title: Alpha-tocopherol supplementation does not affect monocyte endothelial adhesion or C-reactive protein levels but reduces soluble vascular adhesion molecule-1 in the plasma of healthy subjects.
abstract: Vascular monocyte retention in the subintima is pivotal to the development of cardiovascular disease and is facilitated by up-regulation of adhesion molecules on monocytes/endothelial cells during oxidative stress. Epidemiological studies have shown that cardiovascular disease risk is inversely proportional to plasma levels of the dietary micronutrients, vitamin C and vitamin E (alpha-tocopherol). We have tested the hypothesis that alpha-tocopherol supplementation may alter endothelial/monocyte function and interaction in subjects with normal ascorbate levels (> 50 microM), as ascorbate has been shown to regenerate tocopherol from its oxidised tocopheroxyl radical form in vitro. Healthy male subjects received alpha-tocopherol supplements (400 IU RRR-alpha-tocopherol/day for 6 weeks) in a placebo-controlled, double-blind intervention study. There were no significant differences in monocyte CD11b expression, monocyte adhesion to endothelial cells, plasma C-reactive protein or sICAM-1 concentrations post-supplementation. There was no evidence for nuclear translocation of NF-kappaB in isolated resting monocytes, nor any effect of alpha-tocopherol supplementation. However, post-supplementation, sVCAM-1 levels were decreased in all subjects and sE-selectin levels were increased in the vitamin C-replete group only; a weak positive correlation was observed between sE-selectin and alpha-tocopherol concentration. In conclusion, alpha-tocopherol supplementation had little effect on cardiovascular disease risk factors in healthy subjects and the effects of tocopherol were not consistently affected by plasma vitamin C concentration.
authors.affiliation: Life and Health Sciences, Aston University, Birmingham, UK.
authors.forename: Kevin J
authors.initials: KJ
authors.lastname: Woollard
authors.forename: Sarah J
authors.initials: SJ
authors.lastname: Rayment
authors.forename: Ruth
authors.initials: R
authors.lastname: Bevan
authors.forename: Jacqui A
authors.initials: JA
authors.lastname: Shaw
authors.forename: Joseph
authors.initials: J
authors.lastname: Lunec
authors.forename: Helen R
authors.initials: HR
authors.lastname: Griffiths
mesh_terms: D000328:Adult; D000975:Antioxidants / Q000008:administration & dosage / Q000494:pharmacology; D001692:Biological Transport / Q000187:drug effects; D002097:C-Reactive Protein / Q000378:metabolism*; D039481:CD11b Antigen / Q000378:metabolism; D002448:Cell Adhesion / Q000187:drug effects; D002478:Cells, Cultured; D019587:Dietary Supplements; D004311:Double-Blind Method; D024202:Electrophoretic Mobility Shift Assay; D042783:Endothelial Cells / Q000166:cytology / Q000187:drug effects; D004797:Enzyme-Linked Immunosorbent Assay; D005434:Flow Cytometry; D006801:Humans; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D012995:Solubility; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood*; D024502:alpha-Tocopherol / Q000008:administration & dosage / Q000097:blood / Q000494:pharmacology*
chemical_list: D000975:Antioxidants; D039481:CD11b Antigen; D016328:NF-kappa B; D019010:Vascular Cell Adhesion Molecule-1; D002097:C-Reactive Protein; D024502:alpha-Tocopherol