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.