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)

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

Repeated application of hexachlorocyclohexane (HCH; 50 and 100 mg/kg) and malathion (200 and 400 mg/kg) alone or in combination daily for 30 days on the skin of male guinea pigs caused mild to severe signs of toxicity and death of animals. The experimental animals exhibited tremor, dyspnea, salivation, convulsion, diarrhea and paralysis of the limbs. These were associated with significant biochemical and morphological changes in skin, liver, kidney and testes. The inhibition of acetylcholinesterase appeared highly significant in the combined treatment, but was not suggestive of any HCH and malathion potentiation. The highest level of HCH residue was seen in fatty tissue after low dose treatment. This was in contrast to the high level seen in liver after larger doses of HCH. This study suggests that HCH and malathion did not elicit any potentiation effects in the parameters monitored and at the doses tested.
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PMID:Interaction of hexachlorocyclohexane and malathion in male guinea pigs after repeated dermal application. 243 88

A 37-year-old man suffered from photosensitivity and urinary casts with serological findings of positive anti-DNA antibody, LE cells and false positive VD reaction in September of 1979. He developed general fatigue, dyspnea and diplopia with ptosis of bilateral eyelids in November of 1979, which were improved by the anti-cholinesterase drugs. In January of 1980, he had an attack of unconsciousness and his chest X-ray film showed several tumorous shadows in the anterior mediastinum and middle and lower lung fields. Treating him with chemotherapy of VEMP, the pulmonary shadows disappeared. However, he developed severe muscle weakness with an elevated CPK (430 mU/ml) and a myogenic EMG pattern along with an increased anti-acetylcholine receptor antibody (243 n Mol/l), dysphagia and eyelid-ptosis. He died in September of 1985 and his autopsy disclosed a malignant thymoma of mixed type in the anterior mediastinum and an atrophy and fibrosis with infiltration of inflammatory cells in the striated muscles.
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PMID:[An autopsy case of a patient with myasthenia gravis who showed various symptoms of collagen diseases and complicated with malignant thymoma]. 281 7

Three patients with chronic obstructive lung disease (COPD) and myasthenia gravis whose pulmonary symptoms were worsened by therapy with cholinesterase inhibitors were improved by inhaled ipratropium bromide. Two had increases in FEV1 (19 percent, 35 percent) and specific conductance (106 percent, 81 percent) and reductions in dyspnea. The third had no change in airflow with ipratropium, but improved due to decreased bronchial secretions which had limited the use of cholinesterase inhibitors. In contrast, beta agonist bronchodilators had no effect in any of these patients. This experience suggests that ipratropium may be the bronchodilator drug of choice in patients with obstructive lung disease aggravated by cholinesterase inhibitors.
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PMID:Ipratropium in patients with COPD receiving cholinesterase inhibitors. 296 27

Antibodies against acetylcholinesterase were found in the serum of a patient presenting dyspnea, generalized muscle paresis, diminished tendon reflexes, and fasciculations. Electrodiagnostic studies showed a decremental response, an incomplete interference pattern, and reduced motor nerve conduction velocity. Edrophonium administration resulted in extreme cholinergic crisis. Biopsies displayed muscle atrophy and nervous tissue degeneration. Recurrent acute respiratory failure ended in death. The patient's serum pseudocholinesterase and red blood cells acetylcholinesterase levels were generally very low, with periodical fluctuations. Minute quantities of the patient's serum inhibited the activity of cholinesterases from normal human serum and from various fetal tissues. Enzyme inhibition was abolished following preadsorption of the serum immunoglobulins with goat antihuman Fab, and radioiodinated acetylcholinesterase from human erythrocytes was precipitated by the patient's serum, confirming that anticholinesterase antibodies were present. Acetylcholinesterase extracted from fetal striated muscle with detergent and salt was inhibited to a larger extent than the enzymes similarly prepared from other fetal tissues and more efficiently than buffer-soluble muscle enzyme. These findings suggest that the patient's serum contained antibodies which interacted preferentially with the membrane-associated forms of muscle acetylcholinesterase and indicate that autoantibodies against acetylcholinesterase could play a role in the pathogenesis of the disease.
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PMID:Antibodies against acetylcholinesterase and low levels of cholinesterases in a patient with an atypical neuromuscular disorder. 339 Sep 68

Changes in serum cholinesterase (also known as pseudo- or non-specific cholinesterase) activity have been measured in 20 patients after thermal injury. In 19 patients a marked fall was noted at around day 5 post-burn, and recovery to normal levels was variable and in some cases prolonged. A variety of symptoms, for example, dyspnoea and confusion, have been attributed to lowered serum cholinesterase activity and some workers have gone so far as to advocate blood transfusion to treat such a condition (Price et., 1970; Frohlich, 1977). In this study we found 13 patients (65 per cent) with such symptoms coexisting with a low serum cholinesterase activity. However, we do not believe these symptoms were directly attributable to the low enzyme activity for the following reasons: In only three of the 13 patients were symptoms observed at times when the lowest cholinesterase activity was recorded. A conventional explanation for these symptoms was available, except in three cases with abdominal distension. In six cases no symptoms were observed despite very low cholinesterase levels.
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PMID:Serum cholinesterase levels after thermal injury. Is treatment required? 360 63

1. Endosulfan insecticide is a polychlorinated compound used for controlling a variety of insects; it is practically water-insoluble, but readily adheres to clay particles and persists in soil and water for several years. Its mode of action involves repetitive nerve-discharges positively correlated to increase in temperature. This compound is extremely toxic to most fish and can cause massive mortalities. In fish, it causes marked changes in Na and K concentrations, decrease in blood Ca(2+) and Mg levels and inhibits Na, K and Mg-dependent ATPase (in brain). 2. Bioaccumulation of endosulfan is reported for marine animals; however, freshwater animals (e.g., crayfish) accumulate it to some extent, but they lose the compound rapidly during depuration. Endosulfan is generally less toxic to aquatic invertebrates than fish. However, it causes decreases in adenylate energy charge, oxygen consumption, hemolymph amino acids, succinate dehydrogenase, heart-beat (mussel) and altered osmoregulation. 3. Generally, mammals are less susceptible to endosulfan's toxicity than aquatic animals. The majority of studies conducted on laboratory mammals can be summarized. (a) Neurotoxicity: male rats are more sensitive than females to endosulfan, which decreases brain and plasma acetylcholinesterase activity. Endosulfan I (a metabolite) causes a significant change in norepinephrine, 5-HT and GABA. (b) Renal toxicity: inhibition of MFOs activity was noticed in rats; other effects included changes in proximal convoluted tubules and necrosis of the tubular epithelium. (c) Hepatotoxicity: chemically-induced aminopyrine N-demethylase and aniline hydrolase were found in rat liver, and reduction in the glycogen level occurred. (d) Hematologic toxicity: endosulfan exposure resulted in a significant decrease in the level occurred. (d) Hematologic toxicity: endosulfan exposure resulted in a significant decrease in the erythrocyte glutathione reductase, hemoglobin amount, RBC number and mean corpuscular volume. 4. Respiratory toxicity: involved dyspnea, acute emphysema, cyanosis and hemorrhages in teh interalveolar portions of rat's lungs. 5. Biochemical: in rats, endosulfan caused increased glucose-6-phosphate dehydrogenase activity, blood glucose level, phospholipid contents of the microsomal and surfactant system, and profoundly induced the activity of alcohol dehydrogenase and cytosolic glutathione S-transferases. It also decreased significantly Na+, K+ and Mg(2+) ATPases, plasma calcium level and alkaline phosphatase in the intestinal epithelium. 6. Immunologic toxicity: rat serum antibody titer to tetanus toxin, IgG, IgM and gammaglobulins were significantly reduced. 7. Reproductive toxicity: degenerative changes in the seminiferous epithelium, induction of the rate-limiting enzyme in testosterone production (3beta-hydroxysteroid transferase and 17 beta-hydroxysteroid transferase), histological changes in reproductive organs, testicular atrophy and the occurrence of ovarian cysts were noticed in rat. Reduction in the weight of secondary sex organ was also observed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Bioaccumulative potential and toxicity of endosulfan insecticide to non-target animals. 790 Sep 59

Chronic obstructive pulmonary disease (COPD) is a disease involving either or both of chronic bronchitis and emphysema. In the elderly, bronchial asthma is usually called chronic asthma because of sustained asthma attacks and resistance to therapy. Although the absolute value of IgE is low in the asthma in the elderly, IgE values correlated to the symptoms of asthma in the elderly. Therefore, asthma in the elderly is supposed to be primarily caused by allergic reactions. Airway epithelium products histamine methyl-transferase (HMT) and cholinesterase. Allergic reactions and/or virus infection in the airway epithelium reduce productions of these enzymes, which exacerbate bronchoconstriction. Steroid hormones increase these enzymes and relieve bronchoconstriction. Silent aspiration may exacerbate asthma attack in the night and recurrent cough and sputum in COPD. Macrolide antibiotics relieve chronic infections in the elderly. Plural constriction against bullae using thoracoscopy reduce dyspnea dramatically in emphysema.
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PMID:[Clinical strategy of chronic obstructive pulmonary disease in the elderly]. 811 44

A middle aged man who inhaled sarin in a train in a subway station in Tokyo in 1995 and showed a variety of symptoms including psychiatric symptoms was reported. He experienced muscle weakness, dyspnea and unconsciousness of sudden onset immediately after exposure to sarin. Marked miosis was observed on admission. Plasma cholinesterase activity was remarkably decreased at that time. He also experienced delirium consisting of visual hallucination, insomnia and irritability at mid-night for more than seven days. These psychiatric symptoms gradually improved without any medication. To date there is no detailed description of such psychiatric symptoms in sarin poisoning.
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PMID:[Psychiatric symptoms following accidental exposure to sarin--a case report]. 852 73

A 52-year-old woman had a 14-year history of stridor attacks. Pulmonary function tests revealed reversible airway obstruction, and bronchial asthma was diagnosed. She also has bilateral ptosis, diplopia, and moderate weakness of all four limbs; a positive edrophonium test confirmed the diagnosis of myasthenia gravis. Although the parasympathetic system plays an important role in the regulation of bronchial tone, in this patient the edrophonium test did not provoke an asthmatic attack or exacerbate pulmonary function, except for increases in sputum production and in frequency of cough. The general weakness was usually worse in the afternoon. The decrease in grip strength and the shortening of arm elevation time also occurred after asthma attacks, which means that general muscle fatigue was caused by the work of breathing. Furthermore, dyspnea increased and pulmonary function worsened when an anti-cholinesterase inhibitor was discontinued, probably because of respiratory muscle weakness. Accordingly, the clinical status of bronchial asthma seemed to change in parallel with that of the myasthenia gravis.
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PMID:[Bronchial asthma complicated by myasthenia gravis]. 869 67


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