Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Soman, (pinacoloxymethyl-phosphoryl fluoride) (0.1-10 microM) an irreversible cholinesterase inhibitor, reversibly reduced the duration of calcium (Ca2+)- and barium (Ba2+) spikes without significantly affecting spike amplitude in sympathetic postganglionic neurons of the adult bullfrog (Rana catesbeiana). The soman-induced shortening of the spike duration was not prevented by pretreatment with either (+)-tubocurarine (100 microM) or hexamethonium (100 microM) and atropine (10 microM) and was also recorded from acutely-dissociated sympathetic neurons. These results suggest that soman has a direct action to decrease calcium entry through voltage-dependent channels activated during a spike. This effect may contribute to both the decrease in the duration of the spike after-hyperpolarization (AHP) and the enhanced neuronal excitability produced by soman in these neurons.
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PMID:Soman reversibly decreases the duration of Ca2+ and Ba2+ action potentials in bullfrog sympathetic neurons. 166 74

1. The influence of castration on contraction of the guinea pig vas deferens induced by acetylcholine was investigated regarding facilitation of endogenous neurotransmitter release, changes in post-synaptic events and modification in acetylcholine metabolization. 2. Castration prolonged the duration of the isometric contraction of the vas deferens induced by acetylcholine (3 mM) but not the duration of that induced by barium chloride (10 mM). 3. Reserpinization (0.5 mg/kg) of normal and castrated guinea pigs did not change the time-course of acetylcholine-induced contraction in the vas deferens. 4. 4-Aminopyridine (0.05 mM) prolonged the contraction induced by acetylcholine and barium chloride. This effect was blocked by reserpine pretreatment, indicating that in the presence of 4-AP, both acetylcholine and barium release endogenous noradrenaline. Since there was no difference between the effects of 4-AP on organs from normal and castrated animals, prolongation of the acetylcholine-induced contraction is not related to an increase in neutransmitter release. 5. Total cholinesterase and acetylcholinesterase activities were reduced after castration and the time-course of carbachol contraction was not changed. Thus, this decrease in enzyme activity appears to play a relevant role in the prolongation of acetylcholine-induced contraction.
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PMID:The time-course of contractions induced by acetylcholine and barium in the vas deferens of normal and castrated guinea-pigs. 365 28

Brief transmural stimuli, which selectively excited cholinergic fibres, initiated contractions and excitatory junction potentials in preparations of longitudinal muscle isolated from the guinea-pig ileum: these responses were associated with an increase in the internal concentration of calcium ions. When muscle voltage-dependent calcium channels were blocked using the organic calcium antagonist nifedipine, brief stimuli continued to initiate contractions, evoke excitatory junction potentials and cause an increase in the intracellular calcium concentration. Ionophoretically applied acetylcholine caused depolarizations which resembled the excitatory junction potentials evoked by cholinergic nerve stimulation. Both responses had slow time courses and were abolished by muscarinic receptor antagonists. However, the depolarizations produced by ionophoretically applied acetylcholine, unlike those produced by nerve stimulation, were frequently interrupted by transient hyperpolarizations. The transient hyperpolarizations were abolished by barium ions or charybdotoxin. High concentrations of the calcium antagonists nicardipine, verapamil or diltiazem had a tendency to preferentially abolish the excitatory junction potential. When the effects of the cholinesterase inhibitor, eserine, on excitatory junction potentials were examined, it became apparent that when the destruction of acetylcholine was prevented it initiated an additional conductance change to that initiated by acetylcholine in untreated tissues. The results are discussed in relation to the idea that neuronally released acetylcholine and applied acetylcholine might activate different subsets of muscarinic receptors on longitudinal ileal smooth muscle.
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PMID:Neuronally released and applied acetylcholine on the longitudinal muscle of the guinea-pig ileum. 775 96

Studies have shown that inflammatory (cholesterol esterase, CE) and salivary (pseudo-cholinesterase, PCE) enzymes can cause the breakdown of bisphenol-A diglycidyl dimethacrylate (bisGMA) and triethylene glycol dimethacrylate (TEGDMA) components from composite resins. Based on the above consideration, it was desired to show how CE- and PCE-catalyzed hydrolysis of resin components was dependent on the enzymes' concentration and to determine their distinct specificities (if any) towards resin components. Photopolymerized model composite resin samples (60% weight fraction silanated barium glass filler) based on bisGMA and TEGDMA monomers (55/45 weight ratio of the matrix, respectively) were incubated with PBS and either 0.01, 0.05, 0.1 or 1 unit/ml of CE or PCE for 16 days (pH 7.0, 37 degrees C). Incubation solutions were analyzed by high-performance liquid chromatography (HPLC), UV spectroscopy and mass spectrometry. The composite samples were characterized by scanning electron microscopy (SEM). Degradation rates of bisGMA and TEGDMA monomers were assessed. The results showed that CE had a greater specificity towards cleaving bisGMA while PCE showed a greater specificity towards TEGDMA. A strong enzyme concentration dependence was observed which suggests that the level of degradation products generated for a material will depend on the esterase make-up of an individual's saliva in combination with the specific formulation of monomer components used.
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PMID:Biodegradation of a dental composite by esterases: dependence on enzyme concentration and specificity. 1453 61

It has been demonstrated that human saliva contains cholesterol esterase (CE)- and pseudocholinesterase (PCE)-like hydrolase activities. While PCE has been shown to preferentially degrade triethylene glycol dimethacrylate (TEGDMA) and its derivatives, CE has a greater catalytic effect on the breakdown of bis-phenol-A-diglycidyl dimethacrylate (bisGMA) components in composite dental resins. The current study seeks to determine if there is a mutual influence between the different esterases with respect to the biodegradation of resin composite. Photopolymerized model composite resin samples (containing 60% by weight fraction of silanated barium glass filler) based on bisGMA/TEGDMA (bis) or urethane-modified bisGMA/TEGDMA/bisEMA (ubis) monomers were incubated in buffer, CE and/or PCE solutions (pH=7.0, 37 degrees C) for 8 and 16 days. The incubation solutions were analyzed for degradation products using high-performance liquid chromatography, UV spectroscopy and mass spectrometry. In the bis system, higher amounts (p<0.05) of a bisGMA derived product, bishydroxy-propoxyphenyl-propane (bisHPPP), were detected in the combined enzyme group as compared to the sum of the two individual enzyme groups. In the ubis system, similar comparisons showed that higher levels (p<0.05) of bisHPPP were detected in the combined group at 8 days while higher amounts (p<0.05) of a bisEMA derived product, ethoxylated bis-phenol A, were detected in the combined group at 16 days. The study concluded that CE and PCE act synergistically to increase the biodegradation of both composite resin materials.
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PMID:Mutual influence of cholesterol esterase and pseudocholinesterase on the biodegradation of dental composites. 1473 42

The alpha7 nicotinic acetylcholine receptor (nAChR) plays a key role in neural development and neurodegeneration. Here, we identify a novel, modulatory receptor ligand, a 14-amino acid peptide (AEFHRWSSYMVHWK) derived from the C-terminus of acetylcholinesterase (AChE). In three different in vitro preparations, this 'AChE-peptide' is bioactive in a ligand-specific and concentration-dependent manner. First, it modulates acutely the effect of acetylcholine (ACh) on Xenopus oocytes transfected with human alpha7, but not alpha4/beta2, nAChR. The action persists when intracellular calcium is chelated with BAPTA or when calcium is substituted with barium ions. This observation suggests that intracellular Ca(2+) signals do not mediate the interaction between the peptide and nAChR, but rather that the interaction is direct: however, the intervention of other mediators cannot be excluded. Secondly, in recordings from the CA1 region in guinea-pig hippocampal slices, AChE-peptide modulates synaptic plasticity in a alpha-bungarotoxin (alpha-BgTx)-sensitive manner. Thirdly, in organotypic cultures of rat hippocampus, long-term exposure to peptide attenuates neurite outgrowth: this chronic, functional effect is selectively blocked by the alpha7 nAChR antagonists, alpha-BgTx and methyllycaconitine, but not by the alpha4/beta2-preferring blocker dihydro-beta-ethroidine. A scrambled peptide variant, and the analogous peptide from butyrylcholinesterase, are ineffective in all three paradigms. The consequences of this novel modulation of the alpha7 nAChR may be activation of a trophic-toxic axis, of relevance to neurodegeneration.
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PMID:A novel peptide modulates alpha7 nicotinic receptor responses: implications for a possible trophic-toxic mechanism within the brain. 1522 89

Dysphagia is a common problem in elderly patients and a rare manifestation of Graves' disease. We report a case of an 82-year-old male who presented with a 4-week history of dysphagia and weight loss. Workup for his dysphagia with upper endoscopy, MRI brain, electromyography, acetyl-cholinesterase receptor antibodies, and voltage-gated calcium channel antibodies were negative. Modified Barium swallow test showed oropharyngeal dysphagia. Thyroid function tests that revealed hyperthyroidism and antibodies to TSH-receptor were positive. Based on the above findings, we considered Graves' disease as the most likely diagnosis. Patient was treated with methimazole and beta-blockers and subsequently his dysphagia resolved. This paper highlights the importance to clinicians of considering thyrotoxicosis as possible diagnosis in an elderly patient presenting with unexplained dysphagia.
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PMID:Thyrotoxic Dysphagia in an 82-year-old male. 2131 89