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:3.1.1.8 (cholinesterase)
12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cell populations in the dorsal motor nucleus of the vagus (DMNV) of the rat were studied by light microscopy and transmission electron microscopy, including retrograde labeling with horseradish peroxidase and histochemical demonstration of the distribution of the activity of the enzymes acetylcholinesterase (AcChE) and butyrylcholinesterase (BuChE). Two types of neurones were observed: 1) Larger Type A cells, which stain for both AcChE and BuChE and which project into the vagus nerve trunk, and 2) smaller Type B cells, which stain lightly for AcChE but not for BuChE and which do not project into the vagus nerve. Standardised vagal crush at the mid-cervical level causes loss of cholinesterase activity in Type A neurones within a few days but has no effect on Type B neurones. Changes in nuclear morphology of Type A neurones are pronounced at 10 weeks postinjury, indicating that degeneration is irreversible even by this stage. The number of Type A cells projecting to the vagus nerve reduces as a function of time, presumably as these cells die. Only a small number of Type A neurones persist at 2 years postinjury.
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PMID:Ultrastructural and cytochemical study of neurones in the rat dorsal motor nucleus of the vagus after axon crush. 976 28

Reactive phosphonate diesters were designed and prepared as inhibitors of serine proteases and esterases. Inactivation of trypsin, chymotrypsin, and butyrylcholinesterase was determined by residual enzymatic activity as well as by the release of a chromogenic or fluorogenic product of the inhibition reaction. Second-order rate constants were determined from rates of nitrophenol formation. Application of the reaction for active-site titration of enzyme preparations is demonstrated. A basic functional group present in the nitrophenyl tropane phosphonate diester was shown to confer selectivity for inactivation of trypsin and chymotrypsin. Biotinylated derivatives of the phosphonate diesters were prepared to permit analysis of proteins modified in the inhibition reaction. Labeled polypeptides were resolved by SDS-PAGE, electroblotted, and detected by streptavidin-peroxidase staining. A detection limit of less than 4 ng, corresponding to 20 nM of trypsin, was demonstrated. Pretreatment of enzymes with DFP or nonbiotinylated phosphonates specifically blocks the labeling. This technique permits identification of serine proteases in complex mixtures with good sensitivity and specificity.
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PMID:Inhibition and labeling of enzymes and abzymes by phosphonate diesters. 1082 63

Qing Nao Yi Zhi Fang (QNYZ), a traditional Chinese medicine, has been developed as a drug to be used for the prevention and treatment of vascular dementia. However, the mechanisms by which this drug affects vascular dementia remain unknown. We examined the effects of QNYZ serum on glutamate excitotoxicity in rat fetal cerebral neuronal cells in primary culture. Exposure of neuronal cells to glutamate leads to a decrease in the activities of cholinesterase, superoxide dismutase, and streptoavidin peroxidase, and an increase in lactate dehydrogenase release. These enzyme activities were restored to the levels in untreated cells by the addition of QNYZ serum. QNYZ serum suppressed the increased nitric oxide production induced by glutamate and prevented glutamate-mediated apoptosis. QNYZ serum also improved mitochondrial energy metabolism after glutamate exposure. These findings suggest that QNYZ has protective effects against glutamate-mediated excitotoxicity in neuronal cells during ischemic brain injury.
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PMID:Effects of a traditional Chinese medicine, Qing Nao Yi Zhi Fang, on glutamate excitotoxicity in rat fetal cerebral neuronal cells in primary culture. 1092 65

Enzyme tablets with butyrylcholine esterase (CHE) and peroxidase (POD) partly lose enzymatic activity during compaction at a pressure of 495 MPa. Compared to solutions of the original enzyme, no changes of ultraviolet absorbance and fluorescence intensity in the tablet solutions were found. Only small changes were observed in the far ultraviolet circular dichroism spectra. Neither missing nor additional bands were detected with polyacrylamide gel electrophoresis. Heated (150 degrees C) solid starting material with CHE and POD showed still part of its original enzymatic activity. The ultraviolet absorbance increased with continued heating until precipitation occurred. The circular dichroism spectra are changed clearly.
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PMID:[Protein analysis of enzyme tablets]. 1159 90

Stress-induced change in the distribution of the drug pyridostigmine (PYR) has been proposed as a contributing factor to unexplained illnesses in Persian Gulf War veterans. We evaluated the effects of two stress models, forced running and forced swimming, on acute PYR (30 mg/kg, p.o.) toxicity and cholinesterase (ChE) inhibition in the blood and selected brain regions of young adult male Sprague-Dawley rats (6 weeks of age). Plasma corticosterone levels were measured at 0, 1 and 3 h after termination of forced swimming or forced running to confirm the induction of stress. PYR was given either immediately before stress (15 min swimming; 20 min running) or immediately after stress (15 min swimming; 90 min running) and cholinergic toxicity and ChE inhibition were evaluated at 1, 2 or 4 h after PYR exposure. Additionally, rats were subjected to either swimming (15 min) or running (90 min) stress, anesthetized, injected with horseradish peroxidase (HRP, 100 mg/kg, transcardial) and brain-regional HRP activity measured as an indicator of altered blood-brain barrier integrity. Both forced swimming and forced running resulted in significant elevations of plasma corticosterone levels. PYR caused cholinergic toxicity at all time-points evaluated. Swimming and running stress had little influence on expression of PYR-induced toxicity, however. Blood ChE activity was generally inhibited 77-91% at 1-4 h after PYR, but rats pretreated with PYR prior to forced swimming showed lesser inhibition (64%) 1 h after dosing, possibly because of swimming-induced hypothermia and delayed absorption of the drug. Minimal changes in ChE activity were noted in frontal cortex, cerebellum and hippocampus following PYR exposure (maximal inhibition 28%), and neither swimming nor running stress affected the degree of inhibition. Neither stress model increased HRP accumulation in any brain region. The results suggest that stress associated with forced running or forced swimming has little effect on acute PYR toxicity, entry of PYR into the brain or PYR-induced brain-regional ChE inhibition.
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PMID:Neither forced running nor forced swimming affect acute pyridostigmine toxicity or brain-regional cholinesterase inhibition in rats. 1206 28

Compounds acting as antioxidants to lipids often have a prooxidant effect on DNA or protein. In this study, inactivation of creatine kinase was examined as an indicator of protein damage induced by antioxidative stilbene derivatives, including diethylstilboestrol, resveratrol and tamoxifen, with horseradish peroxidase and hydrogen peroxide (horseradish peroxidase-H2O2). Diethylstilboestrol and resveratrol, but not tamoxifen, rapidly inactivated creatine kinase. Also, creatine kinase in heart homogenate was inactivated by diethylstilboestrol and resveratrol. Tamoxifen, which has no phenolic hydroxyl groups in its structure, was about 10 times less active in protecting lipids and creatine kinase than diethylstilboestrol and resveratrol, suggesting that phenolic hydroxyl groups in diethylstilboestrol and resveratrol of stilbene derivatives are anti- and pro-oxidative. Absorption spectra of these stilbene derivatives rapidly changed during the reaction with horseradish peroxidase-H202. Diethylstilboestrol and resveratrol free radicals emitted electron spin resonance signals and creatine kinase effectively diminished the electron spin resonance signals. These results suggest that free radicals of diethylstilboestrol and resveratrol formed through reaction with horseradish peroxidase-H202 inactivated creatine kinase. Presumably, oxidation of essential cysteine and tryptophan residues lead to inactivation of creatine kinase. Other enzymes, including alcohol dehydrogenase and cholinesterase, were also sharply inhibited by diethylstilboestrol and resveratrol with horseradish peroxidase-H202. Free radicals of diethylstilboestrol and resveratrol seem to mediate between anti- and prooxidative actions.
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PMID:Inactivation of creatine kinase induced by stilbene derivatives. 1207 28

Pyridostigmine, a carbamate cholinesterase (ChE) inhibitor, has been used for decades in the treatment of the autoimmune disorder myasthenia gravis and was used prophylactically to protect soldiers from possible organophosphorus nerve agent exposures during the Persian Gulf War. Pyridostigmine is a charged, quaternary compound and thus would not be expected to easily pass the blood-brain barrier. Some studies have suggested, however, that stress may alter blood-brain barrier integrity and allow pyridostigmine to enter the brain. We evaluated the effects of acute and repeated restraint stress on functional signs of cholinergic toxicity (i.e., autonomic dysfunction and involuntary movements) and brain regional cholinesterase inhibition following either acute or repeated pyridostigmine exposures. The acute, oral maximum-tolerated dosage (MTD) of pyridostigmine was estimated at 30 mg/kg. Peak ChE inhibition in whole blood occurred from 0.5 to 4 h after MTD exposure, whereas minimal (<20%) brain ChE inhibition was noted. For acute restraint studies, rats were either (1) restrained for 90 min and then given pyridostigmine (30 mg/kg, po), (2) given pyridostigmine and immediately restrained for 60 min, or (3) restrained for 3 h, given pyridostigmine, and restrained for an additional 60 min. In all cases, rats were evaluated for cholinergic toxicity (SLUD signs and involuntary movements) and sacrificed 1 h after pyridostigmine treatment. Plasma corticosterone was significantly elevated immediately after a single 60-min session of acute restraint stress, but returned to control levels by 1 and 3 h later. Pyridostigmine-induced toxicity was not enhanced nor was brain ChE inhibition altered by acute restraint stress. Blood-brain barrier permeability, assessed by accumulation of horseradish peroxidase in brain regions following intracardiac injection, was not increased by restraint stress. For repeated restraint studies, rats were given pyridostigmine (0, 3, or 10 mg/kg/day) immediately prior to daily restraint (60 min) for 14 consecutive days. Plasma corticosterone was elevated at 1 and 7 days but not at 14 days. Pyridostigmine-treated rats in both dosage groups exhibited slight signs of toxicity for the first 3-5 days, after which cholinergic signs dissipated. Repeated restraint had little effect on functional signs of pyridostigmine toxicity, however. Whole blood and diaphragm ChE were markedly reduced 1 h after the last treatment, but stress had no influence on ChE inhibition in either peripheral or central tissues. The results suggest that acute and repeated restraint stress have little effect on pyridostigmine neurotoxicity or apparent entry of pyridostigmine into the brain.
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PMID:Acute and repeated restraint stress have little effect on pyridostigmine toxicity or brain regional cholinesterase inhibition in rats. 1221 70

To clarify the mechanism of the side effect of chlorpromazine, we examined the inactivation of cholinesterase induced by chlorpromazine. Cholinesterase was inactivated and its activity was lost in rat serum during interaction of chlorpromazine with horseradish peroxidase and H2O2. When chlorpromazine was oxidized by horseradish peroxidase and H2O2, the reaction solution colored pink and the visible absorption spectrum was consistent with the absorption spectrum of the chlorpromazine cation radical (CPZ*+). Adding cholinesterase immediately decreased the pink color of CPZ*+, indicating that CPZ*+ directly attacked cholinesterase to cause loss of the enzyme activity. Tryptophan residues in cholinesterase sharply decreased during the interaction of cholinesterase with horseradish peroxidase and H2O2. Presumably, loss of tryptophan residues changed the conformation of the cholinesterase protein and then the activity of the enzyme was lost. Other phenothiazine derivatives, including promethazine, triflupromazine, trifluoperazine, trimeprazine, thioridazine and perphenazine, also inactivated cholinesterase during the oxidation by horseradish peroxidase and H2O2. These results suggest that phenothiazine cation radicals participate in toxicological signs caused by the drugs.
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PMID:Inactivation of cholinesterase induced by chlorpromazine cation radicals. 1274 80

In order to explore the effects of superoxide dismutase(SOD), catalase(CAT), glutathione-peroxidase (GSH-Px) in rabbits exposed by profenofos and its meaning. 18 rabbits were divided into three groups randomly: A group (high-dose group), B group(low-dose group), C group(control group), each group including 6 rabbits. The activities of SOD, CAT, GSH-Px in plasma, and cholinesterase(ChE) in blood were measured in different exposure period. The results showed that activities of SOD, CAT and GSH-Px increased, ChE decreased markedly compared with those in the same group before experiment and control group (P < 0.05, P < 0.01). The increase of antioxidase activities was earlier than the decease of ChE activity. It suggests that profenofos can result in the increases of the activities of SOD, CAT and GSH-Px, which may be earlier diagnostic index in profenofos poisoning.
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PMID:[An experimental study of the effects of profenofos on antioxidase in rabbits]. 1465 Jan 83

The effect of the organophosphorous insecticide paraoxon on the integrity of the blood-brain barrier (BBB) and permeability of pyridostigmine (PYR), a peripheral inhibitor of cholinesterase activity, was examined in Long Evans rats. The integrity of the BBB was examined by measuring the number of capillaries leaking horseradish peroxidase, which was injected into the heart. Treatment with paraoxon at 100 microg/kg, intramuscularly, resulted in a 3- to 4-fold increase in the number of leaky capillaries in young rats (25 to 30 days old) but not in older rats (90 days old). Interestingly, young rats treated with PYR (30 mg/kg, po) 50 min before treatment with paraoxon showed an inhibited effect of paraoxon on the BBB. Furthermore, no increase in the degree of inhibition of acetylcholinesterase activity was observed in young rats treated with PYR before paraoxon compared with young rats treated with paraoxon alone. Cholinergic toxicity, as assessed by changes in behavior, was not observed in young rats treated with paraoxon alone; but, slight signs of cholinergic toxicity were observed in rats treated with PYR. Young rats treated with both PYR and paraoxon did not exhibit more extensive signs of toxicity than rats treated with paraoxon alone or PYR alone. The results indicate that treatment with paraoxon can compromise BBB permeability at dosages that do not induce cholinergic toxicity, but only in young rats. Also, PYR pre-exposure appears to protect the BBB from the paraoxon-induced alterations.
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PMID:Interactive effects of paraoxon and pyridostigmine on blood-brain barrier integrity and cholinergic toxicity. 1497 54


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