首页> 外文期刊>Comparative biochemistry and physiology, Part B. Biochemistry & molecular biology >Changes in rodent-erythrocyte methemoglobin reductase system produced by two malaria parasites,viz. Plasmodium yoelii nigeriensis and Plasmodium berghei
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Changes in rodent-erythrocyte methemoglobin reductase system produced by two malaria parasites,viz. Plasmodium yoelii nigeriensis and Plasmodium berghei

机译:两种疟疾寄生虫产生的啮齿动物-红细胞高铁血红蛋白还原酶系统的变化,即。约氏疟原虫和伯氏疟原虫

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摘要

The methemoglobin reductase system plays a vital role in maintaining the equilibrium between hemoglobin and methemoglobin in blood. Exposure of red blood cells to oxidative stress (pathological/physiologicaI) may cause impairment to this equilibrium. We studied the status of erythrocytic methemoglobin and the related reductase system during Plasmodium yoelii nigeriensis infection in mice and P. berghei infection in mastomys. Malaria infection was induced by intraperitoneal inoculation with 106 infected erythrocytes. The present investigation revealed a significant decrease in the activity of methemoglobin reductase, with a concomitant rise in methemoglobin content during P. yoelii nigeriensis infection in mice erythrocytes. This was accompanied with a significant increase in reduced glutathione and ascorbate levels. The activity of lactate dehydrogenase, glucose 6-phosphate dehydrogenase and glutathione reductase increased with a progressive rise in parasitemia. However, no methemoglobin or associated reductase activity was detected in normal and P. berghei-infected mastomys. P. berghei infection in mastomys resulted in an increase in the level of reduced glutathione and ascorbate in erythrocytes, and also in the activity of lactate dehydrogenase, glucose 6-phosphate dehydrogenase and glutathione reductase. These results suggest that antioxidants/antioxidant enzymes may prevent or reduce the formation of methemoglobin in the host and thereby protect the host from methemo- globinemia.
机译:高铁血红蛋白还原酶系统在维持血液中血红蛋白和高铁血红蛋白之间的平衡中起着至关重要的作用。红细胞暴露于氧化应激(病理/生理)可能会损害该平衡。我们研究了小鼠约氏疟原虫感染和乳房切除术中伯氏疟原虫感染期间红细胞高铁血红蛋白的状态及相关的还原酶系统。腹膜内接种106株感染的红细胞可诱发疟疾感染。目前的研究表明,高铁血红蛋白还原酶的活性显着降低,在小鼠红细胞感染约氏疟原虫的过程中,高铁血红蛋白含量随之增加。这伴随着减少的谷胱甘肽和抗坏血酸水平的显着增加。乳酸脱氢酶,6-磷酸葡萄糖脱氢酶和谷胱甘肽还原酶的活性随着寄生虫血症的逐步增加而增加。然而,在正常感染和伯氏疟原虫感染的乳腺肌瘤中未检测到高铁血红蛋白或相关的还原酶活性。乳腺造瘘术中的伯氏疟原虫感染导致红细胞中还原型谷胱甘肽和抗坏血酸水平的增加,以及乳酸脱氢酶,6-磷酸葡萄糖脱氢酶和谷胱甘肽还原酶的活性增加。这些结果表明抗氧化剂/抗氧化酶可以预防或减少宿主体内高铁血红蛋白的形成,从而保护宿主免受高铁血红蛋白血症的侵害。

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