Waller Karena L, Kim Kami, McDonald Thomas V
Department of Medicine (Cardiology), Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Exp Parasitol. 2008 Nov;120(3):280-5. doi: 10.1016/j.exppara.2008.07.010. Epub 2008 Jul 30.
Potassium channels are essential for cell survival and regulate the cell membrane potential and electrochemical gradient. During its lifecycle, Plasmodium falciparum parasites must rapidly adapt to dramatically variant ionic conditions within the mosquito mid-gut, the hepatocyte and red blood cell (RBC) cytosols, and the human circulatory system. To probe the participation of K(+) channels in parasite viability, growth response assays were performed in which asexual stage P. falciparum parasites were cultured in the presence of various Ca(2+)-activated K(+) channel blocking compounds. These data describe the novel anti-malarial effects of bicuculline methiodide and tubocurarine chloride and the novel lack of effect of apamine and verruculogen. Taken together, the data herein imply the presence of K(+) channels, or other parasite-specific targets, in P. falciparum-infected RBCs that are sensitive to blockade with Ca(2+)-activated K(+) channel blocking compounds.
钾通道对于细胞存活至关重要，并调节细胞膜电位和电化学梯度。在其生命周期中，恶性疟原虫寄生虫必须迅速适应蚊子中肠、肝细胞和红细胞（RBC）胞质溶胶以及人体循环系统内显著变化的离子条件。为了探究钾通道在寄生虫生存能力中的作用，进行了生长反应试验，其中无性阶段的恶性疟原虫寄生虫在各种钙激活钾通道阻断化合物存在的情况下进行培养。这些数据描述了甲硫酸荷包牡丹碱和氯化筒箭毒碱的新型抗疟作用，以及蜂毒明肽和疣孢菌素的新型无效作用。综上所述，本文数据表明在恶性疟原虫感染的红细胞中存在对钙激活钾通道阻断化合物阻断敏感的钾通道或其他寄生虫特异性靶点。
