The Trypanosoma cruzi infection with an isolate obtained from an endemic produce alterations in the complexes of the cardiac mitochondrial respirator

Reactive oxygen species have direct effects on cellular structure and function; mitochondria are damaged with the entrance of Trypanosoma cruzi into cardiac cells as a consequence of the immflamatory processes that provoke oxidative stress. In the present work we studied the effect of the T. cruzi infection upon the mitochondrial function measured by the enzymatic activity of respiratory chain complexes (CI –CIV) in myocardium from mice infected with an isolate obtained from Santiago del Estero (endemic area).
Albino Swiss mice (n= 30) were used and divided into the following groups, G1= non-infected (n=10); G2= infected with 50 trypomastigotes of Trypanosoma cruzi, SGO Z12 isolate (n=20)
Cardiac tissue samples were obtained from both groups 10 and 30 days post infection (d.p.i.), (acute phase) and 365 d.p.i. (chronic phase). Mitochondria were isolated by subcelullar fractioning determining CI, CII, CIII and CIV enzymatic activity by spectrophotometry.
The enzymatic activities (μm.min-1/mg prot) obtained were: CI in G1=0.04±0.02, in G2 an increment was determined 10 d.p.i. and a significantly decrease at 30 and 365 d.p.i. (p<0.05). CII in G1=1.1 x 10 -9 ±5.7 x 10-11, G2 showed similar activity to G1 at 10 and 30 d.p.i but significantly diminished in the chronic phase (p<0.01). CIII value in G1 was 0.17±0.03, but its activity in G2 was reduced in the acute and chronic phase of the infection (p<0.0001). G1 presented a CIV activity of 0.11±4.4 x 10 -3, similar values were obtained in G2 at 10 and 30 d.p.i., but at 365 d.p.i. decreased (p<0.01).
The functional alterations in the mitochondrial respiratory chain described, surely alter the energy production showing that this organelle is involved in the physiopatogenia and evolution of the cardiopathy in Chagas disease.