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)

The effects in vivo and in vitro of benthiocarb, an organocarbamate, on acetylcholinesterase (AChE) activity and its recovery in vitro in the brain of the freshwater fish Sarotherodon mossambicus have been studied. Findings revealed that the specific activity of AChE was inhibited both in vivo and in vitro in a concentration-dependent manner. Of the different modulators tested, dexamethasone (0.72 mg), prednisolone (0.74 mg), testosterone (0.9 mg), and ADP (9.5 mg) were found to neutralize the inhibitory effect (IC50 = 0.30 microM) of benthiocarb on AChE.
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PMID:Recovery of benthiocarb-inhibited AChE in fish brain: an in vitro study. 274 20

Sarcolemmal membranes were isolated from porcine skeletal muscle by modifications of a LiBr-extraction technique. Latency determinations of acetylcholinesterase, ouabain-sensitive p-nitrophenylphosphatase, [3H]ouabain binding, and (Na+ + K+)-ATPase activities indicated that 65-76% of the membranes were sealed inside-out vesicles. The preparations were enriched in cholesterol and phospholipid, and demonstrated adenylate cyclase activity and both cAMP and cGMP phosphodiesterase activities. An indication of the purity of this fraction was that the Ca2+-ATPase activity (0.13 mumol Pi mg-1 min-1 at 37 degrees C) was 3.8% of that of porcine skeletal muscle sarcoplasmic reticulum preparations. Pertussis toxin specifically catalyzed the ADP-ribosylation of a Mr 41,000 sarcolemmal protein, indicating the presence of the inhibitory guanine nucleotide regulatory protein of adenylate cyclase, Ni. An endogenous ADP-ribosyltransferase activity, with several membrane protein substrates, was also demonstrated. The addition of exogenous cAMP-dependent protein kinase or calmodulin promoted the phosphorylation of a number of sarcolemmal proteins. The calmodulin-dependent phosphorylation exhibited an approximate K 1/2 for Ca2+ of 0.5 microM, and an approximate K 1/2 for calmodulin of 0.1 microM. 125I-Calmodulin affinity labeling of the sarcolemma, using dithiobis(succinimidyl propionate), demonstrated the presence of Mr 160,000 and 280,000 calmodulin-binding components in these membranes. These results demonstrate that this porcine preparation will be valuable in the study of skeletal muscle sarcolemmal ion transport, protein and hormonal receptors, and protein kinase-catalyzed phosphorylation.
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PMID:Components of purified sarcolemma from porcine skeletal muscle. 299 26

An enzymatic method for the determination of serum cholinesterase (ChE) activity is described. The method is based on the liberation of acetate from acetylcholine as a substrate by ChE and the conversion of the acetate to acetylphosphate and ADP in the presence of ATP by acetate kinase. The produced ADP is coupled with pyruvate kinase and lactate dehydrogenase in the presence of phosphoenolpyruvate and NADH. The amount of NADH consumed is determined by absorbance at 340 nm. The reaction proceeds stoichiometrically, and the dilution curve is linear up to 3300 U/liter. The results obtained by this method show a good correlation with those obtained by the usual methods.
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PMID:Ultraviolet spectrophotometric method for determination of cholinesterase activity with acetylcholine as a substrate. 409 50

A new antiaggregating chemical, alpha-(p-(fluoren-9-ylidenemethyl)phenyl)-2-piperidineethanol (RMI 10,393), designated FYPE, was found to be an effective inhibitor of platelet aggregation induced by adenosine diphosphate (ADP), thrombin, collagen, or epinephrine. Effects of the antiaggregant on platelets were concentration dependent. Aggregation was prevented by low concentrations of FYPE that produced in the platelet only minor ultrastructural changes consisting of loss of microtubules and of discoid shape. Low levels of FYPE that prevented platelet aggregation had no effect on platelet ATPase activities but did alter clot retraction, the thrombin-induced shift in electrophoretic mobility and platelet cholinesterase activity. Market decrease in ADP release and increase in adenyl cyclase activity were produced by low levels of FYPE. This study provides a model for evaluation of platelet antiaggregating compounds in vitro.
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PMID:Effect of a new antiaggregating chemical on the structure and function of the human platelet. 425 15

Male Sprague-Dawley rats receiving an acute dose of methomyl (5 mg/Kg, sc) developed overt signs of toxicity within 2 min. The maximum severity, including muscle fasciculations and convulsions, was attained within 7-10 min and lasted for about 30 min. A very rapid recovery followed and by 90 min rats were free from obvious toxicity. During intoxication, the body temperature was significantly below normal. In diaphragm, when the activity of acetylcholinesterase (AChE) was markedly depressed (82%), the levels of high-energy phosphates, adenosine triphosphate (ATP) and phosphocreatine (PCr) were also significantly lowered (27% and 54%, respectively). Significant decreases in the levels of adenosine diphosphate (ADP, 19%), total adenine nucleotides (TAN, 27%), creatine (Cr, 27%), and total creatine compounds (TCrC, 29%) were noted at various intervals. The ratio of PCr/Cr was reduced by 53%. The adenylate energy charge [(ATP + 1/2 ADP)/(ATP + ADP + AMP)], an indicator of high-energy phosphate bond availability, remained unchanged throughout the time course. More than twofold elevation in the activity of Mg(2+)-facilitated creatine kinase (reverse Lohmann reaction) in diaphragm (CK-MM) and more than twofold increase in the levels of glucose in serum, were suggestive of greater synthesis of ATP. Higher activity of CK-MM was also noted in the serum. That high-energy phosphates were partially depleted suggested that the rate of ATP utilization was far greater than its synthesis. Methomyl intoxication also resulted in higher activity of LDH and its isoenzymes in muscle as a result of induced greater synthesis. Elevation of CK and LDH and their isoenzymes in the serum was probably a result of their leakage from the tissues due to loss of membrane permeability caused by significant depletion of ATP and PCr.
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PMID:Energy related metabolic alterations in diaphragm muscle resulting from acute methomyl toxicity. 799 Dec 21

ATPase-ADPase activities in synaptosomes from cerebral cortex was measured in rats of various ages (0-, 7-, 10-, 14- and 21- and 60-90-days). The activities (nmol Pi/min/mg) increased steadily from birth, reaching maximum values at 21 days of age. The increase was primarily due to increases in Vmax; the Km values are the same from birth until adult age. The developmental profile was similar for ATPase-ADPase activities and acetylcholinesterase from the same fraction. Several specific ATPase inhibitors and Ap5A (P1P5-di(adenosine-5)-pentaphosphate) did not interfere with the hydrolysis of ATP and ADP at all ages studied, suggesting that classical ATPases and adenylate kinase were not involved in the degradation of both nucleotides by synaptosomal fraction in the assay conditions. Other phosphatases were also ruled out. It is conceivable that ATPase-ADPase activities play an important role in neurotransmitter metabolism.
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PMID:Postnatal development of ATPase-ADPase activities in synaptosomal fraction from cerebral cortex of rats. 825 29

1. The effect of several central nervous system active drugs was studied in vitro on ATPase-ADPase activity and acetylcholinesterase (AChE) activity from the cerebral cortex of adult rats. 2. Lithium (1.0-10.0 mM) had no effect on either ATPase-ADPase or acetylcholinesterase activity. 3. Imipramine (0.5-5.0 mM), desipramine (0.5-5.0 mM), amitriptyline (0.1-1.0 mM) and diazepam (0.5-2.0 mM) inhibited ATP and ADP hydrolysis at all concentrations tested. 4. AChE activity was altered by imipramine (1.0-2.0 mM) and by diazepam (0.5-2.0 mM). 5. The possible participation of ATP diphosphohydrolase and AChE in the action of these drugs cannot be ruled out. The probable reduction of ATP, ADP and acetylcholine hydrolysis by the inhibitory effect of these drugs is discussed.
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PMID:In vitro effect of central nervous system active drugs on the ATPase-ADPase activity and acetylcholinesterase activity from cerebral cortex of adult rats. 979 15

Incubation of sheep platelet crude membranes with xanthine oxidase (XO)/hypoxanthine/Fe(2+)-ADP revealed: (i) a fast peroxidative response - with a maximal linear rate of 14 nmol malondialdehyde (MDA) equivalents/mg protein, as evidenced by the thiobarbituric acid test - and a decrease in the polyunsaturated fatty acid (PUFA) content of the platelet crude membranes; (ii) a decrease in the lipid fluidity in the deep lipid core of the membranes but not at the membrane surface; (iii) a dramatic inhibitory effect on glucose 6-phosphatase (Glc-6-Pase) but not on acetylcholinesterase activity. Platelets were also aged by storage at 4 degrees C in their own plasma or in Seto additive solution. In these media, platelet aggregates were visible and the effects on platelet phospholipids, PUFA, lipid extract fluorescence, crude membrane fluidity and membrane-bound enzyme activities were assessed for comparison with those observed in in vitro lipid peroxidation. The sensitivity of membranes from stored platelets to lipid peroxidation was also assessed. Storage of platelets in plasma for 5 days was associated with different changes in their crude membranes such as decreases in arachidonic acid contents, the decrease not being avoided by the presence of phospholipase A(2) inhibitors, increases in MDA equivalents, conjugated dienes and lipid extract fluorescence, decreases in the amounts of MDA equivalents formed by platelet crude membranes treated with the oxidizing agents, changes in membrane fluidity and inhibition of Glc-6-Pase. All these alterations were less pronounced or even abolished after platelet storage in Seto. These findings suggest that platelet lipid peroxidation due to XO/hypoxanthine/Fe(2+)-ADP and platelet membrane alterations observed after platelet ageing under storage at 4 degrees C share common features. Also, as regards the prevention of peroxidative processes, Seto solution permits better storage of sheep platelets than plasma.
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PMID:Comparison between in vitro lipid peroxidation in fresh sheep platelets and peroxidative processes during sheep platelet ageing under storage at 4 degrees C. 1040 82

This study examines the effect of new 1,5 benzodiazepines on acetylcholinesterase (AChE) and ATPDase (apyrase) activities from cerebral cortex of adult rats. Simultaneously, the effects of the classical 1,4-benzodiazepine on these enzymes were also studied for comparative purpose. The compounds 2-trichloromethyl-4-phenyl-3H-1,5-benzodiazepin and 2-trichloromethyl-4(p-methyl-phenyl)-3H- 1,5-benzodiazepin significantly inhibited acetylcholinesterase activity (p < 0.01) when tested in the range of 0.18-0.35 mM. The inhibition caused by these two new benzodiazepines was noncompetitive in nature. Similarly, at concentrations ranging from 0.063 to 0.25 mM, the 1,5 benzodiazepines inhibited ATP and ADP hydrolysis by synaptosomes from cerebral cortex (p < 0.01). However, the inhibition of nucleotide hydrolysis was uncompetitive in nature. Our results suggest that, although diazepam and the new benzodiazepines have chemical differences, they both presented an inhibitory effect on acetylcholinesterase and ATPDase activities.
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PMID:New benzodiazepines alter acetylcholinesterase and ATPDase activities. 1095 91

Status epilepticus (SE)-induced neuronal injury may involve excitotoxicity, energy impairment and increased generation of reactive oxygen species (ROS). Potential treatment therefore should consider agents that protect mitochondrial function and ROS scavengers. In the present study, we examined whether the spin trapping agent N-tertbutyl-alpha-phenylnitrone (PBN) and the antioxidant vitamin E (DL-alpha-tocopherol) protect levels of high-energy phosphates during SE. In rats, SE was induced by either of two inhibitors of acetylcholinesterase (AChE), the organophosphate diisopropylphosphorofluoridate (DFP, 1.25 mg/kg, sc)- or the carbamate carbofuran (1.25 mg/kg, sc). Rats were sacrificed 1 h or 3 days after onset of seizures by head-focused microwave (power, 10 kW; duration 1.7 s) and levels of the energy-rich phosphates adenosine triphosphate (ATP) and phosphocreatine (PCr) and their metabolites adenosine diphosphate (ADP) and adenosine monophosphate (AMP), and creatine (Cr), respectively, were determined in the cortex, amygdala and hippocampus. Within 1 h of seizure activity, marked declines were seen in ATP (34-60%) and PCr (25-52%). Total adenine nucleotides (TAN = ATP + ADP + AMP) and total creatine compounds (TCC = PCr + Cr) were also reduced (TAN 38-60% and TCC 25-47%). No changes in ATP/AMP ratio were seen. Three days after the onset of seizures, recovery of ATP and PCr was significant in the amygdala and hippocampus, but not in the cortex. Pretreatment of rats with PBN (200 mg/kg, ip, in a single dose), 30 min before DFP or carbofuran administration, prevented induced seizures and partially prevented depletion of high-energy phosphates. Pretreatment with the natural antioxidant vitamin E (100 mg/kg, ip/day for 3 days), partially prevented loss of high energy phosphates without affecting seizures. In controls, citrulline, a product of nitric oxide synthesis, was found to be highest in the amygdala, followed by hippocampus, and lowest in the cortex. DFP- or carbofuran-induced seizures caused elevation of citrulline levels seven- to eight-fold in the cortex and three- to four-fold in the amygdala and hippocampus. These results suggest a close relationship between SE, excitotoxicity and energy metabolism. The involvement of oxidative stress is supported by the findings that DFP and carbofuran trigger an excessive nitric oxide (NO) production in the seizure relevant regions of the brain.
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PMID:Depletion of energy metabolites following acetylcholinesterase inhibitor-induced status epilepticus: protection by antioxidants. 1140 58


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