Quinidine is an antiarrhythmic drug commonly used for the treatment of cardiac ailments. It affects oxidative phosphorylation, calcium uptake, and ion channels of mitochondria. We have investigated the interaction of Quinidine and mitochondrial voltage-dependent anion channel (VDAC). VDAC was purified from neuronal tissue of Wistar rats and in vitro bilayer electrophysiology experiments were performed on it. 50-mM Quinidine treatment on VDAC leads to a sudden drop in its conductance. The dose of Quinidine leading to a half-maximal current through a single-channel VDAC was calculated using Quinidine at different concentrations. In silico molecular docking studies using Autodock-4.2 software indicate interaction between Quinidine and VDAC. Docking results demonstrate the interaction of Quinidine and VDAC on its Glutamic acid residue (Glu-206 of VDAC). Fluorescence spectroscopy results on Quinidine and Glutamic acid interaction show an increase in the intensity and wavelength of Quinidine fluorescence, whereas no interaction between Quinidine and Cysteine was observed. This further supports the Glutamic acid and Quinidine interaction. In conclusion, we report Quinidine partially blocks VDAC due to the interaction of Glutamic acid and Quinidine in the channel pore.

奎尼丁是一种常用于治疗心脏疾病的抗心律失常药物。它会影响线粒体的氧化磷酸化，钙摄取和离子通道。我们已经研究了奎尼丁和线粒体电压依赖性阴离子通道（VDAC）的相互作用。从Wistar大鼠的神经元组织中纯化VDAC，并对其进行体外双层电生理实验。在VDAC上进行50mM奎尼丁处理会导致其电导突然下降。使用不同浓度的奎尼丁计算导致通过单通道VDAC产生最大电流一半的奎尼丁剂量。使用Autodock-4.2软件进行的计算机分子对接研究表明，奎尼丁与VDAC之间存在相互作用。对接结果表明奎尼丁和VDAC在其谷氨酸残基（VDAC的Glu-206）上相互作用。奎尼丁和谷氨酸相互作用的荧光光谱结果表明，奎尼丁荧光的强度和波长增加，而奎尼丁和半胱氨酸之间没有相互作用。这进一步支持了谷氨酸和奎尼丁的相互作用。总之，我们报告奎尼丁由于谷氨酸和奎尼丁在通道孔中的相互作用而部分阻断了VDAC。