Autor: |
Gonçalves RL; Laboratório de Bioquímica de Resposta ao Estresse, Programa de Biologia Molecular e Biotecnologia, Instituto de Bioquímica Médica, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, Brazil., Barreto RF, Polycarpo CR, Gadelha FR, Castro SL, Oliveira MF |
Jazyk: |
angličtina |
Zdroj: |
Journal of bioenergetics and biomembranes [J Bioenerg Biomembr] 2011 Dec; Vol. 43 (6), pp. 651-61. Date of Electronic Publication: 2011 Nov 12. |
DOI: |
10.1007/s10863-011-9398-8 |
Abstrakt: |
Trypanosoma cruzi is a hemoflagellate protozoan that causes Chagas' disease. The life cycle of T. cruzi is complex and involves different evolutive forms that have to encounter different environmental conditions provided by the host. Herein, we performed a functional assessment of mitochondrial metabolism in the following two distinct evolutive forms of T. cruzi: the insect stage epimastigote and the freshly isolated bloodstream trypomastigote. We observed that in comparison to epimastigotes, bloodstream trypomastigotes facilitate the entry of electrons into the electron transport chain by increasing complex II-III activity. Interestingly, cytochrome c oxidase (CCO) activity and the expression of CCO subunit IV were reduced in bloodstream forms, creating an "electron bottleneck" that favored an increase in electron leakage and H(2)O(2) formation. We propose that the oxidative preconditioning provided by this mechanism confers protection to bloodstream trypomastigotes against the host immune system. In this scenario, mitochondrial remodeling during the T. cruzi life cycle may represent a key metabolic adaptation for parasite survival in different hosts. |
Databáze: |
MEDLINE |
Externí odkaz: |
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