American tegumentary leishmaniasis (ATL) is a neglected disease that is widely distributed in the Americas. The protozoan parasite Leishmania (Viannia) braziliensis is one of the main causative agents of ATL, being responsible for the development of different clinical manifestations of the disease, which ranges from self-healing cutaneous lesions to disseminated and mucocutaneous forms. Because iron is essential for the survival and growth of Leishmania, as it is required for colonization of macrophages and development of lesions in mice, several chelating compounds have been tested for their effects on the growth of these parasites. In the present work, treatment of L. (V.) braziliensis with the iron chelator 2,2-dipyridyl inhibited the growth of promastigote forms in a dose- and time-dependent manner. However, multiplication of the parasites was recovered after reinoculation in fresh culture medium. The iron chelator also induced mitochondrial dysfunction and altered expression of proteins involved in metabolism of nucleic acids and coordination of post-translational modifications. The events described above ultimately caused the death of some parasites, most likely due to mitochondrial dysfunction, whereas others adapted and survived, suggesting a plasticity or resilience of the mitochondrion in this parasite.