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)

In a case of severe poisoning with the organophosphorous insecticide methidathione standardized forced diuresis and peritoneal dialysis were performed for the first time in addition to the usual therapeutical procedures (e.g. repeated gastric lavage, induced diarrhea, atropine and intensive care). The course of the illness as well as the duration of the acute phase were significantly shorter than in comparable cases. No hazardous situation occurred after the first hours of treatment. The presence of the organophosphorous cholinesterase inhibitor or of its metabolites in the urine and the dialysate was proved by thin-layer chromatography.
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PMID:[Standardized forced diuresis and peritoneal dialysis in the therapy of organophosphorous poisoning (author's transl)]. 54 50

This study is based on 17 neonates suffering from total colonic aganglionosis. The male:female ratio was 2:3 and there was a significant familial occurrence. The ages on admission varied between 1 and 90 days. The clinical presentation was extremely variable. Early diagnosis depends on clinical awareness of the condition in neonates who have intestinal obstruction or diarrhea, or both. The most important radiologic indication was retention of barium for 24 hours. Results of manometric studies were misleading. Suction biopsy of the rectum provided the only sure method of diagnosis, although determination of cholinesterase activity in the biopsy specimen and in the patient's serum was of some value. Two patients died before operation and two died from total colonic and small intestinal aganglionosis. Eight patients survived both the initial ileostomy and subsequent pull through operation. Of the various procedures utilized, the Lester Martin operation has proved to be the most satisfactory.
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PMID:Total colonic aganglionosis. 71 62

Clinical signs, pathologic changes and biochemical changes occurred in cattle with natural and experimental triaryl phosphate poisoning. Natural poisoning was caused by triaryl phosphates escaping from a gas pipeline compressor station. The clinical signs were posterior motor paralysis, dyspnea, diarrhea and agalactia. Experimental doses of 1/2-1 gm/kg body weight of these organophosphate compounds caused depression of cholinesterase and axonal degeneration in the spinal cord.
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PMID:Triaryl phosphate poisoning in cattle. 85 97

Aldicarb toxicosis was diagnosed in 200 sheep that died suddenly. Carbamate insecticide toxicosis was suspected based on observed clinical signs (hypersalivation, diarrhea, urination, paddling, seizures, miosis, and deaths occurring within 1 hour). Tissue samples were submitted from 4 Columbian ewes for pathologic and analytical evaluation. Severe diffuse pulmonary edema was observed on gross and histologic examination. Inhibition of cholinesterase activity in retina (21.2-68.1% of normal activity, n = 3), brain (40.6-45.6% of normal activity, n = 3), and whole blood (27% of normal activity, n = 1) supported a diagnosis of carbamate toxicosis. Reversal of brain and whole blood cholinesterase activities (reactivation factor greater than 1.4) following an in vitro 1 hour incubation at 37 C was also consistent with carbamate poisoning. Aldicarb toxicosis was confirmed following its detection in rumen contents at 1.5, 5.5, and 334 ppm using both high-pressure liquid chromatography with UV detection and gas chromatography with nitrogen/phosphorus detection.
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PMID:Aldicarb toxicosis in a flock of sheep. 155 68

A case of prolonged QT syndrome (PQTS) caused by unintentional poisoning with organic phosphate pesticides is reported in a 73 year old farmer. PQTS developed and coexisted with other symptoms of poisoning such as low levels of cholinesterase, vomitus, diarrhoea, miosis, hypersalivation and occurred with typical symptoms. Despite concomitant with PQTS advanced ventricular extrasystoles the most dangerous form of them--ventricular tachycardia "torsades de pointes"--wasn't observed what was attributed among other things to scrupulous control and replenishment of potassium++ and magnesium and avoidance of typical antiarhytmic drugs in ventricular arrhythmia+ treatment. Acquired (most often after drug treatment, toxic and resulting from electrolytic disturbances) forms of PQTS are discussed stressing their heterogeneity and necessity of preventive treatment (different, dependent on etiology).
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PMID:[Long QT syndrome after organophosphate insecticide poisoning]. 164 Jun 67

Pyridostigmine is known as a pre-treatment drug against intoxication with organophosphorus nerve agents. During the Persian Gulf war, we encountered a cluster of nine cases of pyridostigmine self-poisoning, of which three presented with mixed drug poisoning. The clinical and laboratory features of pyridostigmine toxicity are presented. Doses ranged between 390 and 900 mg. Pyridostigmine ingestion resulted in mild to moderate cholinergic symptoms such as abdominal cramps, diarrhea, emesis, nausea, hypersalivation, urinary incontinence, fasciculations, muscle weakness and blurred vision. No central nervous system manifestations were evident. The symptoms developed within several minutes and lasted up to 24 h. All patients underwent gastric emptying followed by administration of activated charcoal. Atropine (1-8 mg) was required in only three patients. Measurement of serum cholinesterase inhibition was found to be a reliable and sensitive diagnostic tool in pyridostigmine poisoning. No clear correlation was found between the extent of cholinesterase inhibition and the incidence or severity of the cholinergic signs. The clinical recovery was faster than the spontaneous recovery of the enzyme. Pyridostigmine intoxication is self-limited and well tolerated by young healthy adults.
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PMID:Acute pyridostigmine overdose: a report of nine cases. 175 42

Aerial application of organophosphates can result in exposure to drift and leaf residues for pilots, ground crews, field workers, and residents near sprayed fields. Exposure can be by either the airborne or dermal route, and can produce illness (headaches, fatigue, diarrhea, cramps, respiratory problems) even with low-grade depressions in cholinesterase. Alkyl phosphate metabolites have been shown to be "gold standard" measures of such exposures. Experience in Israel indicates that reduction of health hazards from exposure to drift and leaf residues may be attained by the use of a comprehensive "mix" of preventive measures. These measures include, first and foremost, reduction in total amount of organophosphates used, followed by substitution of less for more toxic organophosphates, reduction in length of spray season, banning the use of flaggers, and greater reliance on tractor spraying. Cotton yield per hectare cultivated has increased despite a reduction in use of pesticides of all kinds and organophosphates in particular. Enclosure and air-conditioning (to prevent heat stress) of cockpits, protective clothing, training and licensing of pilots have been implemented. Education and communication of information, in keeping with the right-to know principle on hazards and how they should be controlled and monitored, is a part of a comprehensive strategy. Aerial or ground spraying should produce no drift in adjacent residential communities. The criterion for achieving this goal is the absence of urine alkyl phosphate metabolites above the threshold of detection.
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PMID:Hazards associated with aerial spraying of organophosphate insecticides in Israel. 184 56

The reversibility of inhibition of plasma, red blood cell (RBC), and diaphragm cholinesterase (ChE) and clinical signs in mice given anatoxin-a(s) [antx-a(s)], a ChE inhibitor from Anabaena flos-aquae NRC-525-17, were characterized and compared with the effects of 2 known ChE inhibitors, the organophosphorus compound paraoxon and the carbamate pyridostigmine bromide. To follow recovery of ChE activity, mice were given either a control solution or an LD40 dose of one of the toxicants ip and killed at time points up to 8 d postdosing. After dosing, mice were monitored for diarrhea, fasciculations, respiratory difficulty, salivation, and tremors. In general, clinical signs in mice given antx-a(s) persisted longer than in mice given pyridostigmine and were more similar in duration to the clinical signs in mice given paraoxon. Histologic lesions were not detected in tissues of mice killed after administration of antx-a(s). Anatoxin-a(s) inhibited lesions were diaphragm ChE for greater than 1 but less than 2 d and RBC ChE for 8 d. The time required for recovery from Antx-a(s)-induced inhibition of ChE in plasma, RBC, and diaphragm was similar to or longer than that with paraoxon and longer than that with pyridostigmine. Based on the duration of antx-a(s) induced clinical signs and ChE inhibition in mice, antx-a(s) appears to be an in vivo irreversible inhibitor of ChE.
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PMID:Reversal of cholinesterase inhibition and clinical signs and the postmortem findings in mice after intraperitoneal administration of anatoxin-a(s), paraoxon or pyridostigmine. 201 58

A three-month oral subacute toxicity study of mofezolac (N-22), a non-steroidal anti-inflammatory agent, was performed using dose levels of 6, 20, 60 and 200 mg/kg in rats, and recovery was also assessed one month after withdrawal. 1. Toxic signs caused by N-22 administration, observed only in the 200 mg/kg group, were as follows: soiling around the mouth and/or nose, piloerection, anemia, diarrhea, emaciation and decreased spontaneous locomotor activity. Nine males and thirteen females in the 200 mg/kg group excreted bloody diarrhea and died of general exhaustion between weeks four and thirteen of study. 2. In the 200 mg/kg group, decrease in food consumption and suppression of body weight gain were noted in males from about week four and in females from about week six after initiation of administration, and increase in water consumption was noted in males from about week seven. 3. Urinary examination revealed a decline in urinary pH in males of the 20 mg/kg and above groups and elevation of urobilinogen levels in males of the 60 and 200 mg/kg groups. 4. Hematological examination showed decreases in erythrocyte count (RBC), hematocrit value (Ht) and hemoglobin concentration (Hb) and increase in reticulocyte rate in both sexes of the 200 mg/kg group and an increase in neutrophil rate in males of the 200 mg/kg group. 5. Biochemical examination demonstrated a decrease in chloride (Cl-) in males receiving the 20 mg/kg or above doses and a decrease in calcium (Ca++) in males of the 60 and 200 mg/kg groups. Moreover, there were decreases in cholinesterase (ChE) activity, total protein (TP) and albumin (Alb) values, as well as increases in blood urea nitrogen (BUN), uric acid (UA) and potassium (K+) in both sexes of the 200 mg/kg group, along with elevations in GOT and lactate dehydrogenase (LDH) activities in females of the 200 mg/kg group. 6. The absolute and/or relative organ weights for liver, kidneys, spleen and adrenals were increased in the 200 mg/kg group. 7. On pathological examination, perforating ulceration in the jejunum and ileum, turbid ascites, adhesion and inflammatory changes in capsules of the abdominal organs, splenomegaly, mesenteric lymph node hyperplasia and inflammatory changes in the thoracic cavity were observed in dead animals of the 200 mg/kg group. Similar pathological changes were observed in a few survival cases of the 200 mg/kg group. 8. After a one month recovery period, the above-mentioned changes had mostly recovered, indicating that they were reversible.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Three-month oral subacute toxicity study of mofezolac (N-22) in rats]. 223 86

Pyridostigmine bromide, a reversible cholinesterase inhibitor, was administered orally (capsule gavage) to beagle dogs (10-15 months of age) of both sexes once daily at 5, 10, or 20 mg/kg for 14 days; every 8 hr at 2 or 5 mg/kg for 28 days; or every 8 hr at 0.05, 0.5, or 2 mg/kg for 3 months as part of its preclinical safety assessment. A small portion of the dogs receiving pyridostigmine for 3 months were allowed an untreated recovery period of an additional 3 months. Daily doses of 10 or 20 mg/kg were lethal to some of the dogs when given for up to 14 days and caused severe intestinal distress, including diarrhea, emesis, and reddened feces in all animals. The cause of death was intestinal intussusception. Signs of systemic toxicity apparent at these doses included hypersalivation and tremors. Similar but less severe effects were produced by 5 mg/kg per day; plasma cholinesterase activities were inhibited by all three doses in a dose-related manner. Signs of toxicity in the 28-day and 3-month studies were generally limited to the gastrointestinal tract and included diarrhea or soft stools and reddened or mucoid-containing stools; these signs appeared to reverse upon discontinuation of the drug. A single dog at 2 mg/kg every 8 hr developed an apparent intussusception. There were no pathological changes in clinical chemistry, hematology, or urinalysis parameters associated with doses of 0.05, 0.5, or 2 mg/kg every 8 hr for up to 3 months, nor were any drug-related lesions observed upon gross necropsy and microscopic evaluation of the major tissues and organs. Red blood cell (RBC) acetylcholinesterase (AChE) activities in the 3-month study were inhibited by approximately 10, 50, and 70% in the 0.05, 0.5, and 2 mg/kg every 8-hr dose groups, respectively, and these degrees of inhibition were maintained throughout the period of treatment. These data suggest that prolonged oral administration of pyridostigmine at doses sufficient to cause profound and sustained inhibition of RBC AChE activity (i.e., as high as 70%) cause mainly local, gastrointestinal distress related to altered intestinal motility. At the extreme, this can be manifested as a life-threatening intestinal intussusception. Systemic anticholinesterase effects (other than enzyme inhibition) were observed only at doses of 2 mg/kg and greater, while local (gastrointestinal) effects and inhibition of RBC AChE were observed at doses as low as 0.05 mg/kg.
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PMID:Pharmacological and toxicological evaluation of orally administered pyridostigmine in dogs. 230 21


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