1. ¹Taipei City Hospital, Heping Branch, Taipei, Taiwan
2. ²Department of Physiology, National Taiwan University College of Medicine and National Taiwan University Hospital, Taipei, Taiwan
3. ³Department of Internal Medicine, National Yang-Ming University, Taipei, Taiwan
4. ⁴Department of Clinical Research, National Taiwan University College of Medicine and National Taiwan University Hospital, Taipei, Taiwan
5. ⁵Department of Internal Medicine, Far Eastern Memorial Hospital, Taipei, Taiwan
6. ⁶Department of Internal Medicine, National Taiwan University College of Medicine and National Taiwan University Hospital, Taipei, Taiwan
7. ⁷Department of Pathology, National Taiwan University College of Medicine and National Taiwan University Hospital, Taipei, Taiwan
8. ⁸Department of Medical Research, National Taiwan University College of Medicine and National Taiwan University Hospital, Taipei, Taiwan

Correspondence: C-T Chien, Department of Medical Research, National Taiwan University Hospital, 7 Chung-Shan S Road, Taipei, Taiwan. E-mail: ctchien@ha.mc.ntu.edu.tw

⁹These authors contributed equally to this work.

Received 2 June 2005; Revised 7 June 2005; Accepted 14 July 2005; Published online 4 January 2006.

Abstract

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, O₂^- 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.