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)

Preparations from alloxan diabetic rats showed a reduced sensitivity to the neuromuscular blocking action of (+)-tubocurarine but no alteration in sensitivity to the depolarizing neuromuscular blocking drug decamethonium. Physostigmine was less effective in augmenting twitch height in preparations from alloxan diabetic rats and such preparations had a significantly lowered total cholinesterase activity compared with control preparations. An additional observation was a reduction in the effectiveness of the pre-junctionally active agent beta-bungarotoxin in producing neuromuscular blockade in physostigmine-treated preparations from alloxan diabetic rats. All the changes produced by alloxan administration were prevented by treatment with insulin.
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PMID:The effect of acute alloxan diabetes on the sensitivity of the rat skeletal neuromuscular junction to drugs. 21 52

The present study investigated the effect of insulin in vivo on the changes in the cooperativity of a membrane-bound enzyme. The allosteric inhibition by F- of the erythrocyte membrane acetylcholinesterase (acetylcholine hydrolase, EC 3.1.1.7) was studied during intravenous glucose tolerance tests in control and alloxan-induced diabetic rats. In the former group, the value of n decreased from 1.6 to 1.0 whereas it remained about 1.6 in the latter groups. Intravenous injection of insulin (30 U/kg) decreased the values of n in both groups. It is suggested that the in vivo insulin action on membrane cooperative enzymes could also take place in insulin target cells.
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PMID:Biomembrane cooperative enzymes. In vivo modulation of rat erythrocyte acetylcholinesterase by insulin in normal and diabetic conditions. 48 90

Distribution and activity of acetylcholinesterase (AChE) in the neurons of the central vagal nuclei at the level of the medulla oblongata were studied in intact and alloxan-diabetic adult male rats by Gomori's histochemical method. Peculiarities of intracellular distribution of the enzyme in the Nucl. dorsalis n. vagi (ND) and Nucl. ambiguus n. vagi (NA) of intact animals were demonstrated. Changes in the ratio of cholinergic neurons with moderate and strongly-positive AChE staining reactions were revealed in the ND of alloxan-diabetic rats. The dynamics of the changes attested to increased AChE activity of these neurons in response to insulin deficiency. The data obtained are additional evidence for the responsiveness of ND neurons to insulin deficiency, which was demonstrated earlier in alloxan-diabetic rats by karyometry (Akmayev and Rabkina, 1976 b). It is suggested that changes in the plasma glucose or insulin levels may be the stimulus that influences the activity of the ND cholinergic neurons. By means of this mechanism the central vagal nucleus at the medulla oblongata level may be implicated in the feedback control of insulin secretion.
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PMID:CNS--endocrine pancreas system. III. Further studies on the vagal responsiveness to insulin deficiency. 66 40

A syngeneic transplantation of 150 islets into the subcapsular renal space was performed on normoglycemic or alloxan-induced diabetic male C57BL/6 mice. Six, 8, 14, or 20-21 wk after transplantation, the graft-bearing kidney was removed and processed for microscopical examinations with indirect immunofluorescence for neuropeptides and tyrosine hydroxylase, and with acetylcholinesterase staining to visualize nerve fibers within the graft. Six weeks after implantation, only a few scattered nerve fibers were observed within the grafts. A progressive increase in the number of nerves was observed until 14 wk after transplantation, after which, a stable level was reached. Alloxan-induced diabetic mice showed quantitatively and qualitatively similar reinnervation to normoglycemic mice 20 wk after transplantation. The findings demonstrate the presence of sympathetic nerve fibers (containing tyrosine hydroxylase and neuropeptide Y), mainly accompanying ingrowing blood vessels; parasympathetic nerve fibers (containing acetylcholinesterase and vasoactive intestinal peptide), possibly reaching the graft from the adjacent renal capsule; and afferent nerve fibers (containing substance P and calcitonin gene-related peptide), which were less numerous. The data suggest that transplanted islets become reinnervated by ingrowth of nerve fibers from the implantation organ and that several types of nerves are present.
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PMID:Reinnervation of syngeneic mouse pancreatic islets transplanted into renal subcapsular space. 134 84

Acetylcholinesterase activity and pseudocholinesterase activity were examined in plasma and in striated muscles (whole heart and diaphragm muscles) of diabetic KK-CAy mice. Both activities of acetylcholinesterase in heart muscle and pseudocholinesterase in plasma were significantly increased in diabetic KK-CAy mice compared to pre-diabetic KK-CAy mice. Both acetylcholinesterase and pseudocholinesterase activities in skeletal muscle were not changed by the diabetic state. The increases in activity of plasma pseudocholinesterase was significantly correlated to the increase in blood glucose level in alloxan-, streptozotocin (STZ)-diabetic ddY mice and diabetic KK-CAy mice. The increase was not correlated to the body weight in non-diabetic female-KK-CAy mice. Furthermore, the activity of heart acetylcholinesterase was significantly correlated with the activity of plasma pseudocholinesterase (r = 0.79, P less than 0.01). The activities of acetylcholinesterases in heart muscles from STZ- and alloxan-diabetic ddY mice also tended to increase. The hypersensitivity of the pulse rate to a low dose (1 mg/kg) of acetylcholine was correlated to the activity of plasma pseudocholinesterase (r = -0.51, P less than 0.05). These results demonstrate that the activities of plasma pseudocholinesterase were increased by the diabetic state being associated with the increasing alteration of cardiac sensitivity to acetylcholine in the whole body.
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PMID:Increase in the activities of plasma pseudocholinesterase dependent on the blood glucose level and its relation to the hypersensitivity to acetylcholine in striated muscles of KK-CAy mice with diabetes. 215 Feb 10

The anterograde and retrograde axonal flow of acetylcholinesterase were studied in the sciatic nerve of alloxan-diabetic rats after five weeks of experimental diabetes. A slight reduction of the anterograde axonal flow of the enzyme was found in alloxan-diabetic compared to control rats. Sedimentation analysis revealed a major reduction of anterograde axonal flow of the light globular forms of the enzyme (G1 + G2), which are probably conveyed by slow transport. There was also a minor reduction of the anterograde flow of the globular form G4, while no modification of the axonal flow of the heavy asymmetric form A12 was found. Both G4 and A12 molecular forms are conveyed by fast axonal transport. In contrast, no abnormality of the retrograde axonal flow of acetylcholinesterase was observed. Ganglioside treatment antagonized the decline of the anterograde axonal flow of the enzyme in alloxan-diabetic rats. These results are consistent with the view that experimental diabetic neuropathy is associated with axonal transport defects, and suggest a protective effect of ganglioside treatment against neuronal damage(s) related to the diabetic syndrome.
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PMID:Impaired axonal transport of acetylcholinesterase in the sciatic nerve of alloxan-diabetic rats: effect of ganglioside treatment. 242 5

Using histochemical and immunocytochemical methods the intramural neural tissue of the pancreas was investigated in non-diabetic and in alloxan-diabetic rats. It was demonstrated that the non-diabetic pancreas contains an average of 2.71 cells/mm3 tissue that react positive for activity of acetylcholinesterase and 2.38 cells/mm3 tissue that show monoamine oxidase activity. Both cholinergic and monoaminergic cells are found as solitary cells and in clusters of various sizes. All these cells are embedded in the exocrine tissue. Both histochemical methods revealed the presence of intra-insular fiber plexuses. Treatment with alloxan resulted in disappearance of intra-insular cholinergic and monoaminergic activity and also in a 68% reduction of the cholinergic cells and 54% of the monoaminergic cells in the diabetic pancreas. Application of immunocytochemical methods employing antibodies against norepinephrine and dopamine demonstrated the noradrenergic character of at least some of the monoaminergic cell groups. It is discussed how the present data and data from previous innervation studies provide evidence for an intramural ganglionic organization of the sympathetic innervation of the rat pancreas.
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PMID:Autonomic innervation of the pancreas in diabetic and non-diabetic rats. A new view on intramural sympathetic structural organization. 351 79

We examined the effects of alloxan-diabetes on the kinetic properties of the soluble and the membrane-bound forms of acetylcholinesterase (AChE) in rat brain. The Km (0.15 mM) and Vmax. (1.5 mmol/min per mg of protein) of the soluble form of the enzyme were unchanged in the diabetic animals. The membrane-bound enzyme in the control group displayed a lower Km (0.09 mM) and a higher Vmax. (7.2 mmol/min per mg of protein) compared with the soluble form of the enzyme; the diabetic state caused a significant increase (40%) in both Km and Vmax. Kis values were about 3-4 times higher for the membrane-bound enzyme in both control and diabetic animals. The results suggest that membrane binding and membrane alterations in diabetes can significantly influence the kinetic properties of AChE.
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PMID:Alloxan-diabetes alters kinetic properties of the membrane-bound form, but not of the soluble form, of acetylcholinesterase in rat brain. 774 92

1. Diabetic modifications of nicotinic receptor-operated noncontractile Ca2- mobilization observed in the presence of anticholinesterase were investigated by measuring Ca(2+)-aequorin luminescence in diaphragm muscles of mice with diabetes induced by injections of streptozotocin (150 mg kg-1, bolus i.v.) and alloxan (85 mg kg-1, bolus i.v.). 2. The diabetic state accelerated the decline of noncontractile Ca2+ transients without affecting their peak amplitude. Insulin treatment reversed this alteration. 3. The increase in contractile Ca2+ transients by cholinesterase inhibition was attenuated 0.6 fold and became resistant to changes in [Ca2+]o in the diabetic state. 4. Changes in extracellular pH from 7.6 to 5.6 depressed the peak amplitude of noncontractile Ca2+ transients without affecting their duration, and enhanced the peak amplitude of contractile Ca2+ transients. 5. These results suggest that the inactivation process of noncontractile Ca2+ mobilization is promoted in diabetic muscles, presumably by desensitization of the nicotinic acetylcholine receptor.
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PMID:Diabetic state-induced rapid inactivation of noncontractile Ca2+ mobilization operated by nicotinic acetylcholine receptor in mouse diaphragm muscle. 859 Sep 90

The present study was carried out to investigate the effects of Lupinus albus, L. (Lupinus termis), family L. leguminosae, Cymbopogon proximus, (Halfa barr), family Gramineae, and Zygophyllum coccineum L. (Kammun quaramany), family L. Zygophyllacae on biochemical parameters in alloxan-induced diabetic rats. A dose of 1.5 ml of aqueous suspension of each herb/100 g body weight (equivalent to 75 mg/100 g b.wt.) was orally administered daily to alloxan-diabetic rats for 4 weeks. The levels of glucose, urea, creatinine and bilirubin were significantly (P<0.05) increased in plasma of alloxan-diabetic rats compared with the control group. In contrast, total protein and albumin were significantly decreased by 25 and 46%, respectively, versus control. Treatment of the diabetic rats with repeated doses of any one of the three herb suspensions could restore the changes of the above parameters to their normal levels after 4 weeks of treatment. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH) and alkaline phosphatase (AlP) activities were significantly (P<0.05) increased in the plasma of alloxan-diabetic rats. However, acetylcholinesterase activity was significantly (P<0.05) decreased in the plasma compared with the control group, whereas, such activity did not change in brain. The activities of AST, ALT and LDH were significantly (P<0.05) decreased in the liver of alloxan-diabetic rats by 58, 21 and 40%, respectively, and such activities increased in testes by 39, 26 and 26%, respectively, compared with the control group. Also, brain LDH was significantly (P<0.05) increased. Treatment of the diabetic rats with the aqueous suspension of the tested herbs restored the activities of the above enzymes to their normal level in plasma, liver and testes. The present results showed that the herb suspensions exerted antihyperglycemic effects and consequently may alleviate liver and renal damage caused by alloxan-induced diabetes.
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PMID:Biochemical study on the effects of some Egyptian herbs in alloxan-induced diabetic rats. 1178 59


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