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1 Physiology and Functional Genomics, University of Florida, Gainesville, Florida, FL32608, United States; Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University, College of Medicine, Kaohsiung, Taiwan, Taiwan - Republic of China
2 Department of Nutrition, West Virginia University, Morgantown, West Virginia, United States
3 Department of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta, Georgia, United States
4 Dept of Medicine - Div of Cardiology, Emory University, Atlanta, Georgia, United States
5 Physiology and Functional Genomics, University of Florida, Gainesville, Florida, United States
* To whom correspondence should be addressed. E-mail: tainyl{at}ufl.edu.
Chronic kidney disease (CKD) is accompanied by nitric oxide (NO) deficiency and oxidative stress which contribute to progression. We investigated whether the antioxidant vitamin E could preserve renal function and NO bioavailability, and reduce oxidative stress in the 5/6th nephrectomy (NX) rat model. We studied 3 groups of male Sprague-Dawley rats: sham (n=6), 5/6 NX control (n=6), and 5/6 NX treated with vitamin E (5000 IU/kg chow) (n=5). The 5/6 NX group showed increased severity of glomerulosclerosis vs. sham, and this was ameliorated by vitamin E therapy. Both 5/6 NX groups showed similar elevations in plasma creatinine and proteinuria and decreased CCr compared to sham. There was increased NADPH-dependent superoxide production in 5/6 NX rats vs. sham that was prevented by vitamin E. Total NO production was similarly reduced in both 5/6 NX groups. There was unchanged abundance of endothelial (e)NOS in renal cortex and medulla, and neuronal (n)NOS in medulla. However, in kidney cortex, 5/6 NX rats had lower nNOS abundance than sham which was restored by vitamin E. An increased plasma ADMA occurred with 5/6 NX associated with decreased renal DDAH activity as well as increased PRMT1 expression.
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