Goncalves 2011 Abstract IOC65: Difference between revisions
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{{Abstract | {{Abstract | ||
|title=Renata LS Gonçalvesa, Rubem FS Menna Barretoc, Carla R Polycarpod, Solange L Castro, Fernanda R Gadelhae, Marcus F Oliveira (2011) Comparative assessment of mitochondrial function on epimastigotes and bloodstream trypomastigotes of Trypanosoma cruzi. MiPNet16.03. | |title=Renata LS Gonçalvesa, Rubem FS Menna Barretoc, Carla R Polycarpod, Solange L Castro, Fernanda R Gadelhae, Marcus F Oliveira (2011) Comparative assessment of mitochondrial function on epimastigotes and bloodstream trypomastigotes of Trypanosoma cruzi. MiPNet16.03. | ||
|authors= | |authors=Goncalves RL, Rubem FS Menna Barretoc, Carla R Polycarpod, Solange L Castro, Fernanda R Gadelhae, Oliveira MF | ||
|year=2011 | |year=2011 | ||
|event=IOC65 | |event=IOC65 | ||
|abstract=Trypanosoma cruzi is a hemoflagellate protozoan that causes Chagas’ disease. T. cruzi life-cycle is complex involving different evolutive forms that experience striking differences in their environmental condition. Here we carried out a functional assessment of mitochondrial function in two distinct T. cruzi forms: the insect stage, epimastigote and the freshly isolated bloodstream trypomastigote. We observed that in comparison to epimastigotes, bloodstream trypomastigotes facilitate electrons entry into the electron transport chain increasing complex II-III activity. Curiously, cytochrome c oxidase (CCO) activity and the expression of CCO subunit IV were reduced in bloodstream forms, creating an “electron bottleneck” that favored increased electron leak and H2O2 formation. We propose that the oxidative preconditioning provided by this mechanism would confer a protection to the bloodstream trypomastigotes against host immune response. Thus, mitochondrial remodeling during the T. cruzi life-cycle can represent a key metabolic adaptation for parasite survival in different environments. | |abstract=Trypanosoma cruzi is a hemoflagellate protozoan that causes Chagas’ disease. T. cruzi life-cycle is complex involving different evolutive forms that experience striking differences in their environmental condition. Here we carried out a functional assessment of mitochondrial function in two distinct T. cruzi forms: the insect stage, epimastigote and the freshly isolated bloodstream trypomastigote. We observed that in comparison to epimastigotes, bloodstream trypomastigotes facilitate electrons entry into the electron transport chain increasing complex II-III activity. Curiously, cytochrome c oxidase (CCO) activity and the expression of CCO subunit IV were reduced in bloodstream forms, creating an “electron bottleneck” that favored increased electron leak and H2O2 formation. We propose that the oxidative preconditioning provided by this mechanism would confer a protection to the bloodstream trypomastigotes against host immune response. Thus, mitochondrial remodeling during the T. cruzi life-cycle can represent a key metabolic adaptation for parasite survival in different environments. | ||
|keywords=energy metabolism, reactive oxygen species, trypanosomatids | |keywords=energy metabolism, reactive oxygen species, trypanosomatids | ||
|mipnetlab=BR Rio De Janeiro Oliveira MF | |mipnetlab=BR Rio De Janeiro Oliveira MF | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
Revision as of 13:01, 22 November 2011
| Renata LS Gonçalvesa, Rubem FS Menna Barretoc, Carla R Polycarpod, Solange L Castro, Fernanda R Gadelhae, Marcus F Oliveira (2011) Comparative assessment of mitochondrial function on epimastigotes and bloodstream trypomastigotes of Trypanosoma cruzi. MiPNet16.03. |
Link:
Goncalves RL, Rubem FS Menna Barretoc, Carla R Polycarpod, Solange L Castro, Fernanda R Gadelhae, Oliveira MF (2011)
Event: IOC65
Trypanosoma cruzi is a hemoflagellate protozoan that causes Chagas’ disease. T. cruzi life-cycle is complex involving different evolutive forms that experience striking differences in their environmental condition. Here we carried out a functional assessment of mitochondrial function in two distinct T. cruzi forms: the insect stage, epimastigote and the freshly isolated bloodstream trypomastigote. We observed that in comparison to epimastigotes, bloodstream trypomastigotes facilitate electrons entry into the electron transport chain increasing complex II-III activity. Curiously, cytochrome c oxidase (CCO) activity and the expression of CCO subunit IV were reduced in bloodstream forms, creating an “electron bottleneck” that favored increased electron leak and H2O2 formation. We propose that the oxidative preconditioning provided by this mechanism would confer a protection to the bloodstream trypomastigotes against host immune response. Thus, mitochondrial remodeling during the T. cruzi life-cycle can represent a key metabolic adaptation for parasite survival in different environments.
• Keywords: energy metabolism, reactive oxygen species, trypanosomatids
• O2k-Network Lab: BR Rio De Janeiro Oliveira MF
Labels:
HRR: MiPNet-Publication"MiPNet-Publication" is not in the list (Oxygraph-2k, TIP2k, O2k-Fluorometer, pH, NO, TPP, Ca, O2k-Spectrophotometer, O2k-Manual, O2k-Protocol, ...) of allowed values for the "Instrument and method" property.
a.Laboratório de Bioquímica de Resposta ao Estresse UFRJ c. Laboratório de Biologia Celular, Instituto Oswaldo Cruz d. Laboratório de Biologia Molecular, Programa de Biologia Molecular e Biotecnologia, Instituto de Bioquímica Médica e. Departamento de Bioquímica, Instituto de Biologia, Universidade Estadual de Campinas, Campinas, SP, Brasil.
