Cell death in Trypanosoma brucei induced by a thiosemicarbazone involves oxidative stress

M. C. SORAIRES SANTACRUZ, L. M. FINKIELSZTEIN, E. J. BONTEMPI

Congreso; IV International Congress in Translational Medicine; 2018

Trypanosoma brucei is the causative agent of sleeping sickness in man and nagana in cattle. The lack of a vaccine against these diseases and the notable limitations of drug treatments, mean a significant challenge to the proposed goal of eliminating these neglected diseases as a public health problem. A thiosemicarbazone (TSC1) emerged as a promising compound since it has been demonstrated that is capable to inhibit T. brucei proliferation and showed no cytotoxic effects on Vero cells. The present study aims to characterize by flow cytometry, the biochemical and morphological alterations induced by TSC1 in the death of parasite.In the various tests carried out, we observed a reduction of mitochondrial membrane potential, an increase in the formation of reactive oxygen species, phosphatidylserine exposure, reduction of cell volume but no significant changes were observed in cell cycle. Altogether, the alterations induced by TSC1 point to a break in the homeostatic balance of oxidative stress that caused the death of parasite through mechanism that likely involve autophagy or apoptosis.