The activity of the mitochondrial CIII complex is modified by the Trypanosoma cruzi infection in myocardium and lymphocytes

BAEZ AL; LO PRESTI MS; RIVAROLA HW; GUZMAN MENTESANA G; PAGLINI PA

La Plata

Congreso; Meeting ISHR Latin American; 2010

ISHR

Reactive oxygen species have direct effects on cellular structure and function; mitochondria are damaged as a consequence of inflammatory processes that provoke oxidative stress and the Trypanosoma cruzi entrance into cardiac cells generates these kind of processes. In the present work we studied the effect of the T. cruzi infection upon the enzymatic activity of one of the mitochondrial respiratory chain complexes, CIII, very sensitive to the oxidative stress,  in myocardium and lymphocytes from  venous blood samples obtained from mice infected with T.cruzi,, SGO Z12 isolate from Santiago del Estero. Albino Swiss mice (n= 30) were used and divided into the following groups, G1= non-infected (n=10); G2= infected with 50 trypomastigotes (n=20).Cardiac tissue and venous blood samples were obtained from both groups 30 days post infection (d.p.i.), acute phase. Mitochondria were isolated by subcelullar fractioning determining CIII enzymatic activity by spectrophotometry. The enzymatic activities (ìm.min-1/mg prot) obtained were: myocardium CIII value in G1 was 0.38±0.03, and lymphocytes values were 0.33±0.06, but its activity in G2 (in myocardium and lymphocytes) was significantly reduced in the myocardium:0.03±0.01, lymphocytes:0.12±0.02 (p<0.0001). The histological and ultrastructural studies demonstrated inflammatory process and mitochondrial alterations. Present results show the mitochondrial involvement in a systemic manner during the acute phase of the T. cruzi infection, and a correlation between myocardium and lymphocytes mitochondria damage. Mitochondria could be a good marker for cardiac alterations that could be infer by the study of these organelle in a simple blood sample.