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

Whole blood, plasma, or serum levels of various components were measured in fasting, drug-free control subjects and drug-free schizophrenic patients. Compared to normal controls, chronic schizophrenic patients showed increased alpha2-globulins and decreased plasma cholinesterase activity and ceruloplasmin activity, and acute schizophrenic patients showed decreased alpha2-globulins. Compared to chronic patients, acute schizophrenics showed decreased alpha2-globulins and IgA. Compared to normal controls of similar age, chronic schizophrenic patients weighed less, were shorter, and had smaller body surface area. The acute schizophrenic patients were significantly younger than the normal subjects or chronic schizophrenics but there was no difference in the other physical measurements. The present study indicates no gross disturbances in the blood variables studied. That some differences are statistically significant from controls is of scientific interest, but of no clinical value in the diagnosis of schizophrenia.
Arch Gen Psychiatry 1975 Jun
PMID:Blood protein fraction comparisons of normal and schizophrenic patients. 4 63

We describe prolonged apnea following electrotherapy in a patient who was also being treated with a topical organophosphate anticholinesterase, ecothiophate iodide (phospholine iodide), for glaucoma. The increased duration of action of succinylcholine resulted from low levels of serum cholinesterase that had been caused by the organophosphate. Attention is called to other drugs that directly or indirectly (by lowering serum cholinesterase) interact with succinylcholine chloride resulting in prolonged apnea. Other potential hazards of succinylcholine administration, such as hyperkalemia and cardiac arrhythmias, are also discussed.
Arch Gen Psychiatry 1978 Sep
PMID:Hazards of succinylcholine administration during electrotherapy. 68 74

Acute organophosphate poisoning is known to result in substantial behavioral abnormalities. We assessed psychiatric manifestations of exposure in workers less substantially exposed to organophosphate compounds and showing no obvious signs of toxicity. Commercial pesticide sprayers and farmers recently exposed to organophosphate agents were compared to control subjects on personality tests, a structured interview, and cholinesterase level. The commercial sprayers but not the exposed farmers showed elevated of anxiety and lower plasma cholinesterase than control subjects. Assessment of other behavioral manifestations and red blood cell cholinesterase failed to disclose other group differences. These findings are viewed as tentative until confirmed by additional study, but they point to the possibility that organophosphate compounds may produce subtle defects in workers who are not obviously toxic. The findings do not justify public alarm but do suggest an area warranting more systematic and definitive investigation.
Arch Gen Psychiatry 1976 Feb
PMID:Anxiety associated with exposure to organophosphate compounds. 125 99

The effects of some muscarinic M1 and M2 receptor agonists and antagonists on rat brain serotonergic activity was assessed by noting their effects on the levels of 5-hydroxytryptamine (5-HT) and its major metabolite, 5-hydroxyindole acetic acid (5-HIAA), estimated by a high pressure-liquid chromatographic (HPLC) technique. The muscarinic M1 receptor agonists, arecholine and McN-A-343, and the M2 receptor agonists, gallamine and AF-DX 116, induced a dose-related decrease in the concentrations of both 5-HT and 5-HIAA. On the contrary, scopolamine and the selective M1 receptor antagonist, pirenzepine, increased the levels of the amine and its metabolite. The anti-cholinesterase agent, physostigmine, and the putative M2 receptor agonist, carbachol, induced a dose-related dual effect, with the smaller doses decreasing and the higher doses increasing 5-HT and 5-HIAA concentrations. The results indicate that an inverse relationship exists between the cholinergic and serotonergic neurotransmitter systems in the rat brain due to the likely presence of muscarinic heteroreceptors on serotonergic neurones. The data also indicates that though physostigmine and carbachol may function as M2 receptor agonists, they lose their receptor specificity on dose increment.
J Neural Transm Gen Sect 1992
PMID:Effects of muscarinic receptor agonists and antagonists on rat brain serotonergic activity. 128 83

1. The effect of four hypolipidemic agents with different mechanisms of action (fenofibrate, probucol, colestipol and nicotinic acid) on plasma and liver cholinesterase has been studied. 2. Liver weight and liver weight/body weight ratio increased only after treatment with fenofibrate. 3. Plasma and liver cholinesterase activity increased markedly after fenofibrate, a strong peroxisome proliferator, and slightly after nicotinic acid, a weak peroxisome proliferator. 4. The data obtained suggest that increased cholinesterase activity is due to increased rate of fatty acid oxidation caused by peroxisome proliferators.
Gen Pharmacol 1992 Mar
PMID:Effect of hypolipidemic drugs on cholinesterase activity in the rat. 163 35

A case is presented in which a patient who required treatment with electroconvulsive therapy had a history of being treated with pseudocholinesterase-inhibitor eye drops (echothiophate iodide) for glaucoma. As treatment with this antiglaucoma agent contraindicated the use of succinylcholine for a minimum of 10-14 days, the short-acting nondepolarizing agent atracurium was employed instead. The anesthetic management of this patient is described as a guide for clinicians facing similar clinical situations.
Gen Hosp Psychiatry 1992 Jan
PMID:Electroconvulsive therapy and the chronic use of pseudocholinesterase-inhibitor (echothiophate iodide) eye drops for glaucoma. A case report. 173 Apr 2

1. The inhibition of cholinesterase and carboxylesterase activities in the diisopropyl fluorophosphate (DFP) intoxication, and the inducibility of organophosphate (OP) detoxicating enzymes was studied in rats. 2. In phenobarbital (PB)-, but not in beta-naphthoflavone (NF)-pretreated rats, the activities of DFP-inhibited cholinesterases were 70-120% higher than in non-pretreated rats. Also the inhibition of the microsomal and cytosolic carboxylesterase activity in liver was efficiently antagonized by BP, but not by NF. 3. In vitro the microsomes from PB-treated rats detoxicated DFP probably by O-dealkylation, since no fluoride was released from DFP. Glutathione S-transferase did not detoxicate DFP. 4. 7-Pentoxyresorufin O-dealkylase, a specific enzyme of cytochrome P450IIB subfamily, was induced by PB, flumecinol, isosafrole and NF by 167- 61-, 26- and 1.6-fold, respectively. 7-Ethoxyresorufin O-deethylase, a marker enzyme of cytochrome P450IA subfamily, was induced by those agents 5-, 4-, 31- and 94-fold, given in the same order. Glutathione S-transferase, paraoxonase and DFPase activities were increased 0-72% by the tested inducers. 5. The results suggest that the cytochrome P450IIB subfamily, inducible by PB, participates in DFP detoxication by O-dealkylation. Its induction probably causes the protection against the cholinesterase inhibition by OPs.
Gen Pharmacol 1990
PMID:Inhibition of cholinesterases by DRP and induction of organophosphate-detoxicating enzymes in rats. 216 59

1. The effect of cold environment on the acute toxicity of organophosphates (OP), without and with atropine-oxime treatment, was studied in rats and mice by exposing them to +5 and -5 degrees C temperature. The tested OPs and oximes (given intraperitoneally) were diisopropylfluorophosphate (DFP), isopropyl methylphosphonofluoridate (sarin) and dichlorovinyl phosphate (DDVP), pralidoxime (PAM) and obidoxime. 2. An exposure to low environmental temperature decreased the effectiveness of atropine-oxime therapy in OP poisoned rats and mice, evaluated by means of acute LD50 values. 3. The lowering of environmental temperature did not influence the ability of PAM to reactivate tissue cholinesterase in rats intoxicated by 0.5 x LD50 doses of DFP. 4. The acute toxicity of atropine and oximes was not affected by cold environment in rats, but in mice it was increased by 1.1-2.1 times. 5. The decrease in the effectiveness of atropine-oxime therapy at cold environment may be explained by the observation that the cold temperature sensitizes the animals to the inhibition of brain acetylcholinesterase by OP.
Gen Pharmacol 1989
PMID:Cold exposure decreases the effectiveness of atropine-oxime treatment in organophosphate intoxication in rats and mice. 268 80

1. Rats were used for studies on organophosphate (OP) toxicity both in acute and chronic cold exposure. Furthermore the effects of OPs on tissue acetyl- and butyrylcholinesterase activities were studied in the cold environment. 2. No change in the toxicity of dichlorovinyl phosphate (DDVP) was observed whereas that of diisopropylphosphofluoridate (DFP) increased 1.5-fold at +5 degrees C. 3. Chronic exposure to cold produced no change in DFP toxicity. 4. The survival time in acute cold exposure (1.1 x LD50 DFP) was longer than in chronic exposure or at +20 degrees C. 5. In control rats, chronic cold exposure increased blood BuChE and decreased BuChE in lungs. 6. A dose-dependent inhibition of cholinesterases was observed. 7. AcChE in the liver of chronically cold exposed rats was more sensitive to DFP inhibition compared to acute exposure. 8. Blood AcChE activity correlated only to AcChE in brain and lungs in rats.
Gen Pharmacol 1988
PMID:Effect of the cold environment on organophosphate toxicity and inhibition of cholinesterase activity. 321 84

1. Cholinesterase activities in blood and tissues of control and exercising rats with and without organophosphate (OP) exposure were studied. 2. Physical exercise increased total cholinesterase and butyrylcholinesterase activities in rats without OP exposure in blood and diaphragm. In brain physical exercise had no effect on acetylcholinesterase activity. 3. Physical exercise diminished cholinesterase inhibition in blood and tissues after OP exposure.
Gen Pharmacol 1988
PMID:Physical exercise affects cholinesterases and organophosphate response. 322 22


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