Mittal Mukul K, Rai Smita, Gupta Suman, Sundar Shyam, Goyal Neena
Division of Biochemistry, Central Drug Research Institute, Lucknow, India.
Am J Trop Med Hyg. 2007 Apr;76(4):681-8.
Clinical resistance to pentavalent antimonial compounds has long been recognized as a major problem in the treatment of visceral leishmaniasis in India. However, mechanisms of natural resistance are unclear. In this study, we observed that Leishmania donovani clinical isolates not responsive to sodium stibogluconate showed resistance to antimony treatment in both in vitro and in vivo laboratory conditions. The resistant isolates have increased levels of intracellular thiols. This increase in thiol levels was not mediated by the amplification of gamma-glutamylcysteine synthetase, but was accompanied by amplification of trypanothione reductase and an intracellular ATP-binding cassette transporter gene MRPA. The resistance of parasites to antimony could be reversed by the glutathione biosynthesis-specific inhibitor, buthionine sulfoximine, which resulted in increased drug susceptibility. These results suggest the possible role of thiols and MRPA in antimony resistance in field isolates.
长期以来,五价锑化合物的临床耐药性一直被认为是印度治疗内脏利什曼病的一个主要问题。然而,天然耐药机制尚不清楚。在本研究中,我们观察到对葡萄糖酸锑钠无反应的杜氏利什曼原虫临床分离株在体外和体内实验室条件下均表现出对锑治疗的耐药性。耐药分离株的细胞内硫醇水平升高。硫醇水平的这种升高不是由γ-谷氨酰半胱氨酸合成酶的扩增介导的,而是伴随着锥虫硫醇还原酶和细胞内ATP结合盒转运蛋白基因MRPA的扩增。寄生虫对锑的耐药性可被谷胱甘肽生物合成特异性抑制剂丁硫氨酸亚砜胺逆转,从而导致药物敏感性增加。这些结果表明硫醇和MRPA在野外分离株的锑耐药性中可能发挥作用。