Disease relevance of BCHE

• The full clinical significance of the relationship between cholinesterase inhibition in vitro and contrast media toxicity must be reviewed [1].
• Experimental doses of 1/2-1 gm/kg body weight of these organophosphate compounds caused depression of cholinesterase and axonal degeneration in the spinal cord [2].
• From one minute after dosage, all animals showed severe respiratory distress, excitation, weakness, muscle fasciculation and cholinesterase inhibition [3].
• Cholinesterase levels in blood plasma and erythrocytes from calves, normal delivering cows and cows suffering from parturient paresis [4].
• Cholinesterase-positive and a few GABA-immunoreactive nerve cell bodies were seen in the myenteric ganglia, while fluorescent ganglion cells were not observed [5].

High impact information on BCHE

• This matrix was synthesised by coupling the reversible cholinesterase inhibitor, edrophonium chloride, to epoxy-activated Sepharose [6].
• 6. In conclusion, MB may be considered as a cholinesterase inhibitor with additional, relevant affinity for muscarinic binding sites at concentrations at which MB is used for investigations into the endothelial system [7].
• Pseudocholinesterase-mediated hydrolysis is superior to neostigmine for reversal of mivacurium-induced paralysis in vitro [8].
• CONCLUSIONS: Human plasma cholinesterase will reverse mivacurium more effectively than bovine pseudocholinesterase, but both will effectively reverse succinylcholine [8].
• 4. In vitro THA was a potent non-competitive inhibitor of rat brain cholinesterase (IC50: 57 +/- 6 nM) and bovine erythrocyte acetylcholinesterase (IC50: 50 +/- 10 nM) but was a more potent inhibitor of horse serum butyrylcholinesterase (IC50: 7.2 +/- 1.4 nM) [9].

Chemical compound and disease context of BCHE

• The predominant mode of toxicity of dichlorvos is inhibition of cholinesterase [10].
• Atropine promptly and completely reversed these changes, except for muscle fasciculations, central depression and cholinesterase inhibition which disappeared progressively within 24 hours [3].
• The pretreatment of calves with a single dose of 10 mg kg-1 dieldrin or 21 daily doses of 10 mg kg-1 phenobarbitone increased the toxicity of diazinon as reflected by the development of more severe clinical signs and greater depression in whole blood cholinesterase activity in the pretreated calves [11].

Biological context of BCHE

• BACKGROUND: The metabolic hydrolysis of mivacurium (and succinylcholine) is markedly impaired in the presence of hereditary or acquired defects of pseudocholinesterase [8].
• This is the first report of alternative splicing of the N-terminal coding region in a cholinesterase [12].
• Kinetics of 13 new cholinesterase inhibitors [13].
• Eight-month-old Jersey bull calves given ivermectin intravenously or subcutaneously showed signs of depression, ataxia, difficulty in breathing, tachycardia, salivation, diarrhoea, miosis, and an increase in pseudocholinesterase activity [14].

Anatomical context of BCHE

• Affinity and carbamylation rate constants of propoxur in reaction with erythrocyte and serum cholinesterase [15].
• Km and vmax values are given for the hydrolytic activity of porcine liver carboxylic ester hydrolase, wheat germ lipase, candida cylindracea lipase, hog kidney acylase I, and bovine pancreas alpha-chymotrypsin, while others (acetylesterase, trypsin, and cholinesterase) were studied qualitatively [16].
• ACh content in the culture medium after 24 h of incubation in the presence of isoflurophate, a nonspecific cholinesterase inhibitor, was about 16 times higher than that in endothelial cells, indicating that ACh synthesized inside the cells was released rapidly [17].
• The cholinesterase activity among erythrocytes, plasma, and cerebrospinal fluid of these species was also compared statistically [18].
• Five weeks later, the bull had gained weight, the blood cholinesterase activity was 70% of normal, and the results of a semen evaluation indicated he was a satisfactory potential breeder [19].

Associations of BCHE with chemical compounds

• Mechanism of inhibition in vitro of mammalian acetylcholinesterase and cholinesterase in solutions of 0,0-dimethyl 2,2,2-trichloro-1-hydroxyethyl phosphonate (Trichlorphon) [20].
• Iohexol proved to be the most potent inhibitor of cholinesterase; all other conventional ionic agents are not inhibitors or they are weak inhibitors at the concentrations that are apparently achieved locally in clinical practice [1].
• Effects of dichlorvos on blood cholinesterase activities of cattle [21].
• Effects of T-82, a new quinoline derivative, on cholinesterase activity and extracellular acetylcholine concentration in rat brain [22].
• Cattle and sheep poisoned with organophosphate or carbamate insecticides had cholinesterase depression ranging from near 50% to 80% [23].

Other interactions of BCHE

• Cholinesterase activity in the corpus luteum of the sheep and pig [24].

Analytical, diagnostic and therapeutic context of BCHE

• Cholinesterase activity was stable for several days at 25 C and under refrigeration or freezing conditions for longer periods [23].
• Aerial application of the insecticide Nuvacron 40% (monocrotophos) had no significant effect on the cholinesterase level of plasma and erythrocytes of cattle, chicken, buffaloes, and human volunteers exposed to the spray [25].
• The treatments, which had no adverse effects on the health of steers or cellular constituents of their blood, reduced the whole-blood cholinesterase, with the maximum reduction occurring 15 days after treatment [26].
• The latter 3 calves all recovered with no apparent neurological deficit after intravenous injection of plasma pseudocholinesterase [27].
• The daily oral administration of 3, 6 or 12 mg Anthio/kg/d for 90 d caused significant inhibition of serum cholinesterase (10-28%) and carboxylesterase (12-33%) in male calves [28].

References