Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A description is given of an outbreak of equine infectious anaemia (E.I.A.) in Campania [at Naples and Aversa (Caserta)]; it was diagnosed by clinical, pathological and serological examinations (Coggins test). Using the serum of 45 horses with E.I.A. and 11 healthy horses (controls), numerous investigations were carried out on: enzymes, intrinsic coagulation factors, lipids and other substances. The results obtained were very interesting and show that in this disease there are significant increases in many enzymes (LDH, LAP, gamma-GT, CPK, PK and ALD) and copper. Insignificant increases were found in other enzymes (SDH, GLDH, MDH, ICDH, AIP, lysozyme, cholinesterase, GOT and GPT) and also intrinsic coagulation factors, lipid substances (total cholesterol, esterified cholesterol, triglycerides) and glucose. LDH-1-isoenzyme remains unchanged, whilst AcP decreases slightly.
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PMID:Biochemical studies on equine infectious anaemia. 101 May 2

Nonvaccinated pigs were infected with a pathogenic virus of swine fever in order to follow up the changes with some enzymes in their blood serum. It was found that there is a dependable rise in the values of the blood serum GOT (2.6.1. 1.) - From about 38 to approximately 108 mU per cu. cm; GPT (2. 6; 1.2.;-From about 12 up to 66 mU/cu. cm; LAP (3. 4. 1. 1)-from about 13 to 27 mU/cu. cm; and ALD (4. 1; 2. 7.) - from about 6 up to 19 mU/cu. cm. These changes were noticed as early as the 48th hour of infection, prior to the manifestation of the clinical symptoms of swine fever. They remained stable up to the end of the infection process. The activity of LDH (1. 1. 2. 7.) and amylase (3. 2. 1.1 .) was said to rise (not dependable statistically), and that of cholinesterase (3. 1 1. 8) - to drop gradually with the development of the infection process. The two phosphomonoesterases (3. 1. 3. 1 and 3. 1. 3. 2.) showed no essential changes. The changes taking place in the activity of these enzymes did not depend on the extent of the hemorrhagic diathesis characteristic of swine fever. So, this test, which has been unknown so far, is referred to as a characteristic paraclinical symptom of swine fever.
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PMID:[Activity of several serum enzymes in swine with acute plague]. 117 33

Aldicarb (ALD, 2-methyl-2-(methylthio)-propionalaldehyde O-(methyl-carbamoyl) oxime, Temik) is widely used as an insecticide, nematocide and acaricide and it is oxidized to aldicarb sulfoxide (ALX) and aldicarb sulfone (ALU). Neither a toxicokinetic model nor an estimate of the target tissue dose of ALD and its metabolites in exposed organisms is available. The objective of this study was: (i) to develop a physiologically based toxicokinetic (PBTK) model for ALD in the rat and humans, and (ii) to determine the interspecies toxicokinetic uncertainty factor (UF(AH-TK)) of ALD. The model consists of a series of mass balance differential equations that describe the time course behavior of ALD in blood, liver, kidney, lungs, brain, fat, and rest of the body compartments. The physiological parameters of the model (blood flow rates, cardiac output, and tissue volumes) were obtained from the literature, while the maximum velocity (mg/kg/min) and the Michaelis constant (mg/l) for ALD oxidation in rats and humans were determined by in vitro AH-TK microsomal assays. The estimation of the tissue:blood partition coefficient was accomplished within the PBTK model by representing the tissues as a composite of neutral lipids, phospholipids and water, and providing the vegetable oil:water partition coefficient as input parameter. The validity of the rat PBTK model was assessed by comparing the model simulations of ALX time course blood concentrations and the inhibition patterns of acetylcholinesterase (AChE) in erythrocytes and plasma obtained by administering rats ALD (0.1 and 0.4 mg/kg, iv). The human PBTK model was validated by comparing the simulations of AChE inhibition patterns in blood with human experimental data obtained from oral administrations of ALD. The UF(AH-TK) for ALD was determined by dividing the areas under the blood and brain concentration vs time curve (AUCCV, AUCCBR) for ALD and ALX in the rat and in human exposed to the same dose. The results indicate that with respect to parent chemical, equivalent applied doses in rats and humans result in a 9.5-fold difference in the AUC(CV) and AUC(AH-TK) respectively, in the two species, and 17-fold difference in the AUC(CV) and AUC(CBR) with respect to the metabolite. In other words, in order to have toxicokinetic equivalence in rats and humans, the former species must be exposed to a dose that is 9.5 and 17 times higher than the human with respect to the parent chemical and the metabolite respectively. Overall, the present study demonstrates the applicability of PBTK models in the quantitative evaluation of UH(AH-TK), and shows that their current default values are inaccurate, at least with respect to ALD, which has potential negative implications in the alleged protection of risk estimates derived from them.
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PMID:Physiological modeling and derivation of the rat to human toxicokinetic uncertainty factor for the carbamate pesticide aldicarb. 2178 1