Trypanosoma cruzi is the causative agent of Chagas disease, a debilitating illness that affects about 8-10 million people in Latin America having a considerable economic and social impact. T. cruzi epimastigotes have to deal with the reactive oxygen species (ROS) in the invertebrate host intestinal tract derived from the degradation of hemoglobin that generates high levels of heme. The excess of ROS could have deleterious effects to cells since these ROS can oxidize several molecules such as lipids, carbohydrates, proteins and nucleic acids. In DNA, the action of ROS can cause single- and double-strand breaks (SSBs and DSBs, respectively), base excision and oxidation. Like most living organisms, T. cruzi is susceptible to oxidative stress, hence DNA repair is essential for its survival and establishment of the infection. T. cruzi has only one mitochondrion and nowadays, it is clear that it has an important role besides the production of ATP. It is the source of signaling molecules, such as ROS and its integrity is essential for parasite survival. In this research project, the extension to which the mitochondrion contributes to parasite survival (different strains) under H2O2 treatment will be covered. These results will deepen our knowledge regarding the strategies used by T. cruzi for its survival under oxidative stress conditions and will allow the identification of new targets that could lead to the development of a more specific therapy.
News published in Agência FAPESP Newsletter about the scholarship: