Trypanosoma cruzi is the etiological agent of Chagas Disease, which affects 6–7 million people worldwide. Since the early stages of infection and throughout its life cycle, the parasite is exposed to several genotoxic agents. Furthermore, DNA damage is also part of the mechanism of action of at least a few trypanocidal drugs, including Benznidazole. Thus, it is paramount for the parasite to count on an efficient DNA repair machinery to guarantee genome integrity and survival. The present work provides an up-to-date review of both the conserved and peculiar DNA repair mechanisms described in T. cruzi against oxidative stress, ultraviolet and ionizing radiation, DNA adduct-inducing agents, and Benznidazole. The comprehension of the DNA repair mechanisms of the parasite may shed light on the parasite evolution and possibly pave the way for the development of novel and more effective trypanocidal drugs.

克氏锥虫是恰加斯病的病原体，全世界有6-7百万人受其影响。由于感染的早期阶段及其整个生命周期，该寄生虫暴露于多种遗传毒性剂中。此外，DNA损伤也是至少一些锥虫杀菌药物（包括苯并咪唑）作用机理的一部分。因此，寄生虫依靠有效的DNA修复机制来保证基因组的完整性和生存是至关重要的。本工作提供了对T. cruzi中所述的保守和特殊DNA修复机制的最新综述。抗氧化应激，紫外线和电离辐射，DNA加合物诱导剂和苯并咪唑。寄生虫的DNA修复机制的理解可能会阐明寄生虫的进化，并可能为新型和更有效的锥虫病药物的开发铺平道路。