疟原虫约氏疟原虫感染的小鼠红细胞中寄生虫诱导的腺苷渗透过程。
Parasite-induced processes for adenosine permeation in mouse erythrocytes infected with the malarial parasite Plasmodium yoelii.
作者信息
Gati W P, Lin A N, Wang T I, Young J D, Paterson A R
机构信息
McEachern Laboratory, University of Alberta, Edmonton, Canada.
出版信息
Biochem J. 1990 Nov 15;272(1):277-80. doi: 10.1042/bj2720277.
Abstract
In mouse erythrocytes harbouring the malarial parasite Plasmodium yoelii, three processes contributed to inward fluxes of adenosine, one of which is attributed to the native nucleoside transporter, because of the inhibitory effects of nitrobenzylthioinosine (NBMPR). New (parasite-induced) permeation processes of low NBMPR-sensitivity were (i) saturable fluxes with preference for the D enantiomer (D-Ado) and (ii) apparently unsaturable fluxes that proceeded by a channel-like route without enantiomeric selectivity. Parasite-induced fluxes of L- and D-Ado were similarly inhibited by furosemide [IC50 (concn. causing half-maximal inhibition) 15-17 microM], whereas D-Ado fluxes in uninfected erythrocytes were 10-fold less sensitive.
摘要
在携带疟原虫约氏疟原虫的小鼠红细胞中，有三个过程促成了腺苷的内向通量，其中一个归因于天然核苷转运体，这是由于硝基苄硫肌（NBMPR）的抑制作用。新的（寄生虫诱导的）低NBMPR敏感性的通透过程为：（i）对D对映体（D-腺苷）有偏好的饱和通量，以及（ii）通过类似通道的途径进行且无对映体选择性的明显不饱和通量。速尿对寄生虫诱导的L-腺苷和D-腺苷通量有类似的抑制作用[IC50（引起半数最大抑制的浓度）为15 - 17微摩尔]，而未感染红细胞中的D-腺苷通量敏感性则低10倍。
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