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Heart FoF1-ATPase changes during the acute phase of Trypanosoma cruzi infection in rats
Authors:Sérgio A. Uyemura  Maria C. Jordani  Ana C. M. Polizello  Carlos Curti
Affiliation:(1) Department of Clinical, Toxicological and Bromatological Analysis, University of São Paulo, Av. Café, s/n°, 14040-903 Ribeirão Preto, SP, Brasil;(2) Department of Physics and Chemistry, School of Pharmaceutical Science, University of São Paulo, Av. Café, s/n°, 14040-903 Ribeirão Preto, SP, Brasil;(3) Departamento de Física e Quimica, Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, Av. Café, s/n°, 14040-903 Ribeirão Preto, SP, Brasil
Abstract:The kinetic properties of ATP hydrolysis and synthesis by FoF1-ATPase of heart mitochondria were evaluated during the acute phase of T. cruzi infection in rats. Mitochondria and submitochondrial particles were isolated 7 days (early stage) and 25 days (late stage) following infection of rats with 2 × 105 trypomastigote forms of the Y strain of T. cruzi. The kinetic properties for ATP hydrolysis were altered for the early but not the late stage, showing a changed pH profile, increased K0.5 values, and a decreased total Vmax. The Arrhenius' plot for membrane-associated enzyme showed a higher transition temperature with a lower value for the activation energy in body temperature. For the Triton X-100 - solubilized enzyme, the plot was similar to the control. A decrease in the efficiency of ADP phosphorylation by mitochondria, measured by the firefly-luciferase luminescence, was observed only during the late stage and appeared to be correlated with a decrease in the affinity of the FoF1-ATPase for ADP. It is proposed that in the early stage, during the acute phase of T. cruzi infection in rats, heart FoF1-ATPase undergoes a membrane-dependent conformational change in order to maintain the phosphorylation potential of mitochondria, which would compensate for the uncoupling of mitochondrial function. Also, during both the early and late stages, the enzyme seems to be under the regulation of the endogenous inhibitor protein for the preservation of cellular ATP levels.
Keywords:Trypanosoma cruzi   rat heart  mitochondria  oxidative phosphorylation  FoF1-ATPase  ATP hydrolysis  ATP synthesis
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