Abstract #0786

Mitochondrial dysfunction in a rat model of doxorubicin-induced heart failure assessed by hyperpolarized 13C MRS

Kerstin N Timm¹, Charith Perera¹, Vicky Ball¹, John A Henry¹, Matthew Kerr¹, Michael S Dodd¹, Jack J Miller^1,2,3, James West⁴, Angela Logan⁵, Julian L Griffin⁴, Michael P Murphy⁵, Lisa C Heather¹, and Damian J Tyler^1,2

¹Physiology Anatomy and Genetics, University of Oxford, Oxford, United Kingdom, ²Oxford Centre for Magnetic Resonance, John Radcliffe Hospital, Oxford, United Kingdom, ³Department of Physics, University of Oxford, Oxford, United Kingdom, ⁴Department of Biochemistry, University of Cambridge, Cambridge, United Kingdom, ⁵MRC Mitochondrial Biology Unit, University of Cambridge, Cambridge, United Kingdom

Doxorubicin-chemotherapy can lead to serious cardiac side effects in cancer-patients, culminating in heart failure. Cardiac oxidative stress and impaired energetics are hypothesized to be at the core of this toxicity. We established a clinically relevant rat model of doxorubicin-induced heart failure characterized with CINE MRI by decreased cardiac function. We show here that these functional changes are preceded by a shift from oxidative to anaerobic glucose metabolism measured with hyperpolarized MRS. These changes are likely due to a loss and impairment of mitochondria, which cannot be alleviated with the mitochondrially targeted antioxidant, MitoQ.

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