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恶性疟原虫的2-半胱氨酸过氧化物酶参与该寄生虫对热应激的抗性。

2-Cys peroxiredoxin of Plasmodium falciparum is involved in resistance to heat stress of the parasite.

作者信息

Kimura Risa, Komaki-Yasuda Kanako, Kawazu Shin-ichiro, Kano Shigeyuki

机构信息

Research Institute, National Center for Global Health and Medicine, 1-21-1 Toyama, Shinjuku-ku, Tokyo, Japan.

出版信息

Parasitol Int. 2013 Apr;62(2):137-43. doi: 10.1016/j.parint.2012.11.005. Epub 2012 Nov 30.

DOI:10.1016/j.parint.2012.11.005
PMID:23201565
Abstract

In the cytoplasm of Plasmodium falciparum, two peroxiredoxins: PfTPx-1 and Pf1-Cys-Prx, are expressed at different time-points of the parasite cell cycle during the intraerythrocytic stage. In the present study, to gain insight into the functions of Prxs in the cytoplasm of P. falciparum, we investigated the heat stress sensitivity of the previously established PfTPx-1 KO line and found that PfTPx-1 disruption renders the parasite hypersensitive to heat stress. In addition, we established Pf1-Cys-Prx knockout (KO) parasite lines. The phenotypes of Pf1-Cys-Prx KO lines were different to those of the PfTPx-1 KO line and did not show hypersensitivity to reactive oxygen species, reactive nitrogen species, chloroquine or heat stress. These results suggest that the function of Pf1-Cys-Prx in the parasite cytoplasm is independent from that of PfTPx-1. The hyperthermal protective function of the PfTPx-1 is obviously important for the parasite physiology in the human patient body, in which it must survive repeated incidences of fever.

摘要

在恶性疟原虫的细胞质中,两种过氧化物还原酶:PfTPx-1和Pf1-Cys-Prx,在红细胞内期寄生虫细胞周期的不同时间点表达。在本研究中,为了深入了解过氧化物还原酶在恶性疟原虫细胞质中的功能,我们研究了先前建立的PfTPx-1基因敲除系对热应激的敏感性,发现PfTPx-1基因的破坏使寄生虫对热应激高度敏感。此外,我们建立了Pf1-Cys-Prx基因敲除(KO)寄生虫系。Pf1-Cys-Prx基因敲除系的表型与PfTPx-1基因敲除系不同,对活性氧、活性氮、氯喹或热应激均未表现出超敏反应。这些结果表明,Pf1-Cys-Prx在寄生虫细胞质中的功能独立于PfTPx-1。PfTPx-1的热保护功能对人体患者体内的寄生虫生理学显然很重要,因为它必须在反复发热的情况下存活下来。

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