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Mol Cell Biochem. 2014 Jan;385(1-2):17-21. doi: 10.1007/s11010-013-1809-1. Epub 2013 Sep 21.

Vitamin E and regression of hypercholesterolemia-induced oxidative stress in kidney.

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1
Department of Physiology, College of Medicine, University of Saskatchewan, 107 Wiggins Road, Saskatoon, SK, S7N 5E5, Canada, k.prasad@usask.ca.

Abstract

Hypercholesterolemia (HC) is an independent risk factor for the onset and progression of renal disease. HC induces oxidative stress (OS) in the kidney; Vitamin E (Vit.E), an antioxidant, slows the progression of OS in the kidney. This study was to investigate if Vit.E regresses the HC-induced OS, and the regression is associated with an increase in the antioxidant reserve (AR). The studies were carried out in four groups of rabbits. The kidneys were removed under anesthesia. OS and AR in the renal tissue were assessed by measuring malondialdetyde (MDA) and chemiluminescent (CL) activity, respectively. High-cholesterol diet elevated the serum total cholesterol (TC), and the regular diet with or without Vit.E following a high-cholesterol diet reduced the serum TC to control levels. HC increased the MDA levels of kidney by 5.54-fold compared to control. The MDA contents of the kidneys in groups on regular diet with or without Vit.E were, respectively, 56 and 53 % lower than the control group. The CL activity in the control group was 12.15 ± 0.73 × 10(6) RLU/mg protein. The CL activity in HC group was 45.26 % lower than that in control, indicating an increase in AR. The regular diet with or without Vit.E following high-cholesterol diet normalized the CL activity/AR. In conclusion, HC increases OS in the kidney; reduction of serum cholesterol by regular diet regresses the renal OS but Vit.E does not regress HC-induced OS in kidney.

PMID:
24057088
DOI:
10.1007/s11010-013-1809-1
[Indexed for MEDLINE]
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