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约氏疟原虫尼氏亚种感染小鼠期间肝脏血红素和血红素加氧酶的状态

Status of hepatic heme and heme oxygenase during Plasmodium yoelii nigeriensis infection in mice.

作者信息

Sahni S K, Saxena N, Tekwani B L, Dutta G P, Pandey V C

机构信息

Division of Biochemistry, Central Drug Research Institute, Lucknow, India.

出版信息

Exp Mol Pathol. 1991 Aug;55(1):55-62. doi: 10.1016/0014-4800(91)90018-s.

Abstract

Plasmodium yoelii nigeriensis infection in albino mice caused a significant increase in hepatic heme level, the increase being concomitant with a rise in parasitemia. This elevated heme was found to be associated with all the subcellular fractions except the cytosol, where its content remained unaltered. Activity of heme oxygenase, the key enzyme responsible for catabolism of heme, also increased progressively with rise in parasitemia. Treatment of normal mice with cobalt chloride [60 mg (kg body wt)-1; subcutaneously] brought about a 150% increase in the level of heme oxygenase; similar treatment of infected mice at low parasitemia could induce the enzyme activity while at high parasitemia the enzymic activity remained unaltered as compared to untreated infected mice. In spite of an increased level of heme oxygenase in the cobalt-treated mice, the level of heme did not show any noticeable change. Oral administration of chloroquine [64 mg (kg body wt)-1 x 4 days] brought about a 56% reduction in the level of heme oxygenase of normal animals but there was no change in infected animals when compared with the corresponding untreated infected mice. However, the amount of chloroquine present in livers of normal and infected animals was not significantly different.

摘要

约氏疟原虫尼氏亚种感染白化小鼠导致肝脏血红素水平显著升高,这种升高与寄生虫血症的上升同时发生。发现这种升高的血红素与除细胞质溶胶外的所有亚细胞组分相关,其细胞质溶胶中的含量保持不变。血红素加氧酶是负责血红素分解代谢的关键酶,其活性也随着寄生虫血症的升高而逐渐增加。用氯化钴[60毫克/(千克体重);皮下注射]处理正常小鼠会使血红素加氧酶水平增加150%;在低寄生虫血症时对感染小鼠进行类似处理可诱导酶活性,而在高寄生虫血症时,与未处理的感染小鼠相比,酶活性保持不变。尽管在经钴处理的小鼠中血红素加氧酶水平升高,但血红素水平并未显示出任何明显变化。口服氯喹[64毫克/(千克体重)×4天]使正常动物的血红素加氧酶水平降低了56%,但与相应的未处理感染小鼠相比,感染动物没有变化。然而,正常和感染动物肝脏中氯喹的含量没有显著差异。

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