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Interdisciplinary Perspectives on Infectious Diseases
Volume 2009, Article ID 190354, 8 pages
Review Article

Oxidative Stress in Chagas Disease

1Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA
2Department of Pathology, University of Texas Medical Branch, Galveston, TX 77555, USA
3Sealy Center for Vaccine Development, Institute for Human Infections and Immunity, University of Texas Medical Branch, Galveston, TX 77555, USA
43.142C Medical Research Building, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555-1070, USA

Received 19 March 2009; Accepted 23 April 2009

Academic Editor: Herbert B. Tanowitz

Copyright © 2009 Shivali Gupta et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


There is growing evidence to suggest that chagasic myocardia are exposed to sustained oxidative stress induced injuries that may contribute to disease progression. Trypanosoma cruzi invasion- and replication-mediated cellular injuries and immune-mediated cytotoxic reactions are the common source of reactive oxygen species (ROS) during acute infection. Mitochondria are proposed to be the major source of ROS in chronic chagasic hearts. However, it has not been established yet, whether mitochondrial dysfunction is a causative factor in chagasic cardiomyopathy or a consequence of other pathological events. A better understanding of oxidative stress in relation to cardiac tissue damage would be useful in the evaluation of its true role in the pathogenesis of Chagas disease and other heart diseases. In this review, we discuss the evidence for increased oxidative stress in chagasic disease, with emphasis on mitochondrial abnormalities, and its role in sustaining oxidative stress in myocardium.