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诺氏疟原虫:在蛋白酶抑制剂存在的情况下,裂殖子入侵恒河猴红细胞的研究

Plasmodium knowlesi: studies on invasion of rhesus erythrocytes by merozoites in the presence of protease inhibitors.

作者信息

Hadley T, Aikawa M, Miller L H

出版信息

Exp Parasitol. 1983 Jun;55(3):306-11. doi: 10.1016/0014-4894(83)90027-9.

Abstract

The effect of protease inhibitors on invasion of rhesus erythrocytes by Plasmodium knowlesi merozoites was evaluated. Chymostatin, N-alpha-p-tosyl-L-lysine chloromethyl ketone (TLCK), and L-1-tosylamide-2-phenylethylchloromethyl ketone (TPCK) inhibited invasion. Leupeptin, antipain, pepstatin, and phenylmethylsulfonyl fluoride (PMSF) had no effect. TLCK and TPCK inhibited attachment of merozoites to host erythrocytes. Chymostatin had no adverse effect on attachment, and in its presence junction formation between the merozoite and host erythrocyte occurred. Both chymostatin and leupeptin inhibited normal rupture of schizont-infected erythrocytes. It is suggested that proteolytic activity may be important both in the rupture of schizont-infected erythrocytes and in the invasion of erythrocytes by malaria parasites.

摘要

评估了蛋白酶抑制剂对诺氏疟原虫裂殖子侵袭恒河猴红细胞的影响。抑肽酶、N-α-对甲苯磺酰-L-赖氨酸氯甲基酮(TLCK)和L-1-对甲苯磺酰胺-2-苯乙基氯甲基酮(TPCK)可抑制侵袭。亮抑酶肽、抗蛋白酶、胃蛋白酶抑制剂和苯甲基磺酰氟(PMSF)则无作用。TLCK和TPCK可抑制裂殖子与宿主红细胞的附着。抑肽酶对附着无不良影响,且在其存在的情况下,裂殖子与宿主红细胞之间会形成连接。抑肽酶和亮抑酶肽均抑制裂殖体感染红细胞的正常破裂。提示蛋白水解活性在裂殖体感染红细胞的破裂以及疟原虫对红细胞的侵袭过程中可能都很重要。

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