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. 2020 Mar 27;43(1 Suppl 1):e20190163. doi: 10.1590/1678-4685-GMB-2019-0163

Figure 1. Oxidative stress in parasite-host interaction in T. cruzi. After infection, the parasite faces oxidative stress induced by the host cell. Parasites have several defense mechanisms to prevent damage to the nuclear and kinetoplast DNA. The first line of defense is composed of several antioxidants proteins; of these, TcAPX, TcCPX, TcMPX, TcSH, and SOD proteins are the best characterized. ROS that escape from the antioxidant system can cause DNA damage when they encounter parasite DNA molecules (8-oxoG is the most common modification that arises from this stress). To prevent the deleterious effects, the parasite has a specific BER subsystem (GO System), that directly interacts with the modified base within the genome (TcOGG1) or any mispair with this base (TcMYH). The BER repair system has been extensively studied in the parasite and proteins from all steps of this repair pathway have been characterized. The last component of the GO system, the TcMTH protein, has also been identified in T. cruzi. If any damage persists in the parasite’s nuclear or mitochondrial genome, translesion polymerases have also been identified, demonstrating that the parasite has means to survive massive amounts of oxidative stress.

Figure 1