二氮嗪和平尼地尔可使丙酮酸-苹果酸诱导的线粒体呼吸解偶联。
Diazoxide and pinacidil uncouple pyruvate-malate-induced mitochondrial respiration.
作者信息
Kopustinskiene Dalia M, Jovaisiene Jovita, Liobikas Julius, Toleikis Adolfas
机构信息
Institute for Biomedical Research, Kaunas University of Medicine, Lithuania.
出版信息
J Bioenerg Biomembr. 2002 Feb;34(1):49-53. doi: 10.1023/a:1013870704002.
We investigated the effects of K(ATP) channel openers diazoxide and pinacidil on the respiration rate and membrane potential (deltapsi) of rat heart mitochondria, oxidizing pyruvate and malate. Diazoxide and pinacidil (58.8-1348.3 microM) increased the V2 (-ADP) respiration rate accordingly by 13-208% and 30-273% and decreased the deltapsi by 2-17% and 6-55%. These effects were also similar in the respiration medium without K+. Moreover, carboxyatractyloside completely abolished diazoxide- and pinacidil-induced uncoupling, indicating a role for the mitochondrial adenine nucleotide translocase in this process.
我们研究了钾离子通道开放剂二氮嗪和匹那地尔对大鼠心脏线粒体呼吸速率和膜电位（ΔΨ）的影响，这些线粒体氧化丙酮酸和苹果酸。二氮嗪和匹那地尔（58.8 - 1348.3微摩尔）相应地使V2（-ADP）呼吸速率提高了13% - 208%和30% - 273%，并使膜电位降低了2% - 17%和6% - 55%。在无钾离子的呼吸介质中，这些效应也相似。此外，羧基苍术苷完全消除了二氮嗪和匹那地尔诱导的解偶联作用，表明线粒体腺嘌呤核苷酸转位酶在此过程中发挥了作用。
Zotero 插件