Mitochondrial Complex III Defects Contribute to Inefficient Respiration and ATP Synthesis in the Myocardium ofTrypanosoma cruzi

Mitochondrial Complex III Defects Contribute to Inefficient Respiration and ATP Synthesis in the Myocardium ofTrypanosoma cruzi–Infected Mice

Published:2010-01 Issue:1 Volume:12 Page:27-37
ISSN:1523-0864
Container-title:Antioxidants & Redox Signaling
language:en
Short-container-title:Antioxidants & Redox Signaling

Author:

Wen Jian-Jun¹,Garg Nisha Jain¹²³

Affiliation:

1. Department of Microbiology & Immunology, The Center for Biodefense & Emerging Infectious Diseases, and The Sealy Center for Vaccine Development, University of Texas Medical Branch, Galveston, Texas.

2. Department of Pathology, The Center for Biodefense & Emerging Infectious Diseases, and The Sealy Center for Vaccine Development, University of Texas Medical Branch, Galveston, Texas.

3. Member of The Institute for Human Infections and Immunity, The Center for Biodefense & Emerging Infectious Diseases, and The Sealy Center for Vaccine Development, University of Texas Medical Branch, Galveston, Texas.

Publisher

Mary Ann Liebert Inc

Subject

Cell Biology,Clinical Biochemistry,Molecular Biology,Physiology,Biochemistry,Cell Biology,Clinical Biochemistry,Molecular Biology,Physiology,Biochemistry

Link

http://www.liebertpub.com/doi/pdf/10.1089/ars.2008.2418

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3. TNF blockade aggravates experimental chronic Chagas disease cardiomyopathy

4. Trypanosoma cruzi: Cardiac mitochondrial alterations produced by different strains in the acute phase of the infection

5. A compilation of mutations located in the cytochrome b subunit of the bacterial and mitochondrial bc1 complex

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