Santhamma K R, Raj R K
Department of Biochemistry, University of Kerala Kariavattom, Thiruvananthapuram, India.
Biochem Biophys Res Commun. 1993 Jan 15;190(1):201-6. doi: 10.1006/bbrc.1993.1031.
Human filariasis is caused by Wuchereria bancrofti, Brugia malayi and B. timori. Of the several recommended model filarial parasites by WHO, Setaria digitata a bovine one has characteristics such as cyanide insensitivity, lack of detectable cytochromes, presence of two quinones Q8 and Q6. Of the two quinones Q8 seems to have a predominant role in energy production. In vitro inhibitory studies using quinone analogues, coenzyme Q0 and menadione have shown that these compounds paralyse the worms in very low concentrations compared to diethyl carbamazine, the drug of choice for filariasis. The mitochondrial energy production associated with electron transfer is intercepted by quinone analogues. Hence for the treatment of filariasis, this study paves a chemotherapeutic target for the design of drugs which can control the parasites by interacting at the subcellular level by energy depletion.
人类丝虫病由班氏吴策线虫、马来布鲁线虫和帝汶布鲁线虫引起。在世界卫生组织推荐的几种丝虫病模型寄生虫中，牛指状腹腔丝虫具有对氰化物不敏感、缺乏可检测的细胞色素、存在两种醌类物质Q8和Q6等特征。在这两种醌类物质中，Q8似乎在能量产生中起主要作用。使用醌类似物、辅酶Q0和甲萘醌进行的体外抑制研究表明，与丝虫病的首选药物乙胺嗪相比，这些化合物在极低浓度下就能使蠕虫麻痹。与电子传递相关的线粒体能量产生被醌类似物阻断。因此，对于丝虫病的治疗，本研究为设计能够通过在亚细胞水平上通过能量消耗相互作用来控制寄生虫的药物奠定了化疗靶点。
