British Journal of Nutrition

Full Papers

Gene Expression

Dietary vitamin E, brain redox status and expression of Alzheimer's disease-relevant genes in rats

Sonja Gaedickea1, Xiangnan Zhanga2, Patricia Huebbea1, Christine Boesch-Saadatmandia1, Yijia Loua2, Ingrid Wiswedela3, Andreas Gardemanna3, Jan Franka1 and Gerald Rimbacha1 c1

a1 Institute of Human Nutrition and Food Science, Christian-Albrechts-University of Kiel, Hermann-Rodewald-Str. 6, Kiel 24118, Germany

a2 College of Pharmaceutical Sciences, Institute of Pharmacology & Toxicology and Biochemical Pharmaceutics, Zhejiang University, Hangzhou 310058, People's Republic of China

a3 Department of Pathological Biochemistry, Medical Faculty, Otto-von-Guericke-University, Magdeburg 39120, Germany


Oxidative stress is one of the major pathological features of Alzheimer's disease (AD). Here, we investigated whether dietary vitamin E (VE) depletion may induce adverse effects and supplementation with α-tocopherol (αT) may result in beneficial effects on redox status and the regulation of genes relevant in the pathogenesis of AD in healthy rats. Three groups of eight male rats each were fed diets with deficient ( < 1 mg αT equivalents/kg diet), marginal (9 mg αT equivalents/kg diet) or sufficient (18 mg αT equivalents/kg diet) concentrations of natural-source VE for 6 months; a fourth group was fed the VE-sufficient diet fortified with αT (total VE, 146 mg αT equivalents/kg diet). Feeding of the experimental diets dose dependently altered αT concentrations in the cortex and plasma. No significant changes in F2-isoprostane concentrations, activities of antioxidative enzymes (total superoxide dismutase, Se-dependent glutathione peroxidase) and concentrations of glutathione or the expression of AD-relevant genes were observed. In this non-AD model, depletion of VE did not induce adverse effects and supplementation of αT did not induce positive effects on the parameters related to the progression of AD.

(Received September 12 2008)

(Revised November 19 2008)

(Accepted November 20 2008)

(Online publication January 28 2009)


c1 Corresponding author: Gerald Rimbach, fax +49 431 880 26 28, email


Abbreviations: AD, Alzheimer's disease; APP, amyloid β-(A4) precursor protein; Bax, Bcl-2-associated X protein; Bcl-2, B-cell leukaemia/lymphoma 2; BHT, butylated hydroxytoluene; dVE, vitamin E deficient; fVE, vitamin E fortified; HO-1, haeme oxygenase 1; mVE, vitamin E marginal; sVE, vitamin E sufficient; αT, α-tocopherol; γT, γ-tocopherol; Tris, 2-amino-2-hydroxymethyl-propane-1,3-diol; αTTP, αT transfer protein; VE, vitamin E