Mitochondrial dysfunction in Trypanosoma cruzi: The role of Serratia marcescens prodigiosin in the alternative treatment of Chagas disease
Author
dc.contributor.author
Genes, Carlos
Author
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Baquero, Eduard
Author
dc.contributor.author
Echeverri, Fernando
Author
dc.contributor.author
Maya Arango, Juan
Author
dc.contributor.author
Triana, Omar
Admission date
dc.date.accessioned
2019-03-11T13:01:37Z
Available date
dc.date.available
2019-03-11T13:01:37Z
Publication date
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2011
Cita de ítem
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Parasites and Vectors, Volumen 4, Issue 1, 2018,
Identifier
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17563305
Identifier
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10.1186/1756-3305-4-66
Identifier
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https://repositorio.uchile.cl/handle/2250/165222
Abstract
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Background: Chagas disease is a health threat for many people, mostly those living in Latin America. One of the most important problems in treatment is the limitation of existing drugs. Prodigiosin, produced by Serratia marcescens (Rhodnius prolixus endosymbiont), belongs to the red-pigmented bacterial prodiginine family, which displays numerous biological activities, including antibacterial, antifungal, antiprotozoal, antimalarial, immunosuppressive, and anticancer properties. Here we describe its effects on Trypanosoma cruzi mitochondria belonging to Tc I and Tc II. Results: Parasites exposed to prodigiosin altered the mitochondrial function and oxidative phosphorylation could not have a normal course, probably by inhibition of complex III. Prodigiosin did not produce cytotoxic effects in lymphocytes and Vero cells and has better effects than benznidazole. Our data suggest that the action of prodigiosin on the parasites is mediated by mitochondrial structural and functional disruptio