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)

1. The enzymic utilization of O-acetyl-l-carnitine other than via carnitine acetyltransferase (EC 2.3.1.7) was investigated in liver homogenates from rats, sheep and dry cows. 2. An enzymic utilization of O-acetyl-l-carnitine via hydrolysis of the ester bond to yield stoicheiometric quantities of acetate and l-carnitine was demonstrated; 0.55, 0.53 and 0.30mumol of acetyl-l-carnitine were utilized/min per g fresh wt. of liver homogenates from rats, sheep and dry cows respectively. 3. The acetylcarnitine hydrolysis activity was not due to a non-specific esterase or non-specific cholinesterase. O-Acetyl-d-carnitine was not utilized. 4. The activity was associated with the enriched outer mitochondrial membrane fraction from rat liver. Isolation of this fraction resulted in an eightfold purification of acetylcarnitine hydrolase activity. 4. The K(m) for this acetylcarnitine utilization was 2mm and 1.5mm for rat and sheep liver homogenates respectively. 6. There was a significant increase in acetylcarnitine hydrolase in rats on starvation and cows on lactation and a significant decrease in sheep that were severely alloxan-diabetic. 7. The physiological role of an acetylcarnitine hydrolase is discussed in relation to coupling with carnitine acetyltransferase for the relief of ;acetyl pressure'.
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PMID:Enzymic hydrolysis of acetylcarnitine in liver from rats, sheep and cows. 0 59

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

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

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

Elevated serum butyrylcholinesterase (BChE) activity in the diabetic rat, mouse and human is very evident. The source of the increased level of BChE in the diabetic condition is not known. The effect of diabetes on cardiac BChE has not been studied so far, in spite of high BChE levels in the heart. In the present study, we investigated the effect of alloxan-induced diabetes on serum and on the soluble as well as the membrane-bound form of cardiac BChE activity and their substrate kinetics. We included rats of both sexes in the study. Serum BChE activity increased only in male diabetic rats (2.3-fold), while the activities of the soluble as well as the membrane-bound form of cardiac BChE activity increased 2.2- to 2.8-fold in male diabetic rats. A smaller increase (30%) was observed in the activity of the membrane-bound form of cardiac BChE in female diabetic rats. A slight reduction in BChE activity was observed in male and female rats after insulin treatment. The activity ratio of the soluble to the membrane-bound form of cardiac BChE was higher in diabetic and insulin-treated diabetic rats as compared with controls. The K(m) values of component II of the serum and soluble forms of cardiac BChE were comparable. In conclusion, the diabetes-induced increase in serum and cardiac BChE activity was sex dependent. Insulin was not able to rectify the diabetes-induced abnormalities in serum and cardiac BChE activity. The heart could be one of the possible sources of the increased level of serum BChE.
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PMID:Effect of alloxan-induced diabetes on serum and cardiac butyrylcholinesterases in the rat. 1237 9

Our previous study showed that chromium malate improved the regulation of blood glucose in mice with alloxan-induced diabetes. The present study was designed to evaluate the 90-day oral toxicity of chromium malate in Sprague-Dawley rats. The present study inspected the effect of chromium malate on glycometabolism, glycometabolism-related enzymes, lipid metabolism, and learning and memory ability in metabolically healthy Sprague-Dawley rats. The results showed that all rats survived and pathological, toxic, feces, and urine changes were not observed. Chromium malate did not cause measurable damage on liver, brain, and kidney. The fasting blood glucose, serum insulin, insulin resistance index, C-peptide, hepatic glycogen, glucose-6-phosphate dehydrogenase, glucokinase, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglyceride levels of normal rats in chromium malate groups had no significant change when compared with control group and chromium picolinate group under physiologically relevant conditions. The serum and organ content of Cr in chromium malate groups had no significant change compared with control group. No significant changes were found in morris water maze test and superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and true choline esterase (TChE) activity. The results indicated that supplementation with chromium malate did not cause measurable toxicity and has no obvious effect on glycometabolism and related enzymes, learning and memory ability, and related enzymes and lipid metabolism of female and male rats. The results of this study suggest that chromium malate is safe for human consumption.
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PMID:Evaluation of 90-day Repeated Dose Oral Toxicity, Glycometabolism, Learning and Memory Ability, and Related Enzyme of Chromium Malate Supplementation in Sprague-Dawley Rats. 2590 May 79

The present work deal with the effect of alloxan-induced diabetes on kidney oxidative stress and dysfunction of virgin and pregnant rat as well as the protection that may be afforded by high dosage GSSE (4g/kg) treatment. Diabetes affected negatively several kidney function parameters as creatinemia, uremia, uricemia and proteinuria without affecting kidney index. Diabetes also induced an oxidative stress characterized by increased lipid and protein oxidation, a drop in antioxidant enzyme defenses as catalase, superoxide-dismutase, glutathione-peroxidase, an alteration in transition metals as free iron, copper, selenium and associated enzymes and an increase in calpain and acetyl-cholinesterase activities. Tremendously, GSSE treatment protected efficiently against all the deleterious effects of diabetes-induced kidney dysfunction in both virgin and pregnant animals. High dosage GSSE is a safe and potent anti-oxidant that may be further tested in clinical trials for the long-term preservation of kidney function especially in multiple pregnancies.
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PMID:Protective effect of grape seed and skin extract against diabetes-induced oxidative stress and renal dysfunction in virgin and pregnant rat. 2745 14