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Plasmodium falciparum invasion and intraerythrocytic development are impaired by 2 ', 3 '-dialdehyde adenosine

机译:Falciparum侵袭和鼻内肾小球发育的疟原虫侵袭为2',3'-daldehyde腺苷损害

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Purine nucleotide synthesis in protozoa takes place exclusively via the purine salvage pathway and S-adenosyl-L-homocysteine hydrolase (SAHH) is an important enzyme in the Plasmodium salvage pathway which is not present in erythrocytes. Here, we describe the antimalarial effect of 2 ' 3 '-dialdehyde adenosine or oxidized adenosine (oADO), inhibitor of SAHH, on in vitro infection of human erythrocytes by P. falciparum. Treatment of infected erythrocytes with oADO inhibits parasite development and reinvasion of new cells. Erythrocytes pre-treated with oADO have a reduced susceptibility to invasion. Our results suggest that oADO interferes with one or more parasitic enzymes of the purine salvage pathway. (c) 2017 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.
机译:原生动物中的嘌呤核苷酸合成仅通过嘌呤救生途径进行,S-腺苷-1-同型半胱氨酸水解酶(SAHH)是在红细胞中不存在的疟原虫挽救途径中的重要酶。 在这里,我们描述了2'3'-二醛腺苷或氧化腺苷(OADO),Sahh抑制剂,对人红细胞的体外感染的抗疟疾作用,综合症。 用OADO治疗感染的红细胞抑制新细胞的寄生虫发育和再生。 用OADO预处理的红细胞具有降低的侵袭易感性。 我们的结果表明,OADO干扰了嘌呤救生途径的一种或多种寄生酶。 (c)2017年Institut Pasteur。 由Elsevier Masson SA出版。 版权所有。

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