Cardiac mitochondria dysfunction along Trypnosoma cruzi infectio

ALEJANDRA BÁEZ; SILVINA LO PRESTI; CAROLINA BAZÁN; MARIANA STRAUSS; WALTER RIVAROLA; PATRICIA PAGLINI

Salta

Congreso; XXX Congreso Nacional de Cardiología; 2012

Introduction. Trypanosoma  cruzi invasion and replication in cardiomyocytes induce cellular injuries and cytotoxic reactions, with the production of inflammatory cytokines and nitric oxide, both source of reactive oxygen species. The myocyte response to oxidative stress involves the progression of cellular changes primarily targeting mitochondria. We studied the cardiac mitochondrial structure and function through the enzymatic activity of citrate synthase (mitochondrial matrial) and respiratory chain CI–CIV complexes mitochondrial cristae). Materials and Methods. In Albino Swiss mice infected with T. cruzi, Tulahuen strain and SGO Z12 isolate in the acute (30 days post infection dpi, n:10) chronic indeterminate (75 dpi, n:10) and chronic phase (365 dpi N:10). A non infected group (n:10) was also studied). Data were analyzed by ANOVA and Chi-square test for categorical variables. Axiovision 3.0 program was used to quantify mitochondria. Significance level was set at p < 0.05. Results. Activity of complexes I to IV and citrate synthase, measured by spectrophotometric methods, was altered in different ways, according to the strain employed and the alteration were increasing from the acute to the chronic phase (P < 0.01). Changes in mitochondrial structure studied by electronic microscopy were detected in 71 %, 60% and 89% of Tulahuen- and 88%, 60% and 58% of SGO Z12-infected mice for the acute, chronic indeterminate and chronic phase respectively. Parasites were detected all along infection. Conclusions. Here we demonstrate that parasite persistence and inflammation are likely to be involved in the structural and functional alterations in cardiac mitochondria from the acute to the chronically T. cruzi-infected mice, demonstrating that in chagasic cardiopathy the parasite strain determines different mitochondrial changes that are involved in the pathophysiology of heart failure and could be important predictors of the evolution of cardiopathy.