Mitochondrial enzymatic activity of the lymphomonocyte fraction as an early marker of pathology in Chagas disease.

Abstract

The entry of Trypanosoma cruzi (T.cruzi) into cells causes inflammatory reactions that stimulate the production of cytokines and free radicals responsible for oxidative damage; which could lead to heart failure. We studied the activity of complexes I and III (CI, CIII) of the respiratory chain in mitochondria of the lymphomonocyte fraction, of experimental models infected with different strains of T. cruzi, and in patients with positive serology (long standing) for the disease of Chagas, with the objective of determining the participation of mitochondria as probable markers of early evolution and clinical variability of cardiomyopathy produced by T. cruzi.

Albino Swiss mice were infected with the Tulahuen strain and the SGOZ12 and Lucky isolates (n=30 per group); controls (n=30). Patients: n=55 (43 with positive serology, 12 controls) grouped into: Chagas 1 (<40 years), Chagas 2 (>45) and controls 1 and 2 (healthy of both ages). The enzymatic activity was determined by spectrophotometry, the data was analyzed by ANOVA, Fisher Test. Significance level p<0.05.

In the experimental models, CI and III were modified in the infected groups (p<0.05) at all stages, depending on the strain that infected the host. In the group of patients, a significant decrease in activity was observed among the controls (p<0.05), which would show that it decreases with age. While in chagasic patients a decrease in enzyme activity was observed in the older group (Chagas 2), although this difference did not become significant when compared with the Chagas 1 group (<40 years), if instead when compared with the Control group 1 (<40 years).

Inflammatory processes are responsible for causing changes in the mitochondria and can be detected by a blood sample. These changes would be important since, by appearing before the clinical manifestation, they could prevent the evolution of the disease, and the lymphomonocyte fraction could be a simple marker that helps to stop the evolution towards Chagasic cardiomyopathy, especially in the chronic stage without symptomatology.