Mitochondrial dysfunction in skeletal muscle during experimental Chagas disease.

Area of Science:

• Mitochondrial Biology
• Parasitology
• Cardiovascular Disease

Background:

• Trypanosoma cruzi infection leads to cardiac damage through cellular injury and oxidative stress.
• Mitochondrial dysfunction in cardiomyocytes is implicated in Chagasic cardiopathy.
• Skeletal muscle mitochondria may reflect cardiac energetic status.

Purpose of the Study:

• To investigate skeletal muscle mitochondrial structure and enzymatic activity in mice infected with T. cruzi.
• To assess if skeletal muscle mitochondrial changes correlate with Chagasic cardiopathy progression.

Main Methods:

• Albino Swiss mice were infected with T. cruzi (Tulahuen, SGO Z12, Lucky isolates).
• Skeletal muscle mitochondrial structure was analyzed.
• Enzymatic activity of citrate synthase and respiratory chain complexes I-IV (CI-CIV) was measured during acute and chronic infection phases.

Main Results:

• All infected mice showed skeletal muscle mitochondrial structural abnormalities.
• Citrate synthase activity was altered, decreasing in Tulahuen and SGO Z12 during the acute phase and in all groups during the chronic phase.
• Respiratory chain complex activities (CI-CIV) exhibited varied changes across infection phases and isolates, with some complexes showing significant increases or decreases.

Conclusions:

• T. cruzi infection induces structural and functional mitochondrial alterations in skeletal muscle early in the infection.
• These skeletal muscle mitochondrial changes may impact cellular energy production and potentially serve as biomarkers for Chagasic cardiopathy.
• Chagas disease causes systemic effects, including permanent skeletal muscle damage beyond cardiac involvement.