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)

Electromyographic (EMG) examinations were performed on Beagles before and for 7 days after oral administration of one of the following organophosphate (OP) compounds; ronnel (55.0 or 110.0 mg/kg), dichlorvos (29.7, 59.4, or 148.5 mg/kg), or cythioate (24.8 or 33.0 mg/kg). The EMG values determined were evoked potentials, after-discharge activity, F-wave activity, nerve conduction velocity, and motor unit potential activity associated with interosseous and pectineal reflexes. Erythrocyte cholinesterase (ChE) activities were measured in some dogs. Ronnel did not have an effect on ChE activity, whereas dichlorvos and cythioate, at all dosage levels, had an inhibitory effect. Some dogs had minor signs of OP toxicosis. The EMG changes for individual OP compounds were not statistically significant (P greater than 0.05), but pooled results revealed an increased duration of evoked potentials, increased after-discharge activity, and decreased F-wave activity; however, only the effect on duration was significant (P less than 0.05). Reflex motor unit potential activity and nerve conduction velocities were not affected. Effects of neostigmine (0.1 to 0.4 mg/kg) given IV to anesthetized, atropinized Beagles were similar to those effects shown by pooled data for the OP compounds, but considerably more muscle fasciculation was produced. Results of this study indicate that even when erythrocyte ChE activity is reduced by OP compounds at dosage levels that produce no or minimal visible signs of toxicosis, EMG reveals little evidence for increased motor unit irritability.
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PMID:Motor unit irritability in Beagles Before and after exposure to cholinesterase inhibitors. 8 24

Male Sprague-Dawley rats when administered sc a sublethal dose of organophosphorus cholinesterase inhibitors such as the nerve agents, soman (100 micrograms/kg, sc), sarin (110 micrograms/kg, sc), tabun (200 micrograms/kg, sc), or VX (12 micrograms/kg, sc), developed seizures and severe muscle fasciculations within 15-20 min, lasting for 4-6 hr. Marked inhibition of acetylcholinesterase (AChE) and necrotic lesions in skeletal muscles such as soleus, extensor digitorum longus, and diaphragm were evident between 1-24 hr following injection. Pretreatment with memantine HCl (MEM, 18 mg/kg, sc) together with atropine sulfate (ATS, 16 mg/kg, sc), 60 min and 15 min, respectively, prior to nerve agents attenuated AChE inhibition, prevented myonecrosis, and muscle fasciculations as well as other signs of cholinergic toxicity. Pretreatment combining d-tubocurarine (d-TC, 0.075 mg/kg, sc) and ATS (16 mg/kg, sc) prevented the myonecrosis and fasciculation without protecting AChE against inhibition by these nerve agents. Neither MEM, d-TC, nor ATS in the concentration given interfered with the normal behavior of the rats. The role of d-TC and ATS interaction with presynaptic receptors regulating ACh release and MEM's role in modulating neural hyperactivity as protective mechanisms are discussed.
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PMID:Potential of memantine, D-tubocurarine, and atropine in preventing acute toxic myopathy induced by organophosphate nerve agents: soman, sarin, tabun and VX. 147 66

We describe a 54-year-old man with myasthenia gravis, thymoma, systemic muscle twitch particularly of both lower limbs, hyperhidrosis and lower limb pain. The muscle twitch resembled to fasciculation rather than to myokymia and was persistent after discontinuation of anti-acetylcholinesterase drug. No attenuation nor disappearance of the muscle twitch was educed by spinal anesthesia. However, it disappeared when a nondepolarizing type muscle relaxant (pancuronium bromide) was used. The muscle twitch was thus considered to originate from peripheral axons. Thymoma was considered to be involved in the pathogenesis of these unusual clinical manifestations which may constitute a new myasthenic syndrome.
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PMID:Myasthenia gravis, muscle twitch, hyperhidrosis and limb pain associated with thymoma: proposal of possible new myasthenic syndrome. 183 73

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

Cyanobacteria (blue-green algae) implicated in the deaths of 9 dogs at Richmond Lake, SD, on Aug 26, 1985, were analyzed. The dominant cyanobacterial species from the water sample was Anabaena flos-aquae. The lyophilized bloom material or the high-performance liquid chromatography purified toxin peak, when administered to mice IP, induced clinical signs of salivation, lacrimation, urinary incontinence, defecation, convulsion, fasciculation, and respiratory arrest. Further comparison of the semipurified bloom toxin with an irreversible anticholinesterase anatoxin-a(s), produced by A flos-aquae strain NRC-525-17, revealed the bloom toxin and anatoxin-a(s) had similar properties on high-performance liquid chromatography and on the inhibition of electric eel acetylcholinesterase (EC 3.1.1.7).
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PMID:Anticholinesterase poisonings in dogs from a cyanobacterial (blue-green algae) bloom dominated by Anabaena flos-aquae. 313 68

Clinical analysis of 378 acute cases of Malathion insecticide intoxication and pathological and histochemical investigation of skeletal muscles in 7 autopsied victims of acute poisoning have revealed the pronounced neuromuscular disorders. Generalized paresis and paralysis of muscles were observed in trunk and limbs. Muscular fasciculation, hypotonia and hyporeflexia were also generalized. Multiple foci of muscular fibers necrosis and necrobiosis were found with intermuscular nerves and motor endings degenerated, neuromuscular junctions cholinesterase sharply inactivated.
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PMID:[Clinico-morphologic and histochemical changes in the neuromuscular apparatus in acute carbophos poisoning]. 318 79

Clinical and pulmonary function changes induced by intravenous dichlorvos (2,2-dichlorvinyldimethyl phosphate) (DDVP) toxicosis, and reversibility of these changes after atropine treatment were investigated in six Friesian calves one to three months old. From one minute after dosage, all animals showed severe respiratory distress, excitation, weakness, muscle fasciculation and cholinesterase inhibition. Decrease in dynamic lung compliance and arterial oxygen tension and increase in total pulmonary resistance, viscous work of breathing and alveolar arterial oxygen gradient were highly significant (P less than 0.01). On the other hand, body secretions, heart rate, respiratory rate, tidal volume and arterial carbon dioxide tension were not significantly affected by DDVP injection. Atropine promptly and completely reversed these changes, except for muscle fasciculations, central depression and cholinesterase inhibition which disappeared progressively within 24 hours.
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PMID:Pulmonary function changes induced by experimental dichlorvos toxicosis in calves. 373 27

The influence of clonidine on the toxicity produced by two irreversible, organophosphate cholinesterase inhibitors, soman and echothiophate, was studied in mice. At lethal doses, soman produced whole body tremor but no muscle fasciculation; at lethal doses, echothiophate produced muscle fasciculations but no whole body tremor. Pretreatment with clonidine protected against several toxic manifestations of soman, but had little effect on echothiophate toxicity. In addition to its documented effects on acetylcholine metabolism, clonidine was found to be a weak inhibitor of acetylcholinesterase. At certain concentrations, clonidine protected the enzyme from permanent inactivation by soman. These findings indicate that the toxicity of soman and echothiophate reflect primarily central and peripheral actions, respectively, and that clonidine has a much greater protective effect versus the centrally-acting agent. Moreover, direct interactions with acetylcholinesterase may contribute to clonidine protection from cholinesterase inhibitor toxicity.
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PMID:Clonidine protection from soman and echothiophate toxicity in mice. 378 71

Previous studies have shown indirectly that the neuromuscular effects of nonselective cholinesterase inhibitors are mediated through the inhibition of acetylcholinesterase (AChE). To test this hypothesis more directly we studied the effects of the specific inhibitor of AChE, BW 284c51, at the neuromuscular junction of rat diaphragms. BW 284c51 inhibits AChE in a dose-dependent partially reversible manner at all concentrations tested (10(-9) to 10(-4) M). Maximum inhibition was never greater than 92%. The drug increased miniature end-plate potential (MEPP) amplitude and prolonged half-decay time at 10(-7) and 10(-6) M. However, BE 284c51 had no effect on the resting membrane potential at any concentration. BW 284c51 at 10(-7) M reversibly increased MEPP frequency by almost 4-fold. There was a 2-fold increase in the occurrence of giant MEPPs in the presence of BW 284c51. The quantum content (m) of the end-plate potential was increased in 10(-7) M BW 284c51 as were end-plate potential amplitude and quantum size (q). Animals injected subcutaneously with 10 mg/kg of BW 284c51 displayed typical signs of AChE inhibition including salivation, whole body tremor and prostration. Spontaneous muscle fasciculation was more noticeable after in vivo injection of BW 284c51 than after in vitro administration. Furthermore, MEPP frequencies were considerably faster when the drug was injected in vivo than when applied in vitro. The data are discussed with respect to the hypothesis that inhibition of AChE causes presynaptic as well as postsynaptic effects.
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PMID:Presynaptic and postsynaptic neuromuscular effects of a specific inhibitor of acetylcholinesterase. 625 19

Electromyographic potentials of fasciculations were studied in ten patients with amyotrophic lateral sclerosis (ALS). The EMG recordings were made from the extensor digitorum brevis muscle. The EMG recording was so selective that only one motor unit potential appeared on maximal voluntary effort and on supramaximal electrical stimulation of the peroneal nerve. In a series of fasciculations, the shapes of the EMG potentials varied, while in a series of voluntary twitch activations of electrical nerve stimulations the EMG potentials were mainly constant. Fasciculations were followed by antidromic impulses in the test unit axon as judged from collision tests, and they persisted after lidocaine blockades of the nerve to the muscle. The findings are compatible with a conclusion of distal multifocal triggering of fasciculation. Fasciculating motor units had voluntary firing properties close to those of normal low-threshold motor units. Widespread fasciculations were abolished by a nonparalytic dose of a synthetic curare derivative (Pavulon) and augmented by administration of neostigmine in two cases. The fasciculations in ALS thus have the same characteristics as experimental fasciculations evoked by cholinesterase inhibitors, and there is reason to believe that the underlying pathophysiological mechanism is similar in the two cases.
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PMID:Pathophysiology of fasciculations in ALS as studied by electromyography of single motor units. 708 17


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