Dietary vitamin E (VE) is known to regulate gene expression by altering mRNA concentrations. Recently, micro-RNA (miRNA) have been discovered as a means of posttranscriptional gene regulation. Since the effect of VE on miRNA regulation is unknown, we fed rats for 6 months diets deficient or sufficient in VE and determined hepatic concentrations of miRNA involved in processes previously associated with VE (lipid metabolism, miRNA-122a; cancer and inflammation, miRNA-125b). VE-deficiency resulted in reduced concentrations of miRNA-122a and miRNA-125b. The findings of the present study demonstrate that differences in dietary VE may affect hepatic miRNA concentrations in vivo.

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 a-tocopherol (aT) 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 aT equivalents/kg diet), marginal (9 mg aT equivalents/kg diet) or sufficient (18 mg aT equivalents/kg diet) concentrations of natural-source VE for 6 months; a fourth group was fed the VE-sufficient diet fortified with aT (total VE, 146 mg aT equivalents/kg diet). Feeding of the experimental diets dose dependently altered aT concentrations in the cortex and plasma. No significant changes in F 2 -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 aT did not induce positive effects on the parameters related to the progression of AD.

The aim of the present study was to determine the effects of a 6-month dietary vitamin E (VE) deficiency on DNA methylation and gene expression in rat liver. Two enzymes, 5-a-steroid reductase type 1 (SRD5A1) and the regulatory subunit of g-glutamylcysteinyl synthetase (GCLM), which are differentially expressed on the mRNA level, were analysed for promoter methylation in putative cytosine-phospho-guanine (CpG) island regions located at the 5 0 end using base-specific cleavage and matrix-assisted laser desorption ionisation time-of-flight MS. A twofold increase in the mRNA level of SRD5A1 gene and a twofold decrease in the mRNA level of GCLM gene in VE-deficient animals were not associated with different CpG methylation of the analysed promoter region. Furthermore, global DNA methylation was not significantly different in these two groups. Thus, the present results indicate that the VE-induced regulation of SRD5A1 and GCLM in rat liver is not directly mediated by changes in promoter DNA methylation.