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Abstract #4048

Mitochondria-Targeted Antioxidant Promotes Recovery of Skeletal Muscle Mitochondrial Function After Burn Trauma

Valeria Righi1, 2, Caterina Constantinou1, 3, Dionyssios Mintzopoulos1, 2, Laurence G. Rahme3, Hazel H. Szeto4, Ronald G. Tompkins, Aria A. Tzika1, 2

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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