Saliba Kevin J, Krishna Sanjeev, Kirk Kiaran
School of Biochemistry and Molecular Biology, Faculty of Science, Australian National University, Canberra ACT 0200, Australia.
FEBS Lett. 2004 Jul 16;570(1-3):93-6. doi: 10.1016/j.febslet.2004.06.032.
An O-3-hexose derivative, shown previously to inhibit a malaria parasite hexose transporter expressed in Xenopus oocytes as well as to suppress the multiplication of parasites, both in vitro and in vivo, was shown here to block the uptake of hexose sugars into isolated blood-stage parasites. This led to a decline in ATP levels and the loss of intracellular pH control. The results are consistent with those obtained with the cloned transporter. They support the notion that the transporter mediates uptake of glucose into the intraerythrocytic parasite and provide further support for the view that it is a suitable antimalarial drug target.
一种O-3-己糖衍生物,此前已证明其可抑制非洲爪蟾卵母细胞中表达的疟原虫己糖转运蛋白,并在体外和体内抑制疟原虫的增殖,在此研究中发现它可阻断己糖进入分离的血液期疟原虫。这导致ATP水平下降以及细胞内pH控制丧失。这些结果与克隆转运蛋白所获得的结果一致。它们支持该转运蛋白介导葡萄糖进入红细胞内疟原虫的观点,并为其是合适的抗疟药物靶点这一观点提供了进一步支持。