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INTRODUCTION
Chagas disease is a neglected infectious disease caused by the flagellated protozoan Trypanosoma cruzi (Bern, 2015). Due to the lack of prophylactic agents and effective chemotherapy, there is no cure after the parasite spread and install in the organs of the vertebrate host (Novaes et al. 2016a , b ; WHO, 2016). In response to continuous immigration of infected people from Central and South American endemic regions, Chagas disease has also become a serious health problem in non-endemic areas, especially in the USA and European countries (Hotez et al. 2012). Beyond the 6-7 million people infected with T. cruzi in Central and South America, 70 million people are at risk of contracting the infection worldwide (Bern, 2015).
Due to myotropic parasitic behaviour, muscle tissues are intensely parasitized by T. cruzi, generating skeletal myositis, myocarditis, cardiomyocytes atrophy and necrosis in animals and humans (Novaes et al. 2013; Bern, 2015). Cardiac damage is associated with the direct cell parasitism (i.e. cardiomyocytolysis) and unspecific immunomediated mechanisms, in which the exacerbated Th1 inflammatory response against the parasite induces secondary damage to host cells (Marin-Neto et al. 2007; Dutra et al. 2014). In this mechanism, the overproduction of reactive metabolites (i.e. free radicals) by inflammatory cells and the resultant oxidative tissue damage has been implicated as a pivotal mechanism involved in the pathogenesis of Chagas cardiomyopathy (Gupta et al. 2009a , b ; Machado et al. 2013).
It has been indicated that beyond the reactive oxygen (ROS) and nitrogen (RNS) species produced by the inflammatory cells, mitochondrial dysfunction in parasitized cardiomyocytes provides an additional source of reactive mediators (Gupta et al. 2009a , b ; Wen et al. 2010). Considering that ROS and RNS exerts a pivotal role in the physiopathology of Chagas cardiomyopathy, there is limited and controversial evidence that antioxidant and anti-inflammatory therapy is beneficial to attenuate reactive tissue damage and the pathological remodelling associated with the myocarditis induced by T. cruzi infection (Gusmão et al. 2012; Marim et al. 2012; Budni et al. 2013). By using a murine model of T. cruzi infection we compared the relevance of vitamins C, E (abundant and low-cost antioxidants) or ibuprofen (a...