Leishmaniasis is a neglected infection that is caused by Leishmania protozoa, affecting millions of people worldwide, mainly in tropical and subtropical regions. This disease has different clinical forms: cutaneous, mucocutaneous, and visceral. The drugs that are currently available for the treatment of this infection have limitations, such as high toxicity, long-term treatment, and leads to drug-resistant strains. Numerous studies, in various experimental models, have sought to develop more effective and less toxic chemotherapeutic agents against leishmaniasis. In the present study, we evaluated the mechanism of cell death that is induced by n-benzyl 1-(4-methoxy)phenyl-9H-β-carboline-3-carboxamide (C5) against Leishmania amazonensis. C5 increased reactive oxygen species production, depolarization of the mitochondrial membrane, DNA fragmentation, decrease of cell volume, lipoperoxidation, the accumulation of lipid bodies, and acidic vesicular organelles (AVOs) and caused the intense formation of autophagic compartments in L. amazonensis promastigotes. The results indicate that C5 causes L. amazonensis death through different pathways.
Keywords: Cell death; Leishmania amazonensis; Oxidative damage; β-carboline.
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