Laboratório de Ultraestrutura Celular Hertha Meyer, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, CEP 21949-900, Brazil.
Int J Antimicrob Agents. 2013 Feb;41(2):183-7. doi: 10.1016/j.ijantimicag.2012.09.018. Epub 2012 Dec 4.
Chagas disease, caused by the protozoan Trypanosoma cruzi, is an endemic illness in Latin America. Efforts have been made by several groups to develop new effective and safe anti-T. cruzi drugs. In the present work, we show that thiazolidine LPSF SF29 inhibited growth of the epimastigote and amastigote forms and caused lysis in the trypomastigote form of T. cruzi, leading to death of the protozoan. Mitochondrial dysfunction was also observed. The thiazolidine induced ultrastructural alterations such as detachment of the flagellar membrane, intense mitochondrial swelling, formation of myelin-like figures and the appearance of autophagosomes. Taken together, these results suggest that this new thiazolidine is active against T. cruzi and constitutes a promising drug for the therapy of Chagas disease.
恰加斯病由原生动物克氏锥虫引起,是拉丁美洲的一种地方病。几个小组已经在努力开发新的有效和安全的抗克氏锥虫药物。在本工作中,我们表明噻唑烷 LPSF SF29 抑制了滋养体和无鞭毛体形式的生长,并导致克氏锥虫的锥鞭毛体形式的裂解,导致原生动物的死亡。还观察到线粒体功能障碍。噻唑烷诱导了超微结构的改变,如鞭毛膜的脱落、线粒体的强烈肿胀、髓鞘样结构的形成和自噬体的出现。总之,这些结果表明,这种新的噻唑烷对克氏锥虫具有活性,是一种治疗恰加斯病的有前途的药物。