Programmed cell death in Trypanosoma cruzi induced by Bothrops jararaca venom

Cells die through a programmed process or accidental death, know as apoptosis or necrosis, respectively. Bothrops jararaca is a snake whose venom inhibits the growth of Trypanosoma cruzi epimastigote forms causing mitochondrion swelling and cell death. The aim of the present work was to determine th...

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Bibliographic Details
Published in:Memórias do Instituto Oswaldo Cruz 2005-02, Vol.100 (1), p.33-38
Main Authors: Deolindo, Poliana, Teixeira-Ferreira, André S, Melo, Edésio J T, Arnholdt, Andrea Cristina Veto, Souza, Wanderley de, Alves, Elias W, DaMatta, Renato A
Format: Article
Language:English
Subjects:
Animals
Antiprotozoal Agents - pharmacology
Apoptosis - drug effects
Bothrops
Bothrops jararaca
Cell Membrane - drug effects
Cell Membrane - ultrastructure
Crotalid Venoms - pharmacology
Flow Cytometry
Microscopy, Electron, Transmission
Mitochondria - drug effects
Mitochondria - ultrastructure
PARASITOLOGY
programmed cell death
snake venom
Time Factors
TROPICAL MEDICINE
Trypanosoma cruzi
Trypanosoma cruzi - drug effects
Trypanosoma cruzi - programmed cell death -Bothrops jararaca - snake venom
Trypanosoma cruzi - ultrastructure
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Summary:Cells die through a programmed process or accidental death, know as apoptosis or necrosis, respectively. Bothrops jararaca is a snake whose venom inhibits the growth of Trypanosoma cruzi epimastigote forms causing mitochondrion swelling and cell death. The aim of the present work was to determine the type of death induced in epimastigotes of T. cruzi by this venom. Parasite growth was inhibited after venom treatment, and 50% growth inhibition was obtained with 10 μg/ml. Ultrastructural observations confirmed mitochondrion swelling and kinetoplast disorganization. Furthermore, cytoplasmic condensation, loss of mitochondrion membrane potential, time-dependent increase in phosphatidylserine exposure at the outer leaflet plasma membrane followed by permeabilization, activation of caspase like protein and DNA fragmentation were observed in epimastigotes throughout a 24 h period of venom treatment. Taken together, these results indicate that the stress induced in epimastigote by this venom, triggers a programmed cell death process, similar to metazoan apoptosis, which leads to parasite death.
ISSN:1678-8060
0074-0276
0074-0276
1678-8060
DOI:10.1590/S0074-02762005000100006