Different cell death pathways induced by drugs in Trypanosoma cruzi: an ultrastructural study.

摘要: Electron microscopy has proven to be a reliable and essential tool determine morphological alterations target organelles in the investigation of new drugs for Chagas disease. In this review, we focused on evaluating different agents that induce death Trypanosoma cruzi, i.e. lysophospholipids analogues, naphthoquinones derivatives, cytoskeletal inhibitors natural products. Apoptosis-like presents as characteristics DNA fragmentation, membrane blebbing apoptotic body formation. Autophagy involves autophagosome formation, with appearance membranes surrounding cytosolic structures. Necrosis causes loss osmotic balance, an increase cytoplasmic vacuolization plasma disruption. Mitochondrion appears central checkpoint both apoptosis necrosis. Our evidences ultrastructural changes T. cruzi treated classes compounds point dramatic mitochondrial similar autophagic phenotypes. Lysophospholipid analogues interfere lipid biosynthesis epimastigotes, altering amount phospholipids sterols, consequently physical properties membrane. Naphthoquinone derivatives led strong fragmentation trypomastigotes release cysteine proteases from reservosomes cytosol starting proteolytic process which results parasite death. The susceptibility was also observed parasites propolis, suggesting impairment metabolism, compromising fluidity leading lysis. blocked mitosis arresting cell cycle impairing proliferation. variety drug stimuli converge same pathway suggests intense cross-talking between three types PCD protozoa.