Lehane Adele M, Saliba Kevin J, Allen Richard J W, Kirk Kiaran
School of Biochemistry and Molecular Biology, Faculty of Science, Australian National University, Canberra, ACT 0200, Australia.
Biochem Biophys Res Commun. 2004 Jul 23;320(2):311-7. doi: 10.1016/j.bbrc.2004.05.164.
The uptake by the intraerythrocytic malaria parasite of the phospholipid precursor choline was investigated in parasites 'isolated' from their host cells by saponin permeabilization of the erythrocyte membrane. Choline is transported across the parasite plasma membrane then phosphorylated and thereby trapped within the parasite. Choline influx was inhibited competitively by quinine. It increased with increasing extracellular pH, decreased on depolarization of the parasite plasma membrane with a protonophore or by increasing extracellular [K+], and increased in response to hyperpolarization of the membrane by decreasing extracellular [K+] or by addition of the K+ channel blocker Cs+. In ATP-depleted parasites choline was taken up but not phosphorylated. Under these conditions, imposition of an inwardly negative membrane potential using the K+ ionophore valinomycin resulted in the accumulation of choline to an intracellular concentration more than 15-fold higher than the extracellular concentration. Choline influx is therefore an electrogenic process, energized by the parasite plasma membrane potential.
通过对红细胞膜进行皂素通透处理，从宿主细胞“分离”出疟原虫，研究了红细胞内疟原虫对磷脂前体胆碱的摄取情况。胆碱穿过疟原虫的质膜，然后被磷酸化，从而被困在疟原虫内。奎宁竞争性抑制胆碱内流。胆碱内流随细胞外pH升高而增加，用质子载体使疟原虫质膜去极化或增加细胞外[K⁺]时内流减少，通过降低细胞外[K⁺]或添加K⁺通道阻滞剂Cs⁺使膜超极化时内流增加。在ATP耗竭的疟原虫中，胆碱被摄取但未被磷酸化。在这些条件下，使用K⁺离子载体缬氨霉素施加内向负膜电位会导致胆碱在细胞内积累，其浓度比细胞外浓度高15倍以上。因此，胆碱内流是一个由疟原虫质膜电位驱动的生电过程。
