Glutathione export from uninfected human erythrocytes was compared with that from cells infected with the malaria parasite Plasmodium falciparum using two separate methods that distinguish between oxidized (GSSG) and reduced (GSH) glutathione. One involved enzymatic recycling with or without thiol-masking; the other involved rapid derivatization followed by HPLC. Glutathione efflux from uninfected erythrocytes under physiological conditions occurred predominantly as GSH. On exposure of the cells to oxidative challenge, efflux of GSSG exceeded that of GSH. Efflux of both species was blocked by MK571, an inhibitor of mammalian multidrug-resistance proteins. Glutathione efflux from parasitized erythrocytes was substantially greater than that from uninfected erythrocytes. Under physiological conditions, the exported species was GSH, whereas under energy-depleted conditions, GSSG efflux occurred. Glutathione export from parasitized cells was inhibited partially by MK571 and more so by furosemide, an inhibitor of the 'new permeability pathways' induced by the parasite in the host erythrocyte membrane. Efflux from isolated parasites occurred as GSH. On exposure to oxidative challenge, this GSH efflux decreased, but no GSSG export was detected. These results are consistent with the view that the parasite supplies its host erythrocyte with GSH, much of which is exported from the infected cell via parasite-induced pathways.

译文

:使用两种分别区分氧化型(GSSG)和还原型(GSH)谷胱甘肽的方法,将未感染的人类红细胞的谷胱甘肽输出与感染疟原虫恶性疟原虫的细胞的谷胱甘肽输出进行了比较。一种涉及有或没有硫醇掩蔽的酶循环。另一个涉及快速衍生化,然后进行HPLC。在生理条件下,未感染红细胞的谷胱甘肽外排主要以GSH形式发生。当细胞暴露于氧化性刺激后,GSSG的流出超过了GSH。两种物种的外流都被MK571阻断,MK571是一种哺乳动物多药抗性蛋白的抑制剂。寄生的红细胞的谷胱甘肽外排显着大于未感染的红细胞的谷胱甘肽外排。在生理条件下,出口物种为GSH,而在能量消耗条件下,发生了GSSG外排。谷胱甘肽从寄生虫细胞中的输出受到MK571的部分抑制,而速尿则更受抑制,速尿是由宿主红细胞膜中的寄生虫诱导的“新通透性途径”的抑制剂。来自分离的寄生虫的外排以GSH发生。暴露于氧化刺激后,该GSH外排量减少,但未检测到GSSG出口。这些结果与以下观点一致:寄生虫为其宿主红细胞提供了GSH,其中GSH大部分是通过寄生虫诱导的途径从被感染的细胞中输出的。

+1
+2
100研值 100研值 ¥99课程
检索文献一次
下载文献一次

去下载>

成功解锁2个技能,为你点赞

《SCI写作十大必备语法》
解决你的SCI语法难题!

技能熟练度+1

视频课《玩转文献检索》
让你成为检索达人!

恭喜完成新手挑战

手机微信扫一扫,添加好友领取

免费领《Endnote文献管理工具+教程》

微信扫码, 免费领取

手机登录

获取验证码
登录