4.7 Article

Effects of vitamin C infusion and vitamin E-coated membrane on hemodialysis-induced oxidative stress

Journal

KIDNEY INTERNATIONAL
Volume 69, Issue 4, Pages 706-714

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1038/sj.ki.5000109

Keywords

hemodialysis; methemoglobin; oxidative stress; vitamin C; vitamin E

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Chronic hemodialysis ( HD) patients manifest anemia and atherosclerosis with associated oxidative stress. We explored whether intravenous infusion of vitamin C ( VC) and/or use of vitamin E ( VE)-coated dialysis membrane could palliate HD-evoked oxidative stress. Eighty patients undergoing chronic HD were enrolled and randomly assigned into four groups: HD with intravenous VC ( n = 20), HD with VE-coated dialyzer ( n = 20), HD with both ( n = 20), and HD with neither ( n = 20). We evaluated oxidative stress in blood and plasma, erythrocyte methemoglobin/ferricyanide reductase ( red blood cells ( RBC)-MFR) activity, plasma methemoglobin, and pro-inflammatory cytokines in these patients. All patients showed marked increases ( 14-fold) in blood reactive oxygen species ( ROS) after HD. The types of ROS were mostly hydrogen peroxide, and in lesser amounts, O-2(center dot-) and HOCl. HD resulted in decreased plasma VC, total antioxidant status, and RBC-MFR activity and increased plasma and erythrocyte levels of phosphatidylcholine hydroperoxide ( PCOOH) and methemoglobin. Intravenous VC significantly palliated HD-induced oxidative stress, plasma and RBC levels of PCOOH, and plasma methemoglobin levels and preserved RBC-MFR activity. The VE-coated dialyzer effectively prevented RBCs from oxidative stress, although it showed a partial effect on the reduction of total ROS activity in whole blood. In conclusion, intravenous VC plus a VE-coated dialyzer is effective in palliating HD-evoked oxidative stress, as indicated by hemolysis and lipid peroxidation, and by overexpression of proinflammation cytokines in HD patients. Using VE-coated dialyzer per se is, however, effective in reducing lipid peroxidation and oxidative damage to RBCs.

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