Abstract: Chagas’ disease is a major parasitic cause of death and hardship, especially in the impoverished regions of Latin America. Trypanosoma cruzi is the etiologic agent of this disease. Characteristically, this hemoflagellate has an indirect life cycle with mammals as definitive hosts where attacks the heart, skeletal, smooth and cardiac muscles and the central nervous system. The drugs currently in use to treat this disease are nifurtimox and benznidazole. However, they have many side effects and are potentially toxic. Their mode of action includes free radical and electrophilic metabolites generation, which are toxic for the parasite. The parasite is more sensitive to the oxidative stress than the host. Gutathione and its spermidine derivative, trypanothione are the main antioxidative mechanisms in the parasite. Any modification in the parasite capacity to synthesise this thiols could induce a more susceptible environment to the action of the trypanocidal drugs. This effect may shorten treatment length or lower the required doses to treat this disease.