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Abstract #0983

In vivo assessment of diabetes-induced renal oxidative stress and response to therapy using hyperpolarized 13C dehydroascorbate magnetic resonance imaging

Kayvan R Keshari 1 , David M Wilson 2 , Victor Sai 2 , Robert Bok 2 , Kuang-Yu Jen 3 , Peder Larson 2 , Mark Van Criekinge 2 , John Kurhanewicz 2 , and Zhen Jane Wang 2

1 Radiology and Medical Physics, Memorial Sloan Kettering Cancer Center, New York, NY, United States, 2 Radiology, UCSF Medical Center, San Francisco, CA, United States, 3 Pathology, UCSF Medical Center, San Francisco, CA, United States

Oxidative stress is proposed as a unifying cause for diabetic nephropathy. We apply an endogenous redox sensor, HP 13C-dehydroascorbate (DHA), to interrogate the renal redox capacity in a mouse diabetes model. The diabetic mice demonstrate decreased redox capacity, with lower 13C-DHA reduction to the antioxidant Vitamin C. This correlates to lower reduced glutathione (GSH) concentration and higher Nox4 expression, consistent with increased generation of superoxide and oxidative stress. ACE inhibition normalizes 13C-DHA reduction to Vitamin C, GSH concentration, and Nox4 expression. HP 13C DHA enables rapid in vivo assessment of altered redox capacity in diabetic nephropathy and following successful treatment.

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