ABSTRACT: Clinically, the disease is divided into the acute stages, indeterminate and chronic. The acute phase is characterized by the sign of Romanã and chagoma inoculation, high parasitemia, and general symptoms and systemic alterations. The indeterminate phase is characterized by absence symptoms, normal electrocardiogram, chest radiographs and gut normal but with positive serology for Chagas disease and the chronic phase may manifest on the cardiac form, with electrocardiographic changes or chest radiograph with cardiomegaly, and the digestive form, with megaesophagus or megacolon. In the acute phase, the QM1 T. cruzi strain presents tropism for cardiac muscle and striated, and in the chronic phase, over these tissues, also infects the colon. At these sites, phagocytosis of T. cruzi by macrophages triggers immune response mediated by Th-1 lymphocytes, able to destroy much of the parasites in the acute phase, however, the permanence of microfocus parasite would be the incentive for continuous production of IL-12 and Th-1 profile is consistent with a delayed hypersensitivity, which leads to tissue damage in the chronic phase. The damage to the myocardium and other tissues in Chagas disease is a consequence of the degree of oxidative stress and antioxidant capacity of the affected tissue. It was observed that in Chagas disease the activation of cellular antioxidant systems is not sufficient to eliminate ERMO of infected tissues. Studies of supplementation with vitamins C and E showed the efficiency of non-enzymatic antioxidants in neutralizing the oxidative insult caused by Chagas disease. But other studies show that were found in T. cruzi peroxiredoxins (Prx) type 1-Cys, which are reduced by ascorbic acid, become active in the decomposition of peroxides and protect them from oxidative action triggered by the immune system.
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