Mitochondrial bioenergetics and redox state are unaltered in Trypanosoma cruzi isolates with compromised mitochondrial complex I subunit genes.
In trypanosomatids the involvement of mitochondrial complex I in NADH oxidation has long been debated. Here, we took advantage of natural Trypanosoma cruzi mutants which present conspicuous deletions in ND4, ND5 and ND7 genes coding for complex I subunits to further investigate its functionality. Mitochondrial bioenergetics of wild type and complex I mutants showed no significant differences in oxygen consumption or respiratory control ratios in the presence of NADH-linked substrates or FADH(2)-generating succinate. No correlation could be established between mitochondrial membrane potentials and ND deletions. Since release of reactive oxygen species occurs at complex I, we measured mitochondrial H(2)O(2) formation induced by different substrates. Significant differences not associated to ND deletions were observed among the parasite isolates, demonstrating that these mutations are not important for the control of oxidant production. Our data support the notion that complex I has a limited function in T. cruzi.
Carranza
Julio César
JC
Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, São Paulo, SP, Brasil.
Kowaltowski
Alicia J
AJ
Mendonça
Marco Aurélio G
MA
de Oliveira
Thays C
TC
Gadelha
Fernanda R
FR
Zingales
Bianca
B
D000818:Animals; D019069:Cell Respiration / Q000502:physiology; D042967:Electron Transport Complex I / Q000235:genetics*; D004734:Energy Metabolism / Q000235:genetics / Q000502:physiology*; D006861:Hydrogen Peroxide / Q000378:metabolism; D053078:Membrane Potential, Mitochondrial / Q000502:physiology; D008928:Mitochondria / Q000502:physiology*; D010084:Oxidation-Reduction; D010101:Oxygen Consumption / Q000502:physiology; D021122:Protein Subunits / Q000172:deficiency / Q000235:genetics; D014349:Trypanosoma cruzi / Q000502:physiology*
D021122:Protein Subunits; D006861:Hydrogen Peroxide; D042967:Electron Transport Complex I