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四聚体重组人丁酰胆碱酯酶作为一种生物药物用于改善急性有机磷中毒症状的应用。

Application of Tetrameric Recombinant Human Butyrylcholinesterase as a Biopharmaceutical for Amelioration of Symptoms of Acute Organophosphate Poisoning.

作者信息

Terekhov S S, Palikov V A, Palikova Y A, Dyachenko I A, Shamborant O G, Smirnov I V, Masson P, Gabibov A G

机构信息

V. V. Shemyakin and Yu. A. Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, Moscow, Russia.

Affiliated Branch of V. V. Shemyakin and Yu. A. Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, Pushchino, Moscow Region, Russia.

出版信息

Bull Exp Biol Med. 2017 Aug;163(4):430-435. doi: 10.1007/s10517-017-3821-z. Epub 2017 Aug 29.

DOI:10.1007/s10517-017-3821-z
PMID:28853097
Abstract

We present a procedure for optimizing the expression of recombinant tetrameric butyrylcholinesterase that enables large-scale production with the yield >30 mg/liter (>90 mg/roller bottle). Intravenous injection of the preparation significantly increased survival and decreased the severity of symptoms of poisoning with paraoxon, an organophosphorus toxin.

摘要

我们提出了一种优化重组四聚体丁酰胆碱酯酶表达的方法，该方法能够实现大规模生产，产量>30毫克/升（>90毫克/滚瓶）。静脉注射该制剂可显著提高对氧磷（一种有机磷毒素）中毒后的生存率并减轻中毒症状的严重程度。

相似文献

1
Application of Tetrameric Recombinant Human Butyrylcholinesterase as a Biopharmaceutical for Amelioration of Symptoms of Acute Organophosphate Poisoning.四聚体重组人丁酰胆碱酯酶作为一种生物药物用于改善急性有机磷中毒症状的应用。
Bull Exp Biol Med. 2017 Aug;163(4):430-435. doi: 10.1007/s10517-017-3821-z. Epub 2017 Aug 29.
2
A novel expression cassette delivers efficient production of exclusively tetrameric human butyrylcholinesterase with improved pharmacokinetics for protection against organophosphate poisoning.一种新型表达盒可高效产生纯四聚体人丁酰胆碱酯酶，其药代动力学得到改善，可用于预防有机磷中毒。
Biochimie. 2015 Nov;118:51-9. doi: 10.1016/j.biochi.2015.07.028. Epub 2015 Aug 1.
3
Protection against paraoxon toxicity by an intravenous pretreatment with polyethylene-glycol-conjugated recombinant butyrylcholinesterase in macaques.静脉内预处理聚乙二醇化重组丁酰胆碱酯酶对猕猴的对氧磷毒性的保护作用。
Chem Biol Interact. 2014 Mar 5;210:20-5. doi: 10.1016/j.cbi.2013.12.010. Epub 2013 Dec 30.
4
Increased organophosphate scavenging in a butyrylcholinesterase mutant.丁酰胆碱酯酶突变体中有机磷酸清除增加。
Chem Biol Interact. 2008 Sep 25;175(1-3):376-9. doi: 10.1016/j.cbi.2008.04.012. Epub 2008 Apr 22.
5
Recombinant human butyrylcholinesterase from milk of transgenic animals to protect against organophosphate poisoning.来自转基因动物乳汁的重组人丁酰胆碱酯酶用于预防有机磷中毒。
Proc Natl Acad Sci U S A. 2007 Aug 21;104(34):13603-8. doi: 10.1073/pnas.0702756104. Epub 2007 Jul 27.
6
Aerosolized recombinant human butyrylcholinesterase delivered by a nebulizer provides long term protection against inhaled paraoxon in macaques.雾化吸入重组人丁酰胆碱酯酶通过雾化器对恒河猴吸入对氧磷提供长期保护。
Chem Biol Interact. 2019 Aug 25;309:108712. doi: 10.1016/j.cbi.2019.06.025. Epub 2019 Jun 12.
7
A single amino acid substitution, Gly117His, confers phosphotriesterase (organophosphorus acid anhydride hydrolase) activity on human butyrylcholinesterase.单个氨基酸取代，即甘氨酸117被组氨酸取代，赋予了人丁酰胆碱酯酶磷酸三酯酶（有机磷酸酐水解酶）活性。
Biochemistry. 1997 Jan 28;36(4):786-95. doi: 10.1021/bi961412g.
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Strategies for developing a recombinant butyrylcholinesterase medical countermeasure for Organophosphorus poisoning.开发用于有机磷中毒的重组丁酰胆碱酯酶医学对策的策略。
Chem Biol Interact. 2022 Aug 25;363:109996. doi: 10.1016/j.cbi.2022.109996. Epub 2022 May 30.
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Weak inhibitors protect cholinesterases from strong inhibitors (paraoxon): in vitro effect of tiapride.弱抑制剂可保护胆碱酯酶免受强抑制剂（对氧磷）的影响：硫必利的体外效应
J Appl Toxicol. 2005 Nov-Dec;25(6):562-7. doi: 10.1002/jat.1097.
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Adeno-associated virus-mediated expression of human butyrylcholinesterase to treat organophosphate poisoning.腺相关病毒介导的人丁酰胆碱酯酶表达治疗有机磷中毒。
PLoS One. 2019 Nov 25;14(11):e0225188. doi: 10.1371/journal.pone.0225188. eCollection 2019.

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Atomistic Origins of Resurrection of Aged Acetylcholinesterase by Quinone Methide Precursors.醌甲醚前体引发衰老乙酰胆碱酯酶复活的原子起源。
Molecules. 2024 Aug 3;29(15):3684. doi: 10.3390/molecules29153684.
2
Trends in the Recent Patent Literature on Cholinesterase Reactivators (2016-2019).近年来关于胆碱酯酶重激活剂的专利文献趋势（2016-2019）。
Biomolecules. 2020 Mar 12;10(3):436. doi: 10.3390/biom10030436.