1NMR
Surgical Laboratory, Department of Surgery, Massachusetts General Hospital
and Shriners Burn Institute, Harvard Medical School, Boston, MA, United
States; 2Department of Radiology, Athinoula A. Martinos Center of
Biomedical Imaging, Boston, MA, United States; 3Molecular Surgery
Laboratory, Department of Surgery, Massachusetts General Hospital and
Shriners Burn Institute, Harvard Medical School, Boston, MA, United States; 4Department
of Pharmacology, Joan and Sanford I, Weill Medical College of Cornell
University, New York, NY, United States
Severe burn injury causes a major systemic catabolic response that is associated with mitochondrial dysfunction in skeletal muscle. We investigated the effects of the mitochondria-targeted peptide antioxidant, SS-31, on skeletal muscle in a mouse model of burn using in vivo 31P NMR spectroscopy, to noninvasively measure high-energy phosphates, and mitochondrial aconitase activity measurements which directly correlates with TCA cycle flux. At 6 hours after burn, ATP synthesis rate was significantly increased in burned mice injected with a single dose of SS-31, as compared to burned mice alone. SS-31 administration in burned animals decreased mitochondrial aconitase activity back to control levels.
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