal cortex and plasma at lower dosages (i.e., 4.5 and 9 mg/kg) 3 d following PS treatment. Time-course studies (3, 7, and 11 d after PS exposure, 18 mg/kg, sc) indicated significantly greater brain and plasma AChE inhibition in glucose-fed animals at later time points. In contrast, glucose feeding had no effect on the degree of AChE inhibition following PO exposure. Neither liver microsomal oxidative desulfuration of PS, nor liver or plasma paraoxonase, nor liver or plasma carboxylesterase activities were measurably affected by glucose feeding. Downregulation of muscarinic receptors 7 d after PS exposure (18 mg/kg, sc) was more extensive in GF rats. It is postulated that excessiveglucose consumption decreases the intake of other dietary components, in particular amino acids, limiting the de novo synthesis of AChE and consequent recovery of synaptic transmission. Due to the shorter duration of inhibition following PO exposure, sponta neous reactivation of AChE may be more important than de novo protein synthesis in recovery of function, and thus with the effects of glucose feeding on its toxicity. Individuals that derive a large proportion of their calories from sugars may be at higher risk of acute toxicity from organophosphorus pesticides such as PS.
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PMID:Glucose feeding exacerbates parathion-induced neurotoxicity. 1143 59

The determination of organophosphate (paraoxon, chlorpyrifos, diazinon) and carbamate (carbaryl, carbofuran) pesticides in spiked drinking water and fruit juices was carried out using a photothermal biosensor. The biosensor consists of a cartridge containing immobilised enzyme acetylcholinesterase (AChE) placed in a flow-injection analysis (FIA) manifold and a photothermal detector based on thermal lens spectrometry. With this approach, 0.2 ng/ml of paraoxon can be detected in less than 15 min. Limits of detection for other organophosphate (chlorpyrifos, diazinon) and carbamate (carbaryl, carbofuran) pesticides varied, depending on their antiacetylcholinesterase (AntiAChE) toxicity, from 1 ng/ml to 4 microg/ml. The biosensor was used for the direct detection of pesticides in spiked tap water and fruit juices without any pretreatment steps. In these cases, the LOD3sigma of 1.5, 2.8 and 4 ng/ml paraoxon in tap water, orange juice and apple juice were obtained, respectively.
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PMID:Determination of organophosphate and carbamate pesticides in spiked samples of tap water and fruit juices by a biosensor with photothermal detection. 1145 2

A biosensor for the detection of insecticides based on an ion-sensitive field-effect transistor (ISFET) was developed. The resulting device combines the simplicity of potentiometric sensors and the use of associated electronic systems as powerful tools for the acquisition and the processing of data. The enzyme acetylcholinesterase (AChE) was entrapped in a membrane placed on the gate of the ISFET forming an enzyme field-effect transistor (EnFET). The biosensor is applied to the determination of pesticides in spiked real samples. Organophosphorous and carbamate insecticides were measured with a detection limit of 10(-8) mol L(-1). The measurement is based on the production of hydrogen ions due to the hydrolysis of acetylthiocholine by the enzyme. The resulting local pH change is picked up by the underlying pH-sensitive ISFET and transduced as potential variations. The preparation of the membrane is simple and reproducible. The analysis in spiked real samples was performed in tap water and showed detection limits comparable to those obtained by other researchers.
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PMID:Development of an EnFET for the detection of organophosphorous and carbamate insecticides. 1274 54

Effects of chronic exposure to corticosterone in drinking water on corticosterone kinetics, blood chemistry, and concentrations of catecholamines in parts of brain were studied in Long-Evans rats. Rats were randomly grouped into 3 x 2 treatments (n=4), with three treatments of drinking water (tap water, or 2.5% ethanol, or 400 microg/mL of corticosterone in 2.5% ethanol) for 28 days and two treatments of gavage with a single dose of either corn oil or corticosterone 20 mg/kg on day 28. Blood samples were collected at 0, 15, 30, 60, 120, 240, 480, and 720 min after dosing to determine plasma corticosterone concentrations. Blood samples were collected for clinical pathology on day 42. Hippocampus, cerebral cortex, caudate-putamen, and pons were examined to determine concentrations of catecholamines and activities of esterases. Concentrations of plasma corticosterone before gavage of the corticosterone-drinking rats (47.61 +/- 1.13 ng/mL) were lower than the water (418.47 +/- 1.13 ng/mL) or the ethanol rats (383.71 +/- 1.13 ng/mL, P < 0.0001). Plasma corticosterone rose to peak concentrations by 15 min after gavage in all three groups of drinking rats. Corticosterone-drinking rats had concentrations of plasma corticosterone that returned to basal levels slower than water- and ethanol-drinking rats. Plasma sodium and chloride concentrations were lower in the corticosterone-drinking rats than the water-drinking rats (P < 0.01). Plasma albumin, globulin, and total protein were highest in the corticosterone-drinking rats when compared to the other groups of drinking rats (P < 0.001, P < 0.05, and P < 0.001, respectively). Corticosterone in drinking water did not affect activities of brain neurotoxic esterase, carboxylesterase, acetylcholinesterase, or concentrations of monoamines and their metabolites. A single oral dose of corticosterone reduced neurotoxic esterase activity in the cerebral cortex (P < 0.05) and increased norepinephrine concentrations in the hippocampus (P < 0.05).
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PMID:Corticosterone in drinking water: altered kinetics of a single oral dose of corticosterone and concentrations of plasma sodium, albumin, globulin, and total protein. 1574 78

The acetylcholinesterase (AChE) inhibitors sarin and pyridostigmine bromide (PB) have been proposed as causes of neurobehavioral dysfunction in Persian Gulf War veterans. To test possible delayed effects of these agents, we exposed rats to low (subsymptomatic) levels of sarin (0.5 LD50 s.c. 3 times weekly) and/or PB (80 mg/L in drinking water) for 3 weeks. Controls received saline s.c. and tap water. At 2, 4 and 16 weeks after exposure, regional cerebral blood flow (rCBF) and glucose utilization (rCGU) were measured in conscious animals with the Iodo-14C-antipyrine and 14C-2 deoxyglucose methods, respectively. Two weeks after exposure, PB+sarin caused significant rCBF elevations, but no changes in rCGU, in neocortex, with lesser effects on allocortex. Four weeks after exposure, the same general pattern was found with sarin. Only a few changes were found at 16 weeks post-treatment. The predominant effects of sarin or PB+sarin on rCBF at earlier times after treatment are consistent with the well known direct cerebral vascular effect of cholinergic agonists. The lack of changes in rCBF and rCGU observed at 16 weeks after treatment does not support the hypothesis that repeat exposure to low-dose cholinesterase inhibitors can generate permanent alterations in cerebral activity.
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PMID:Low-dose cholinesterase inhibitors do not induce delayed effects on cerebral blood flow and metabolism. 1582 May 22

Malathion toxicity has been related to the inhibition of acetylcholinesterase and induction of oxidative stress, while zinc has been shown to possess neuroprotective effects in experimental and clinical studies. In the present study the effect of zinc chloride (zinc) was addressed in adult male Wistar rats following a long-term treatment (30 days, 300mg/L in tap water ad libitum) against an acute insult caused by a single malathion exposure (250mg/kg, i.p.). Malathion produced a significant decrease in hippocampal acetylcholinesterase, as well as a decrease in the activity of several hippocampal antioxidant enzymes: glutathione reductase, glutathione S-transferase, catalase and superoxide dismutase. The pretreatment with zinc did not completely prevent acetylcholinesterase activity impairment; however, antioxidant activity was completely restored. Zinc administration significantly increased HSP60, but not HSP70, expression. The HSP60 increase suggests a novel zinc-dependent pathway, which may be related to a counteracting mechanism against malathion effects. Based on these results the following hypothesis can be presented: the published "pro-oxidative" effect of malathion may be related, among others, to compromised antioxidant defenses, while the zinc "antioxidant" action may be related to the preservation of antioxidant defenses. In conclusion, our data points to the inhibition of antioxidant enzymes as an important non-cholinergic effect of malathion, which can be rescued by oral zinc treatment.
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PMID:Zinc reverses malathion-induced impairment in antioxidant defenses. 1942 56


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