Department of Animal Physiology and Development, Adam Mickiewicz University, Poznan, Poland.
J Insect Physiol. 2013 Nov;59(11):1125-32. doi: 10.1016/j.jinsphys.2013.08.007. Epub 2013 Aug 22.
In the present study, we describe the existence of mitochondrial ATP-dependent K(+) channel (mitoKATP) in two different insect tissues, fat body and muscle of cockroach Gromphadorhina coquereliana. We found that pharmacological substances known to modulate potassium channel activity influenced mitochondrial resting respiration. In isolated mitochondria oxygen consumption increased by about 13% in the presence of potassium channel openers (KCOs) such as diazoxide and pinacidil. The opening of mitoKATP was reversed by glibenclamide (potassium channel blocker) and 1 mM ATP. Immunological studies with antibodies raised against the Kir6.1 and SUR1 subunits of the mammalian ATP-sensitive potassium channel, indicated the existence of mitoKATP in insect mitochondria. MitoKATP activation by KCOs resulted in a decrease in superoxide anion production, suggesting that protection against mitochondrial oxidative stress may be a physiological role of mitochondrial ATP-sensitive potassium channel in insects.
在本研究中,我们描述了在两种不同的昆虫组织中存在线粒体 ATP 依赖性钾通道(mitoKATP),即蟑螂 Gromphadorhina coquereliana 的脂肪体和肌肉。我们发现,已知能调节钾通道活性的药理学物质会影响线粒体的静息呼吸。在分离的线粒体中,钾通道开放剂(KCOs)如二氮嗪和匹那地尔的存在使氧消耗增加了约 13%。mitoKATP 的开放可以被格列本脲(钾通道阻断剂)和 1 mM ATP 逆转。针对哺乳动物 ATP 敏感性钾通道的 Kir6.1 和 SUR1 亚基的抗体的免疫研究表明,昆虫线粒体中存在 mitoKATP。KCOs 激活 mitoKATP 会导致超氧阴离子产生减少,这表明对线粒体氧化应激的保护可能是昆虫线粒体 ATP 敏感性钾通道的生理作用。