血漿コリンエステラーゼ

WordNet

(physical chemistry) a fourth state of matter distinct from solid or liquid or gas and present in stars and fusion reactors; a gas becomes a plasma when it is heated until the atoms lose all their electrons, leaving a highly electrified collection of nuclei and free electrons; "particles in space exist in the form of a plasma"
a green slightly translucent variety of chalcedony used as a gemstone
the colorless watery fluid of the blood and lymph that contains no cells, but in which the blood cells (erythrocytes, leukocytes, and thrombocytes) are suspended (同)plasm, blood_plasma
an enzyme that hydrolyses acetylcholine (into choline and acetic acid)

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(また『blood plasma』)血漿,リンパ漿 / 原形質

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2012/12/15 14:38:56」(JST)

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This article is about a human gene. For Bachelor of Chemical Engineering (BChE) degree, see Bachelor of Engineering.

Butyrylcholinesterase (also known as pseudocholinesterase, plasma cholinesterase,^[1] BCHE, or BuChE) is a non-specific cholinesterase enzyme that hydrolyses many different choline esters. In humans, it is found primarily in the liver^[1] and is encoded by the BCHE gene.^[2]

It is very similar to the neuronal acetylcholinesterase, which is also known as RBC or erythrocyte cholinesterase.^[1] The term "serum cholinesterase" is generally used in reference to a clinical test that reflects levels of both of these enzymes in the blood.^[1]

Butyrylcholine is a synthetic compound and does not occur in the body naturally. It is used as a tool to distinguish between acetyl- and butyrylcholinesterase.

Clinical significance

Pseudocholinesterase deficiency results in delayed metabolism of only a few compounds of clinical significance, including the following: succinylcholine, mivacurium, procaine, and cocaine. Of these, its most clinically important substrate is the depolarizing neuromuscular blocking agent, succinylcholine, which the pseudocholinesterase enzyme hydrolyzes to succinylmonocholine and then to succinic acid.

In individuals with normal plasma levels of normally functioning pseudocholinesterase enzyme, hydrolysis and inactivation of approximately 90-95% of an intravenous dose of succinylcholine occurs before it reaches the neuromuscular junction. The remaining 5-10% of the succinylcholine dose acts as an acetylcholine receptor agonist at the neuromuscular junction, causing prolonged depolarization of the postsynaptic junction of the motor-end plate. This depolarization initially triggers fasciculation of skeletal muscle. As a result of prolonged depolarization, endogenous acetylcholine released from the presynaptic membrane of the motor neuron does not produce any additional change in membrane potential after binding to its receptor on the myocyte. Flaccid paralysis of skeletal muscles develops within 1 minute. In normal subjects, skeletal muscle function returns to normal approximately 5 minutes after a single bolus injection of succinylcholine as it passively diffuses away from the neuromuscular junction. Pseudocholinesterase deficiency can result in higher levels of intact succinylcholine molecules reaching receptors in the neuromuscular junction, causing the duration of paralytic effect to continue for as long as 8 hours. This condition is recognized clinically when paralysis of the respiratory and other skeletal muscles fails to spontaneously resolve after succinylcholine is administered as an adjunctive paralytic agent during anesthesia procedures. In such cases respiratory assistance is required.^[3]

In 2008, an experimental new drug was discovered for the potential treatment of cocaine abuse and overdose based on the pseudocholiesterase structure. It was shown to remove cocaine from the body 2000 times as fast as the natural form of BChE. Studies in rats have shown that the drug prevented convulsions and death when administered cocaine overdoses.^[4] This enzyme also metabolizes succinylcholine which accounts for its rapid degradation in the liver and plasma. There may be genetic variability in the kinetics of this enzyme that can lead to prolonged muscle blockade and potentially dangerous respiratory depression that needs to be treated with assisted ventilation.

Mutant alleles at the BCHE locus are responsible for suxamethonium sensitivity. Homozygous persons sustain prolonged apnea after administration of the muscle relaxant suxamethonium in connection with surgical anesthesia. The activity of pseudocholinesterase in the serum is low and its substrate behavior is atypical. In the absence of the relaxant, the homozygote is at no known disadvantage.^[5]

Finally, pseudocholinesterase metabolism of procaine results in formation of paraaminobenzoic acid (PABA). If the patient receiving procaine is on sulfonamide antibiotics such as bactrim the antibiotic effect will be antagonized by providing a new source of PABA to the microbe for subsequent synthesis of folic acid.

Interactive pathway map

Click on genes, proteins and metabolites below to link to respective articles. ^[6]

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Irinotecan Pathway edit

References

^ ^a ^b ^c ^d http://www.umm.edu/ency/article/003358.htm
^ Allderdice PW, Gardner HA, Galutira D, Lockridge O, LaDu BN, McAlpine PJ (October 1991). "The cloned butyrylcholinesterase (BCHE) gene maps to a single chromosome site, 3q26". Genomics 11 (2): 452–4. doi:10.1016/0888-7543(91)90154-7. PMID 1769657.
^ emedicine.medscape.com, Pseudocholinesterase deficiency;
^ Zheng F, Yang W, Ko MC, Liu J, Cho H, Gao D, Tong M, Tai HH, Woods JH, Zhan CG (September 2008). "Most efficient cocaine hydrolase designed by virtual screening of transition states". J. Am. Chem. Soc. 130 (36): 12148–55. doi:10.1021/ja803646t. PMC 2646118. PMID 18710224. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2646118/. Lay summary – ScienceDaily.
^ "Entrez Gene: BCHE butyrylcholinesterase". http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=590.
^ The interactive pathway map can be edited at WikiPathways: "IrinotecanPathway_WP46359". http://www.wikipathways.org/index.php/Pathway:WP46359.

External links

Butyrylcholinesterase at the US National Library of Medicine Medical Subject Headings (MeSH)

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「cholinesterase」

Butyrylcholinesterase
	; PDB rendering based on 1p0i.
Available structures
PDB	Ortholog search: PDBe, RCSB
List of PDB id codes
	1P0I, 1P0M, 1P0P, 1P0Q, 1XLU, 1XLV, 1XLW, 2J4C, 2PM8, 2WID, 2WIF, 2WIG, 2WIJ, 2WIK, 2WIL, 2WSL, 2XMB, 2XMC, 2XMD, 2XMG, 2XQF, 2XQG, 2XQI, 2XQJ, 2XQK, 2Y1K, 3DJY, 3DKK, 3O9M, 4AQD, 4AXB, 4B0O, 4B0P
Identifiers
Symbols	BCHE; CHE1; E1
External IDs	OMIM: 177400 MGI: 894278 HomoloGene: 20065 ChEMBL: 1914 GeneCards: BCHE Gene
EC number	3.1.1.8
Gene Ontology
Molecular function	• beta-amyloid binding; • catalytic activity; • acetylcholinesterase activity; • carboxylesterase activity; • cholinesterase activity; • enzyme binding; • choline binding;
Cellular component	• extracellular region; • extracellular space; • nuclear envelope lumen; • endoplasmic reticulum lumen; • membrane;
Biological process	• synaptic transmission, cholinergic; • learning; • choline metabolic process; • response to drug; • response to alkaloid; • cocaine metabolic process; • negative regulation of synaptic transmission; • response to glucocorticoid stimulus; • response to folic acid;
	Sources: Amigo / QuickGO
RNA expression pattern
	More reference expression data
Orthologs
	This box: view; talk; edit;

　　[★] コリンエステラーゼ　

「cholinesterases」