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)

Monitoring observations made on 60 operators involved in pesticide application work in godowns and warehouses and 60 matched control workers are reported. Occupational exposure history and medical history are noted. Biochemical investigations, plasma and RBC cholinesterase estimations are included along with medical examination of the workers. Workers were found to be mostly exposed to Celphos, DDVP, Malathion, Pyrethrum, etc, and the use of protective devices were very limited. Cases of significant reduction in plasma and RBC cholinesterase activity were found. Frequency of symptoms like dizziness, headache, lachrymation, burning sensation in eyes, nausea and anorexia, etc, were much more in the exposed workers. No cases of clinical poisoning attributable to occupational exposure to pesticides were reported by the workers.
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PMID:A monitoring study of workers handling pesticides in warehouses and godowns. 46 78

Carbaryl, a widely used insecticide, is reputed to have a wide safety margin. It can induce acute cholinesterase poisoning, which is rapidly reversible on discontinuation of exposure. Long-term sequelae from long-term exposure have not previously been described in humans. This report describes the experience of a 75-year-old man who had long-term excessive exposure to carbaryl and in whom a debilitating syndrome, including headaches, memory loss, proximal muscle weakness, muscle fasciculation, muscle cramps, and anorexia with marked weight loss, developed. At the time of diagnosis, serum pseudocholinesterase levels were low, and his major symptoms resolved on termination of exposure. Late clinical features were sleep apnea and progressive development of a peripheral neuropathy. The difficulty in diagnosing the cause of a group of relatively nonspecific symptoms raises the question of whether chronic carbaryl neurotoxicity might be occurring more frequently than previously suspected.
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PMID:Subacute neurotoxicity following long-term exposure to carbaryl. 308 76

A group of 16 cauliflower workers poisoned by residues of the organophosphate insecticides mevinphos and phosphamidon was followed in weekly clinics with interviews and determinations of plasma and erythrocyte cholinesterase levels. None had preexposure baseline values. Although six had initial erythrocyte cholinesterase values within the laboratory normal range, subsequent testing showed their erythrocyte activity had been significantly inhibited. While the most severe symptoms of the 16 subjects resolved after 28 days, their erythrocyte cholinesterase levels did not reach a plateau until an average of 66 days after exposure, after which most patients continued to report blurred vision, headache, weakness or anorexia. These findings support the view that the diagnostic utility of single cholinesterase levels is limited in the absence of baseline values.
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PMID:Clinical management of field worker organophosphate poisoning. 401 66

Patients with severe virus hepatitis and a prothrombin concentration below 25% have a bad prognosis. This is due to direct consequences of hepatic failure and to the rather frequent complications of this disease. The clinical course of such patients is essentially dependent upon the degree of liver regeneration, which again is dependent upon the mass of hepatocytes which are able to regenerate and upon the so called hepatotrophic factors. Patients with severe hepatitis suffer during the first weeks rather frequently from nausea and loss of appetite and for that reason their nutrition is insufficient. In the study recorded here 9 cases were investigated (7 patients with hepatitis B, 2 patients with hepatitis non A non B). The question was asked, if partial parenteral nutrition in addition to a liver diet not containing meat would improve liver function. It could be shown that the prothrombin concentration, which could not be improved by vitamine K1 supplements, was increased during a 7 day parenteral nutrition period from 19,3 +/- 2,9% to 41,5 +/- 8,1% (p less than 0,05), serum albumine and cholinesterase activity improved as well. During the first day of treatment there was a significant fall of ammoniac from 115 +/- 10 mumol to 73 +/- 10 mumol/l (p less than 0,05), at the same time production of urea did not increase. All patients survived. The results show, that parenteral nutrition can improve liver function and decrease the catabolic status of metabolism.
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PMID:[Partial parenteral nutrition in severe virus hepatitis]. 643 23

The acute toxicity of quinuronium was investigated by measurements of lethal doses (LD50) in mice and rats, cholinesterase activity in vivo in whole blood, and protection from anticholinesterase activity by atropinisation in sheep and rabbits. The LD50s in mice injected i.p. and s.c. were 4.80 and 5.40 mg/kg and in rats 6.3 and 6.5 mg/kg for i.p. and s.c. routes, respectively. Signs of salivation, defecation, anorexia and muscular spasms were observed in sheep. In rabbits anorexia and depression only were observed. There was species variation in normal cholinesterase activity, rabbits being low in activity. Quinuronium inhibited cholinesterase activity from 10 min to 24 h after treatment in sheep by 24% of the normal baseline values. The enzyme activity returned to normal at 48 h. Atropinisation partially protected against anticholinesterase activity in sheep; cholinesterase activity was inhibited by only 14% of the normal baseline values 10 min to 2 h after treatment. This study indicates that quinuronium is highly toxic and that rabbits are moderately resistant.
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PMID:Acute toxicity studies with quinuronium sulfate in laboratory animals and sheep. 669 98

Extracts of Sesbania drummondii administered to chickens by oral intubation are lethal within several days. Effects are dose-dependent; a dose of 1% of body weight is uniformly lethal in 5 days. Signs of poisoning include weakness, depression (CNS), anorexia, diarrhea, ruffled feathers, cold feet, and rapid loss of body weight. Microscopic examination indicates damage to kidney glomeruli and leakage of protein into the kidney tubules. Packed cell volume and plasma glucose concentrations show no difference between controls and treated chickens; however, creatine kinase is increased and plasma cholinesterase and total plasma protein values are severely depressed in poisoned birds. Neither a specific toxin nor a mechanism of action for toxicity has yet been identified.
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PMID:Determination of the oral toxicity of Sesbania drummondii seeds in chickens. 673 32

The intraperitoneal administration of spermine (SPM) produced a dual-phasic feeding suppression. The first suppression appeared immediately after the administration and disappeared on the 2nd day. The next suppression was observed on the 3rd day and continued for 2-4 days. The 50% dose which induced suppression on the 3rd day was 64.9 (60.9-69.2) mumol/kg. Drinking behavior was also suppressed on the 1st day, but was facilitated on the 2nd day and lasted for 4-5 days. Serum glucose and free fatty acids concentrations increased after the administration of SPM (80 mumol/kg). Their maximal values obtained at 3 hours after the dosing were 116% and 156% of the control values, respectively. These increases in both substances were not observed in the adrenal-demedullated rats. The same dose of SPM enhanced serum glutamic oxaloacetic transaminase and glutamic pyruvic transaminase activities. The maximal values obtained at 2 hours after the dosing were 264% and 142% of the control values, respectively. On the contrary, serum cholinesterase activity decreased to 44% of the control value at the same hour. These variations of the enzyme activities disappeared at 3 hour, but were again observed between the 1st and 4th days. The results suggest that SPM releases catecholamines from the adrenal medulla, and exerts a toxic action on the liver. The anorexia induced by SPM may be due to these actions on the viscera.
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PMID:[Effects of intraperitoneally administered spermine on ingestive behavior, serum glucose and free fatty acids concentrations in rats (author's transl)]. 728 44

Acute cholestatic hepatitis developed in two patients, a 58-year-old man and a 54-year-old woman, who had been treated for hypercholesterolaemia with the cholesterol-synthesis inhibitor lovastatin for 3 years and 2 months, respectively. Both of them at first complained only of tiredness and loss of appetite, but then developed jaundice with colourless stool and dark urine. Alkaline phosphatase concentration rose up to maximally 1227 and 569 U/l, gamma-GT to 403 and 410 U/l, respectively. The transaminases and glutamate dehydrogenase were also elevated, while serum cholinesterase had fallen to 2346 and 2418 U/l, respectively. Histological examination of liver biopsies 6 months and 4 weeks, respectively, after onset of jaundice also suggested drug-toxic liver damage. There was no evidence for other causes. After lovastatin had been discontinued the various cholestasis parameters regressed only slowly.
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PMID:[Lovastatin-induced acute cholestatic hepatitis]. 786 82

Neuropeptide Y is one of the most powerful neurochemical stimulants of food intake known. The neuronal substrate for this action is believed to be the neuropeptide Y-expressing cell population in the hypothalamic arcuate nucleus. In this study, mice homozygous for the anorexia mutation (anx) were investigated histochemically; anx is a recessive mutation that causes decreased food intake and starvation, leading to death 22 days after birth. We were interested to see whether any hypothalamic neurochemical abnormalities could be detected in this genetic model of starvation. By using immunohistochemistry and in situ hybridization, the hypothalamic distributions of neuropeptide Y, cholecystokinin, galanin, and serotonin, all messenger molecules postulated to be involved in the regulation of food intake and energy metabolism, were investigated. Immunoreactivities for somatostatin, the excitatory amino acid aspartate, and acetylcholinesterase were also studied. Neuropeptide Y-like immunoreactivity was increased markedly in arcuate cell bodies and decreased in terminals in the arcuate nucleus and other hypothalamic regions of anx/anx mice compared with normal litter mates. In situ hybridization for neuropeptide Y mRNA, however, showed no significant difference in gene expression in the arcuate nucleus. In addition, immunoreactivities for aspartate, acetylcholinesterase, and somatostatin in the arcuate nucleus were decreased in anx/anx mice. For cholecystokinin, galanin, and serotonin, no certain differences in hypothalamic immunoreactivity could be seen. These data suggest that a defect in neuropeptide Y-ergic signalling in the arcuate neurons may contribute to the failure to thrive in anx/anx mice.
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PMID:Hypothalamic neurohistochemistry of the murine anorexia (anx/anx) mutation: altered processing of neuropeptide Y in the arcuate nucleus. 933 Nov 76

The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, drug interactions, and dosage and administration of donepezil are reviewed. Donepezil is a synthetic noncovalent reversible inhibitor of acetylcholinesterase (AChE) for the treatment of mild to moderate dementia associated with Alzheimer's disease. In contrast to tacrine hydrochloride, the only comparable agent currently approved by FDA, donepezil exhibits a relatively high degree of selectivity for neuronal AChE as opposed to butyrylcholinesterase. It has a half-life of 60 hours in young adults and 104 hours in elderly patients. In clinical trials, donepezil has been associated with significant improvements in Alzheimer's Disease Assessment Scale-cognitive subscale and Clinical Interview-Based Impression of Change scores. The most common adverse effects associated with donepezil are nausea, diarrhea, anorexia, and vomiting, which are most likely to occur during dose initiation or adjustment. Hepatotoxicity, a dose-limiting adverse effect that sometimes requires discontinuation of tacrine, has not been reported with donepezil. Donepezil does not appear to interact with theophylline, cimetidine, warfarin, or digoxin. Ketoconazole and quinidine inhibit the metabolism of donepezil in vitro, but there is a lack of clinical data showing that these drugs decrease the clearance of donepezil. The initial recommended dosage is 5 mg daily before bedtime, with a dosage increase to 10 mg after four to six weeks according to the patient's response and tolerance. Donepezil appears to be preferable to tacrine as the initial agent for patients with mild to moderate dementia associated with Alzheimer's disease.
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PMID:Donepezil: an anticholinesterase inhibitor for Alzheimer's disease. 942 50


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