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 enzyme activities of cultured early erythroid progenitor cells (burst-forming unit erythroid, BFU-E) were measured and were compared with the activities of mature erythrocytes. The enzyme activity of acetylcholinesterase was not detectable in the erythroblasts. The ratios of phosphofructokinase and glutathione peroxidase were low due to low enzyme activities in both the erythroblasts and erythrocytes. The ratios of triose phosphate isomerase, phosphoglycerate kinase, and adenylate kinase were low due to high enzyme activities in both the erythroblasts and erythrocytes. The ratios of hexokinase, glucose phosphate isomerase, monophosphoglyceromutase, pyruvate kinase, and adenosine deaminase were high due to high enzyme activities in the erythroblasts. The isozyme of erythroblast hexokinase was of the prototype isozyme I, while pyruvate kinase was predominantly of the prototype M2, with two hybrid isozymes to the anodal side by electrophoresis. These facts suggest that there is a greatly different metabolic pattern during the maturation of the erythroid cells.
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PMID:Enzyme activities of cultured erythroblasts. 403 55

The different doses of chlorfenvinphos given in diets with low-protein and optimal-protein level to young Wistar rats of both sexes were, after 10 or 30 days, without the significant influence on the activity of several serum enzymes used as diagnostic markers in determining the liver damage or disease, as for example:sorbitol dehydrogenase, glutamic dehydrogenase, glucosephosphate isomerase (PHI), aspartate and alanine aminotransferase. Not even important changes were found in the activity of aromatic amino acids aminotransferases in the brain and in protein content in the brain and liver of rats fed diets contaminated with chlorfenvinphos, irrespective of the protein concentration in the diet. Only in some cases at the highest concentration of chlorfenvinphos in the diets the decreased activity of aromatic amino acids aminotransferases appeared in the liver, more evident in low-protein rats. The decrease of the PHI activity in the brain and the inhibition of acetylcholinesterase activity in the serum and brain depended mainly on the amount of chlorfenvinphos in the diets and to a lower degree on the amount of protein. All changes caused by chlorfenvinphos normalized during two weeks after its elimination from the diets.
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PMID:Alterations in some biochemical processes in the organism of rats being under the influence of chlorfenvinphos administered in diets with variable protein content. 648 45

The acute oral toxicity (LD50) of chlorfenvinphos (Chl) showed no significant difference between Wistar rats (males and females) aged 42 days kept for 30 days on 4.5% or 26%-protein diet, but a twofold difference appeared after 60 days on these diets (LD50 was lower in low-protein rats) showing that a longer period of protein deficiency more increases the susceptibility of rats to the lethal action of Chl. During acute poisoning produced by intragastric administration of single convulsive dose of Chl (30 mg/kg body weight) to rats kept for 30 days on low-protein or optimal-protein diet, changes were observed in the activity of some enzymes in the serum and brain. Protein deficient diet increased the Chl-produced inhibition of acetylcholinesterase (AChE) activity in the brain; the augmented activity of aspartate aminotransferase (AspAT) and alanine aminotransferase (AlaAT) and glucosephosphate isomerase (PHI) appeared only in the serum of low-protein rats--these changes were more marked in females. Other enzymatic alterations caused by Chl were similar independently of the diets and also more evident in females; for comparison the rats received also standard Murigran diet. Activity of the brain aromatic amino acids aminotransferases (AAA) showed a decreasing trend in Chl-poisoned rats, while in the liver the activity of these enzymes rose, but chiefly in the rats receiving previously the diet with 26% of protein or standard diet. In the rats surviving the acute Chl poisoning, with the evidently seen convulsions, the activity of nearly all enzymes was normal after 14 days.
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PMID:Relationship between dietary protein level and enzymatic changes in acute poisoning of rats with chlorfenvinphos. 651 1

Here we describe two cases of carbamate poisoning. Patients AMF and PVM were accidentally poisoned by cholinesterase inhibitors. The medical diagnosis in both cases was overcholinergic syndrome, as demonstrated by exposure to cholinesterase inhibitors. The widespread use of cholinesterase inhibitors, especially as pesticides, produces a great number of human poisoning events annually. The main known neurotoxic effect of these substances is cholinesterase inhibition, which causes cholinergic overstimulation. Once AMF and PVM had recovered from acute intoxication, they were subjected to extensive neuropsychological evaluation 3 and 12 months after the poisoning event. These assessments point to a cognitive deficit in attention, memory, perceptual, and motor domains 3 months after intoxication. One year later these sequelae remained, even though the brain magnetic resonance imaging (MRI) and computed tomography (CT) scans were interpreted as being within normal limits. We present these cases as examples of neuropsychological profiles of long-term sequelae related to acute poisoning by cholinesterase inhibitor pesticides and show the usefulness of neuropsychological assessment in detecting central nervous system dysfunction in the absence of biochemical or structural markers.
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PMID:Chronic neuropsychological sequelae of cholinesterase inhibitors in the absence of structural brain damage: two cases of acute poisoning. 1592 1