Difference between revisions of "Goncalves 2011 Abstract IOC65"
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{{Abstract | {{Abstract | ||
|title= | |title=Gonçalves 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= | |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 Chagasâ 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 | |abstract=''Trypanosoma cruzi'' is a hemoflagellate protozoan that causes Chagasâ 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 âelectron bottleneckâ 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= | |keywords=Energy metabolism, Reactive oxygen species, Trypanosomatids | ||
|mipnetlab=BR Rio | |mipnetlab=BR Rio de Janeiro Oliveira MF | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|instruments= | |area=Respiration, Developmental biology | ||
|organism=Protists | |||
|enzymes=Complex IV;cytochrome c oxidase | |||
|instruments=Oxygraph-2k | |||
}} | }} | ||
a.LaboratĂłrio de BioquĂmica de Resposta ao Estresse UFRJ c. LaboratĂłrio de Biologia Celular, Instituto Oswaldo Cruz d. LaboratĂłrio de Biologia Molecular, Programa de Biologia Molecular e Biotecnologia, Instituto de BioquĂmica MĂ©dica e. Departamento de BioquĂmica, Instituto de Biologia, Universidade Estadual de Campinas, Campinas, SP, Brasil. | a.LaboratĂłrio de BioquĂmica de Resposta ao Estresse UFRJ c. LaboratĂłrio de Biologia Celular, Instituto Oswaldo Cruz d. LaboratĂłrio de Biologia Molecular, Programa de Biologia Molecular e Biotecnologia, Instituto de BioquĂmica MĂ©dica e. Departamento de BioquĂmica, Instituto de Biologia, Universidade Estadual de Campinas, Campinas, SP, Brasil. |
Latest revision as of 17:27, 19 February 2018
Gonçalves 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 Chagasâ 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 âelectron bottleneckâ 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.
âą Keywords: Energy metabolism, Reactive oxygen species, Trypanosomatids
âą O2k-Network Lab: BR Rio de Janeiro Oliveira MF
Labels: MiParea: Respiration, Developmental biology
Organism: Protists
Enzyme: Complex IV;cytochrome c oxidase
HRR: Oxygraph-2k
a.LaboratĂłrio de BioquĂmica de Resposta ao Estresse UFRJ c. LaboratĂłrio de Biologia Celular, Instituto Oswaldo Cruz d. LaboratĂłrio de Biologia Molecular, Programa de Biologia Molecular e Biotecnologia, Instituto de BioquĂmica MĂ©dica e. Departamento de BioquĂmica, Instituto de Biologia, Universidade Estadual de Campinas, Campinas, SP, Brasil.