Trypanosoma cruzi is a protozoan of great medical interest since it is the causative agent of Chagas disease, an endemic condition in Latin America. This parasite undergoes epigenetic events, such as phosphorylation, methylation and acetylation, which play a role in several cellular processes including replication, transcription and gene expression. Histone deacetylases (HDAC) are involved in chromatin compaction and post-translational modifications of cytoplasmic proteins, such as tubulin. Tubastatin A (TST) is a specific HDAC6 inhibitor that affects cell growth and promotes structural modifications in cancer cells and parasites. In the present study, we demonstrated that T. cruzi epimastigote cell proliferation and viability are reduced after 72 h of TST treatment. The results obtained through different microscopy methodologies suggest that this inhibitor impairs the polymerization dynamics of cytoskeleton microtubules, generating protozoa displaying atypical morphology and cellular patterns that include polynucleated parasites. Furthermore, the microtubules of treated protozoa were more intensely acetylated, especially at the anterior portion of the cell body. A cell cycle analysis demonstrated an increase in the number of trypanosomatids in the G2/M phase. Together, our results suggest that TST should be explored as a tool to study trypanosomatid cell biology, including microtubule cytoskeleton dynamics, and as an antiparasitic drug.

克氏锥虫是一种具有重要医学意义的原生动物，因为它是南美一种地方病恰加斯病的病原体。这种寄生虫经历表观遗传事件，如磷酸化、甲基化和乙酰化，这些事件在包括复制、转录和基因表达在内的几个细胞过程中发挥作用。组蛋白去乙酰化酶 (HDAC) 参与染色质压实和细胞质蛋白（如微管蛋白）的翻译后修饰。Tubastatin A (TST) 是一种特异性 HDAC6 抑制剂，可影响细胞生长并促进癌细胞和寄生虫的结构改变。在本研究中，我们证明了T. cruziTST 处理 72 小时后，上鞭毛体细胞增殖和活力降低。通过不同的显微镜方法获得的结果表明，这种抑制剂会损害细胞骨架微管的聚合动力学，产生显示非典型形态和细胞模式的原生动物，其中包括多核寄生虫。此外，处理过的原生动物的微管被更强烈地乙酰化，尤其是在细胞体的前部。细胞周期分析表明 G2/M 期锥虫数量增加。总之，我们的结果表明，应将 TST 作为研究锥虫细胞生物学（包括微管细胞骨架动力学）的工具和抗寄生虫药物进行探索。