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Vitamin E supplementation increases circulating vitamin E metabolites tenfold in end‐stage renal disease patients
Author(s) -
Smith Kylie Sherée,
Lee ChiaLin,
Ridlington James W.,
Leonard Scott W.,
Devaraj Sridevi,
Traber Maret G.
Publication year - 2003
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/s11745-003-1130-9
Subject(s) - medicine , endocrinology , ascorbic acid , vitamin e , chemistry , oxidative stress , antioxidant , vitamin , ferritin , vitamin c , metabolite , tocopherol , hemodialysis , biochemistry , food science
Abstract Vitamin E supplementation could elevate circulating vitamin E metabolites while modulating oxidative and inflammatory status in end‐stage renal failure patients undergoing hemodialysis. Plasma concentrations of carboxyethyl‐hydroxychromanols (α‐and γ‐CEHC), ascorbic acid, α‐and γ‐tocopherols, E 2 ‐isoprostanes, and inflammatory biomarkers [tumor necrosis factor‐α (TNF‐α), interleukin‐6 (IL‐6), ferritin, and C‐reactive protein (CRP)] were measured in blood samples obtained from patients ( n =11) before and after dialysis on two occasions prior to, and at 1 and 2 mon of daily vitamin E supplementation (400 IU RRR ‐α‐tocopherol). Supplementation nearly doubled plasma α‐tocopherol concentrations (from 18±0.5 to 31±1.7 μM, P <0.0001), whereas γ‐tocopherol concentrations decreased (from 2.8±0.3 to 1.7±0.2 μM, P =0.001). Serum α‐CEHC increased 10‐fold from 68±3 to 771±175 nM ( P <0.0001), and γ‐CEHC increased from 837±164 to 1136±230 nM ( P =0.008). Vitamin E supplementation also increased postdialysis hematocrits from 38±1% to 41±1% ( P <0.001). Dietary antioxidant intakes (vitamins E and C) were low in most subjects; plasma ascorbic acid levels (88±27 μM) decreased significantly with dialysis (33±11 μM, P =0.01). Plasma Il‐6, CRP, TNF‐α, and free F 2 ‐isoprostane concentrations were elevated throughout the study. There is a complex relationship between chronic inflammation and oxidative stress that is not mitigated by short‐term vitamin E supplementation. Importantly, serum vitamin E metabolite concentrations that increased 10‐fold within 30 d of supplementation did not increase further, suggesting routes other than urine for removal of metabolites.