Disease relevance of Bche

• In the present study, ganglionic butyrylcholinesterase was near-totally inactivated by the injection of tetramonoisopropyl pyyrophosphoramide (6.0 mumol/kg of body weight) intravenously [1].
• Neither the liver CarbEs, which showed high affinity to iso-OMPA, nor the inhibition of butyrylcholinesterase (BuChE) by iso-OMPA in plasma and liver potentiated paraoxon toxicity [2].
• In the present study we investigate the effect of homocysteine (Hcy) administration, the main metabolite accumulating in homocystinuria, on butyrylcholinesterase (BuChE) activity in serum of rats [3].
• Reduction of butyrylcholinesterase activity in rat serum subjected to hyperhomocysteinemia [3].
• The results confirmed prior reports that hyperglycemia significantly enhances TBARS levels in brain and retinal tissue and decreases AChE and BChE activity [4].

Psychiatry related information on Bche

• In rats pretreated intravenously with 5,000 IU of horse serum-derived BChE, the locomotor activity effect was significantly attenuated [5].

High impact information on Bche

• Identification of the probable site of synthesis of butyrylcholinesterase in the superior cervical and ciliary ganglia of the cat [1].
• The activity of butyrylcholinesterase (BCHE), a liver fetal isozyme (Zone L-V) of a nonspecific esterase, was studied histochemically and cytochemically in rat hepatocellular carcinomas induced by 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB) [6].
• The significance of the appearance of BCHE activity in hepatocellular carcinomas induced by 3'-Me-DAB is discussed [6].
• Histochemical and cytochemical study of butyrylcholinesterase activity in rat hepatocellular carcinomas induced by 3'-methyl-4-dimethylaminoazobenzene [6].
• In normal adult rats, BCHE activity was very prominent in cells of the intestinal mucosa but was not detectable in the liver [6].

Chemical compound and disease context of Bche

• It is concluded that the cycloheximide pretreatment potentiates DFP toxicity by a mechanism that is related to inhibition of the synthesis of proteins such as AChE, BuChE, and CarbE [7].
• Attenuation of cocaine-induced locomotor activity by butyrylcholinesterase [5].
• In the present work we investigated the in vitro effects of homocysteine (Hcy) and methionine (Met), metabolites accumulated in homocystinuria, on butyrylcholinesterase (BuChE) activity in rat serum [8].
• The rats of both sexes were given a single and multiple doses of DDVP (8.0 mg/kg body weight) with two-day intervals between administrations, ensuring the continuous inhibition of BuChE activity without lethal outcome [9].
• The paper describes the catalytic activity of butyrylcholinesterase (BuChE) measured in plasma, liver, white adipose tissue, heart, and brain of rats intraperitoneally administered a single non-lethal dose of cycloheximide (2.0 mg/kg body weight; CHM) [10].

Biological context of Bche

• Regulation of the rat oligodendroglia cell line OLN-93 by antisense transfection of butyrylcholinesterase [11].
• The possible biomedical impact of BChE protein, e.g., on CNS nerve regeneration, is briefly discussed [11].
• For neuroepithelial cells, BChE has been shown to regulate cell division and expression of the postmitotic marker acetylcholinesterase (AChE), while similar studies are lacking for glial cells [11].
• In particular, immunoreactivities of the intermediate filament proteins vimentin and the cell adhesion protein F11 were detected, indicating that BChE-inhibited OLN-93 cells have shifted toward an astrocytic phenotype [11].
• Sex differences in the BuChE activity of serum and liver were even larger (ten times more activity in females), but the activity of other tissues was similar in both sexes [12].

Anatomical context of Bche

• These data support a role of the glia marker BChE in CNS glial cell proliferation and differentiation, achieved via a nonenzymatic mechanism [11].
• This finding indicates that the regulation of BuChE may be strongly affected by hormones under the control of the pituitary gland [12].
• Peak inhibition of maternal spinal cord AChE and BuChE activities occurred 2 h and 1 h after dosing, respectively [13].
• Acetylcholinesterase activity in erythrocytes as well as butyrylcholinesterase activity in plasma were significantly decreased in both groups of animals after intoxication with sarin [14].
• The concentration of exogenous ACh needed to reduce the spontaneous frequency of contractions of the isolated right atrium by 30, 60, or 90/min fell by 78%, 79% and 84% respectively after BW 284 C51 inhibition of AChE and by 95%, 94% and 94% after simultaneous inhibition of AChE and BuChE [15].

Associations of Bche with chemical compounds

• These results indicated that AChE, rather than BuChE, plays an important role in controlling ACh-induced contractions of rat urinary bladder [16].
• The purpose of this work was to study the catalytic properties of rat butyrylcholinesterase with benzoylcholine (BzCh) and N-alkyl derivatives of BzCh (BCHn) as substrates [17].
• Neostigmine, a non-selective ChE inhibitor, caused concentration-dependent contractions in rat urinary bladder strips, whereas tetraisopropylpyrophosphoramide (iso-OMPA; a BuChE inhibitor) failed to affect the resting tone of the preparations [16].
• The presence of a long lag phase, with no oscillations, in substrate hydrolysis by rat butyrylcholinesterase was also observed with N-methylindoxyl acetate as substrate [17].
• The carbaphen compounds are hence prototype drugs that can interact with either muscarinic receptors or butyrylcholinesterase [18].

Other interactions of Bche

• In Sprague-Dawley rats there were also large individual variations with up to a fivefold range of AChE activities and up to a 100-fold range of BuChE activities in a given tissue [19].
• There were no significant changes in the acetyl- and butyrylcholinesterase activities in the olfactory bulb, or in the choline acetyltransferase activity in all three brain areas [20].
• Total carnitine acetyltransferase and butyrylcholinesterase activities were markedly decreased [21].
• Acute chlorpyrifos administration produced a 85.01% inhibition of AChE and a 43.4% inhibition of BuChE but had no effect on MAO-A activity and 5-HT uptake [22].

Analytical, diagnostic and therapeutic context of Bche

• Most of the effects of hypophysectomy on mean BuChE activity were opposite in direction in the two sexes [12].
• The individual molecular forms (10S and 4S) of maternal and fetal brain AChE and BuChE activities were significantly decreased 1 h after treatment [13].
• Denervation of muscle caused a dramatic reduction in the presence of AchE molecular forms with no discernable influence on the presence of BuchE molecular forms [23].
• At 1 1/2 hr after the treatments, the BuChE activity was too low to be detected on the gels, but 24 hr thereafter, the quantitative determination of the different forms, performed by scanning densitometry, showed a significant increase of the two faster migrating ones [24].
• Heparin-Sepharose chromatography, nondenaturing electrophoresis and sucrose gradient centrifugation were used to study heparin interaction with the G2 form BChE [25].

References