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药物敏感和耐药疟疾中的宿主血红素分解代谢

Host heme catabolism in drug-sensitive and drug-resistant malaria.

作者信息

Eckman J R, Modler S, Eaton J W, Berger E, Engel R R

出版信息

J Lab Clin Med. 1977 Oct;90(4):767-70.

PMID:333045
Abstract

Chloroquine resistance has arisen in both human and murine forms of malaria. CR Plasmodium berghei in mice does not produce the malaria pigment which is characteristic of the CS form. Determinations of carbon monoxide production (i.e., host heme catabolism) by individual mice revealed that those infected with CS P. berghei produce only one fourth as much carbon monoxide as do CR infected mice at all levels of infection. These observations confirm the idea that malaria pigment is composed of precipitated host cell hemoglobin and suggest that drug resistance is accompanied by a basic alteration in parasite-mediated hemoglobin catabolism.

摘要

氯喹抗性已在人类和鼠类疟疾病例中出现。小鼠体内的氯喹抗性伯氏疟原虫不会产生作为氯喹敏感型特征的疟色素。对个体小鼠一氧化碳生成量(即宿主血红素分解代谢)的测定显示,在所有感染水平下,感染氯喹敏感型伯氏疟原虫的小鼠产生的一氧化碳量仅为感染氯喹抗性型小鼠的四分之一。这些观察结果证实了疟色素由沉淀的宿主细胞血红蛋白组成这一观点,并表明耐药性伴随着寄生虫介导的血红蛋白分解代谢的基本改变。

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Host heme catabolism in drug-sensitive and drug-resistant malaria.药物敏感和耐药疟疾中的宿主血红素分解代谢
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2
Hemoglobin catabolism and host-parasite heme balance in chloroquine-sensitive and chloroquine-resistant Plasmodium berghei infections.氯喹敏感和氯喹耐药伯氏疟原虫感染中的血红蛋白分解代谢及宿主-寄生虫血红素平衡
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Chloroquine resistance and host cell hemoglobin catabolism in Plasmodium berghei.伯氏疟原虫中的氯喹抗性与宿主细胞血红蛋白分解代谢
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