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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