钒化合物对拮抗剂与人脑毒蕈碱受体结合的抑制作用。

Inhibition of antagonist binding to human brain muscarinic receptor by vanadium compounds.

作者信息

Venters H, Ala T A, Frey W H

机构信息

Department of Neurology, The Alzheimer's Treatment and Research Center, St. Paul Ramsey Medical Center, MN 55101-2595, USA.

出版信息

Recept Signal Transduct. 1997;7(3):137-42.

PMID:9440500

Abstract

Metavanadate, orthovanadate, and pervanadate all inhibited [3H]QNB antagonist binding to the human brain muscarinic acetylcholine receptor (mAChR) in the presence of glutathione, with the order of decreasing potency and the concentration required for 50% inhibition (I[50]) being: pervanadate (95 microM) > orthovanadate (132 microM) > metavanadate (452 microM). Omission of glutathione decreased the inhibition of the vanadium compounds 2-6-fold. Preincubating the vanadium compounds with the mAChR in the presence of glutathione at 37 degrees for 1 h markedly decreased the I(50) values as follows: pervanadate (13 microM) > orthovanadate (46 microM) > metavanadate (118 microM). Inhibition by the vanadium compounds was blocked by EDTA, Mn2+, and Trolox, a water-soluble vitamin E analog. Vanadium use in treating diabetes is discussed regarding its inhibition of mAChR function.

摘要

在存在谷胱甘肽的情况下，偏钒酸盐、正钒酸盐和过钒酸盐均抑制[3H]QNB拮抗剂与人脑毒蕈碱型乙酰胆碱受体（mAChR）的结合，其效力递减顺序以及50%抑制所需浓度（I[50]）如下：过钒酸盐（95微摩尔）>正钒酸盐（132微摩尔）>偏钒酸盐（452微摩尔）。去除谷胱甘肽会使钒化合物的抑制作用降低2至6倍。在37摄氏度下，将钒化合物与mAChR在存在谷胱甘肽的情况下预孵育1小时，会显著降低I(50)值，如下所示：过钒酸盐（13微摩尔）>正钒酸盐（46微摩尔）>偏钒酸盐（118微摩尔）。钒化合物的抑制作用可被EDTA、Mn2+和水溶性维生素E类似物Trolox阻断。讨论了钒在治疗糖尿病方面对mAChR功能的抑制作用。