Vitamin E attenuates oxidative stress induced by intravenous iron in patients on hemodialysis

Intravenous iron application to anemic patients on hemodialysis leads to an "oversaturation" of transferrin. As a result, non-transferrin-bound, redox -active iron might induce lipid peroxidation. To test the hypothesis that v itamin E attenuates lipid peroxidation in patients receiving 100 mg of iron (III) hydroxide sucrose complex intravenously during a hemodialysis session , 22 patients were investigated in a randomized cross-over design, either w ith or without a single oral dose of 1200 IU of all-rac-alpha-tocopheryl ac etate taken 6 h before the hemodialysis session. Blood was drawn before and 30, 60, 90, 135, and 180 min after the start of the iron infusion, and are as under the curve (AUC(0-180 min)) of ratios of plasma malondialdehyde (MD A) to cholesterol and plasma total peroxides to cholesterol (two markers of lipid peroxidation) were determined as the outcome variables. At baseline of the session without vitamin E supplementation, plasma alpha-tocopherol c oncentrations (27.6 +/- 1.8 mu mol/L) and ratios of alpha-tocopherol to cho lesterol (5.88 +/- 1.09 mmol/mol) were normal, plasma MDA concentrations we re above normal (1.20 +/- 0.28 mu mol/L), and bleomycin-detectable iron (BD I), indicating the presence of redox-active iron, was not detectable. Upon iron infusion, BDI and MDA concentrations increased significantly (P < 0.00 1). BDI concentrations explained the increase over baseline in MDA concentr ations (MDA = 1.29 + 0.075 x BDI). Vitamin E supplementation, leading to a 68% increase in plasma alpha-tocopherol concentrations, significantly reduc ed the AUC(0-180 min) of MDA to cholesterol (P = 0.004) and peroxides to ch olesterol (P = 0.002), These data demonstrate that a single oral dose of vi tamin E attenuates lipid peroxidation in patients on hemodialysis receiving intravenous iron. Given that intravenous iron is applied repeatedly to pat ients on hemodialysis, this therapeutic approach may protect against oxidat ive stress-related degenerative disease in the long term.