Journal
DIABETES
Volume 64, Issue 2, Pages 344-352Publisher
AMER DIABETES ASSOC
DOI: 10.2337/db13-1829
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Funding
- National Institutes of Health [R00-EB-014328, R01-CA-166766, R00-EB-012064, P41-EB-013598, R01-DK-097357]
- Society of Abdominal Radiology Morton A. Bosniak Research Grant
- INSERM [P41EB013598]
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Oxidative stress has been proposed to be a unifying cause for diabetic nephropathy and a target for novel therapies. Here we apply a new endogenous reduction-oxidation (redox) sensor, hyperpolarized (HP) C-13 dehydroascorbate (DHA), in conjunction with MRI to noninvasively interrogate the renal redox capacity in a mouse diabetes model. The diabetic mice demonstrate an early decrease in renal redox capacity, as shown by the lower in vivo HP C-13 DHA reduction to the antioxidant vitamin C (VitC), prior to histological evidence of nephropathy. This correlates with lower tissue reduced glutathione (GSH) concentration and higher NADPH oxidase 4 (Nox4) expression, consistent with increased superoxide generation and oxidative stress. ACE inhibition restores the HP C-13 DHA reduction to VitC with concomitant normalization of GSH concentration and Nox4 expression in diabetic mice. HP C-13 DHA enables rapid in vivo assessment of altered redox capacity in diabetic renal injury and after successful treatment.
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