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Effect of Crotalus viridis viridis snake venom on the ultrastructure and intracellular survival of Trypanosoma cruzi

Published online by Cambridge University Press:  21 July 2010

CAMILA M. ADADE
Affiliation:
Laboratório de Biologia Celular e Ultraestrutura, Departamento de Microbiologia Geral, Instituto de Microbiologia Prof. Paulo de Góes, Centro de Ciências da Saúde, bloco I, Universidade Federal do Rio de Janeiro, Ilha do Fundão, Rio de Janeiro, Brazil
BRUNO LEMOS CONS
Affiliation:
Laboratório de Farmacologia das Toxinas e Substâncias Antagonistas, Centro de Ciências da Saúde, bloco J, Universidade Federal do Rio de Janeiro, Ilha do Fundão, Rio de Janeiro, Brazil
PAULO A. MELO
Affiliation:
Laboratório de Farmacologia das Toxinas e Substâncias Antagonistas, Centro de Ciências da Saúde, bloco J, Universidade Federal do Rio de Janeiro, Ilha do Fundão, Rio de Janeiro, Brazil
THAÏS SOUTO-PADRÓN*
Affiliation:
Laboratório de Biologia Celular e Ultraestrutura, Departamento de Microbiologia Geral, Instituto de Microbiologia Prof. Paulo de Góes, Centro de Ciências da Saúde, bloco I, Universidade Federal do Rio de Janeiro, Ilha do Fundão, Rio de Janeiro, Brazil
*
*Corresponding author: Laboratório de Biologia Celular e Ultraestrutura, Instituto de Microbiologia Prof. Paulo de Góes, CCS, Bloco I, UFRJ, Ilha do Fundão, Rio de Janeiro, RJ, Brazil. Tel: +55 21 2562 6738. Fax: +5521 2560 8344. E-mail: souto.padron@micro.ufrj.br

Summary

Chagas' disease, caused by Trypanosoma cruzi, affects 16–18 million people in Central and South America. Patient treatment is based on drugs that have toxic effects and limited efficacy. Therefore, new chemotherapeutic agents need to be developed. Snake venoms are sources of natural compounds used in various medical treatments. We observed that Crotalus viridis viridis venom was effective against all developmental forms of T. cruzi. Ultrastructural analysis revealed swelling of mitochondria, blebbing and disruption of the plasma membrane, loss of cytoplasm components and morphological changes of the cell. Staining with propidium iodide and rhodamine 123 confirmed the observed alterations in the plasma and mitochondrial membranes, respectively. The effects of the venom on the parasite intracellular cycle were also analysed. Pre-infected LLC-MK2 cells incubated with Cvv venom showed a 76–93% reduction in the number of parasites per infected cell and a 94–97·4% reduction in the number of parasites per 100 cells after 96 h of infection. Free trypomastigotes harvested from the supernatants of Cvv venom-treated cells were incapable of initiating a new infection cycle. Our data demonstrate that Cvv venom can access the host cell cytoplasm at concentrations that cause toxicity only to the amastigote forms of T. cruzi, and yields altered parasites with limited infective capacity, suggesting the potential use of Cvv venom in Chagas' disease chemotherapy.

Type
Research Article
Copyright
Copyright © Cambridge University Press 2010

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