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通过抑制脑醛脱氢酶来抑制饮酒。

Suppression of alcohol drinking with brain aldehyde dehydrogenase inhibition.

作者信息

Sinclair J D, Lindros K O

出版信息

Pharmacol Biochem Behav. 1981 Mar;14(3):377-83. doi: 10.1016/0091-3057(81)90405-6.

DOI:10.1016/0091-3057(81)90405-6
PMID:7232463
Abstract

Calcium cyanamide, an aldehyde dehydrogenase (ALDH) inhibitor used in the treatment of alcoholism, strongly suppressed voluntary ethanol drinking by rats. Such inhibitors have generally been believed to act primarily by limiting drinking through acetaldehyde accumulation after ethanol consumption. Administration of a low dose of 4-methylpyrazole (4-MP) that abolished acetaldehyde accumulation did not, however, remove the suppression produced by cyanamide. 4-MP alone did not affect the unsuppressed alcohol intake by Long Evans rats or the drinking by rats of the ANA strain developed for low levels of ethanol consumption. When given from the start with cyanamide, 4-MP did affect the development of the suppression, but probably by its effect in lessening the degree of brain ALDH inhibition: a high correlation (r = +0.825, p less than 0.001) was found between brain ALDH activity and ethanol consumption. The results suggest that cyanamide suppresses alcohol drinking also in the absence of acetaldehyde accumulation probably by some action related to its direct inhibition of brain ALDH.

摘要

氰胺化钙是一种用于治疗酒精中毒的醛脱氢酶(ALDH)抑制剂,它能强烈抑制大鼠的自愿乙醇摄入。人们普遍认为,这类抑制剂主要通过在乙醇摄入后限制乙醛积累来限制饮酒。然而,给予低剂量的4-甲基吡唑(4-MP)以消除乙醛积累,并不能消除氰胺产生的抑制作用。单独使用4-MP对长Evans大鼠未受抑制的酒精摄入量或为低水平乙醇消费而培育的ANA品系大鼠的饮酒量没有影响。当与氰胺同时给药时,4-MP确实影响了抑制作用的发展,但可能是通过其减轻脑ALDH抑制程度的作用:发现脑ALDH活性与乙醇摄入量之间存在高度相关性(r = +0.825,p小于0.001)。结果表明,氰胺在没有乙醛积累的情况下也能抑制酒精摄入,这可能与其直接抑制脑ALDH的某种作用有关。

相似文献

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Suppression of alcohol drinking with brain aldehyde dehydrogenase inhibition.通过抑制脑醛脱氢酶来抑制饮酒。
Pharmacol Biochem Behav. 1981 Mar;14(3):377-83. doi: 10.1016/0091-3057(81)90405-6.
2
Aldehyde dehydrogenase inhibitors and voluntary ethanol drinking by rats.醛脱氢酶抑制剂与大鼠的自愿乙醇摄入
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Alterations in brain aldehyde dehydrogenase activity modify the locomotor effects produced by ethanol in rats.大脑醛脱氢酶活性的改变会改变乙醇对大鼠产生的运动效应。
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The metabolism of acetaldehyde and not acetaldehyde itself is responsible for in vivo ethanol-induced lipid peroxidation in rats.乙醛的代谢而非乙醛本身,是大鼠体内乙醇诱导脂质过氧化的原因。
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Generation of protein adducts with malondialdehyde and acetaldehyde in muscles with predominantly type I or type II fibers in rats exposed to ethanol and the acetaldehyde dehydrogenase inhibitor cyanamide.在暴露于乙醇和乙醛脱氢酶抑制剂氨甲环酸的大鼠中,主要含有I型或II型纤维的肌肉中与丙二醛和乙醛生成蛋白质加合物的情况。
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Mystic Acetaldehyde: The Never-Ending Story on Alcoholism.神秘的乙醛:关于酗酒的无尽故事
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Glucagon-like peptide-1 (GLP-1) receptor agonist prevents development of tolerance to anti-anxiety effect of ethanol and withdrawal-induced anxiety in rats.胰高血糖素样肽-1(GLP-1)受体激动剂可预防大鼠对乙醇抗焦虑作用产生耐受性以及戒断所致的焦虑。
Metab Brain Dis. 2015 Jun;30(3):719-30. doi: 10.1007/s11011-014-9627-z. Epub 2014 Nov 8.
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Dipeptidyl-peptidase IV (DPP-IV) inhibitor delays tolerance to anxiolytic effect of ethanol and withdrawal-induced anxiety in rats.
二肽基肽酶IV(DPP-IV)抑制剂可延缓大鼠对乙醇抗焦虑作用的耐受性及戒断所致焦虑。
Metab Brain Dis. 2015 Jun;30(3):659-67. doi: 10.1007/s11011-014-9603-7. Epub 2014 Aug 17.
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Role of acetaldehyde in ethanol-induced conditioned taste aversion in rats.乙醛在大鼠乙醇诱导的条件性味觉厌恶中的作用。
Psychopharmacology (Berl). 2003 May;167(2):130-6. doi: 10.1007/s00213-003-1427-9. Epub 2003 Mar 25.
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Daidzin suppresses ethanol consumption by Syrian golden hamsters without blocking acetaldehyde metabolism.大豆苷元可抑制叙利亚金黄地鼠的乙醇摄入,而不阻断乙醛代谢。
Proc Natl Acad Sci U S A. 1995 Sep 12;92(19):8990-3. doi: 10.1073/pnas.92.19.8990.
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Catalase activity measured in rats naive to ethanol correlates with later voluntary ethanol consumption: possible evidence for a biological marker system of ethanol intake.在未接触过乙醇的大鼠中测得的过氧化氢酶活性与后来的自愿乙醇摄入量相关:这可能是乙醇摄入量生物标志物系统的证据。
Psychopharmacology (Berl). 1988;95(4):512-5. doi: 10.1007/BF00172965.
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Psychopharmacology (Berl). 1989;98(2):176-82. doi: 10.1007/BF00444688.