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疟原虫感染的红细胞的热特性。

Thermal properties of red blood cells infected by malaria parasites.

作者信息

Forte T, Roca L

机构信息

Istituto Superiore di Sanità, Laboratorio di Biologia Cellulare, Rome, Italy.

出版信息

Exp Parasitol. 1989 Oct;69(3):272-80. doi: 10.1016/0014-4894(89)90073-8.

Abstract

Three membrane thermotropic transitions at 8, 20, and 40 degrees C have been detected in human red blood cells (RBC) by using spin-labeled stearic acids. Red blood cells infected in vitro by Plasmodium falciparum showed the disappearance of the 8 degrees C transition and a lowering of the 40 degrees C transition to 32 degrees C. The disappearance of the 8 degrees C transition was observed in synchronized cultures of P. falciparum trophozoites as well as in mouse RBC infected in vivo by an asynchronous population of P. berghei. Furthermore, erythrocytes infected by P. falciparum showed an increase in the phosphorylation of protein 4.1. This protein was shown previously to be involved in the 8 degrees C transition, (T. Forte, T. L. Leto, M. Minetti, and V. T. Marchesi, Biochemistry 24, 7876-7880 (1985). Our results suggest that the malaria parasite invasion produces a disorganization of the protein 4.1-membrane interaction.

摘要

通过使用自旋标记的硬脂酸,在人类红细胞(RBC)中检测到了三个膜热致转变,分别在8、20和40摄氏度。体外被恶性疟原虫感染的红细胞显示8摄氏度转变消失,40摄氏度转变降至32摄氏度。在恶性疟原虫滋养体的同步培养物以及体内被伯氏疟原虫异步群体感染的小鼠红细胞中,也观察到了8摄氏度转变的消失。此外,被恶性疟原虫感染的红细胞中蛋白质4.1的磷酸化增加。该蛋白质先前已被证明参与8摄氏度的转变(T. Forte、T. L. Leto、M. Minetti和V. T. Marchesi,《生物化学》24,7876 - 7880(1985))。我们的结果表明,疟原虫入侵会导致蛋白质4.1与膜的相互作用紊乱。

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