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=Gonçalvesa RL, Barretoc RFSM, Polycarpod CR, Castro SL, Gadelhae FR, Oliveira MF (2011) Comparative assessment of mitochondrial function on epimastigotes and bloodstream trypomastigotes of Trypanosoma cruzi. MiPNet16.03.
|authors=Goncalves RL, Rubem FS Menna Barretoc, Carla R Polycarpod, Solange L Castro, Fernanda R Gadelhae, Oliveira MF
|authors=Goncalves RL, Barretoc RFSM, Polycarpod CR, Castro SL, Gadelhae FR, 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 (CIV) activity and the expression of CIV 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

Revision as of 07:54, 20 December 2011

Gonçalvesa RL, Barretoc RFSM, Polycarpod CR, Castro SL, Gadelhae FR, Oliveira MF (2011) Comparative assessment of mitochondrial function on epimastigotes and bloodstream trypomastigotes of Trypanosoma cruzi. MiPNet16.03.

Link:

Goncalves RL, Barretoc RFSM, Polycarpod CR, Castro SL, Gadelhae FR, 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 (CIV) activity and the expression of CIV 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


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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.

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