tocotrienol--alpha and 6-hydroxy-2-5-7-8-tetramethylchroman-2-carboxylic-acid

Measurements of the singlet oxygen ((1)O2) quenching rates (kQ (S)) and the relative singlet oxygen absorption capacity (SOAC) values were performed for 11 antioxidants (AOs) (eight vitamin E homologues (α-, β-, γ-, and δ-tocopherols and -tocotrienols (-Tocs and -Toc-3s)), two vitamin E metabolites (α- and γ-carboxyethyl-6-hydroxychroman), and trolox) in ethanol/chloroform/D2O (50:50:1, v/v/v) and ethanol solutions at 35 °C. Similar measurements were performed for five palm oil extracts 1-5 and one soybean extract 6, which included different concentrations of Tocs, Toc-3s, and carotenoids. Furthermore, the concentrations (wt%) of Tocs, Toc-3s, and carotenoids included in extracts 1-6 were determined. From the results, it has been clarified that the (1)O2-quenching rates (kQ (S)) (that is, the relative SOAC value) obtained for extracts 1-6 may be explained as the sum of the product {Σ kQ(AO-i) (S) [AO-i]/100} of the rate constant (kQ(AO-i) (S)) and the concentration ([AO-i]/100) of AO-i (Tocs, Toc-3s, and carotenoid) included.

Topics: Carotenoids; Chromans; Free Radical Scavengers; Glycine max; Kinetics; Palm Oil; Plant Extracts; Plant Oils; Singlet Oxygen; Solutions; Tocopherols; Tocotrienols; Vitamin E

The antioxidant activity of vitamin E (VE) homologs α, γ and δ-tocotrienamines (4b-6b), never studied before, and α, γ and δ-tocopheramines (4a-7a) was investigated by means of different total antioxidant capacity (TAC) tests. In all the test model systems, compounds 4a-7a and 4b-6b showed similar or higher TAC values than the parental vitamin E forms and their physiological metabolites. α-Homologs of VE amines showed markedly higher activity than the VE congeners in the TEAC test, which is tailored for liposoluble antioxidants, while γ-homologs of the amine analogs showed higher activity in the FRAP tests. Kinetics analysis of the reaction with DPPH(·) showed higher second order rate k for 4a than for α-tocopherol (1a). α-Tocopherolquinone 1f was the common main oxidation product for both 1a and α-tocopheramine (4a) exposed to ferric ions or DPPH(·), and the implied oxidative deamination of 4a was accompanied by a nitration reaction of phenolic substrates that were added to the reaction medium. Possible mechanisms of these reactions were studied.

Topics: Amines; Biphenyl Compounds; Chromans; Electron Spin Resonance Spectroscopy; Ferric Compounds; Free Radical Scavengers; Kinetics; Magnetic Resonance Spectroscopy; Oxidation-Reduction; Picrates; Vitamin E

The role of vitamin E in the CNS has not been fully elucidated. In the present study, we found that pre-treatment with vitamin E analogs including alphaT (alpha-tocopherol), alphaT3 (alpha -tocotrienol), gammaT, and gammaT3 for 24 h prevented the cultured cortical neurons from cell death in oxidative stress stimulated by H2O2, while Trolox, a cell-permeable analog of alphaT, did not. The preventive effect of alphaT was dependent on de novo protein synthesis. Furthermore, we found that alphaT exposure induced the activation of both the MAP kinase (MAPK) and PI3 kinase (PI3K) pathways and that the alphaT-dependent survival effect was blocked by the inhibitors, U0126 (an MAPK pathway inhibitor) or LY294002 (a PI3K pathway inhibitor). Interestingly, the up-regulation of Bcl-2 (survival promoting molecule) was induced by alphaT application. The up-regulation of Bcl-2 did not occur in the presence of U0126 or LY294002, suggesting that alphaT-up-regulated Bcl-2 is mediated by these kinase pathways. These observations suggest that vitamin E analogs play an essential role in neuronal maintenance and survival in the CNS.

Topics: alpha-Tocopherol; Animals; Animals, Newborn; Cell Death; Cell Survival; Cells, Cultured; Cerebral Cortex; Chromans; Cytoprotection; Enzyme Inhibitors; MAP Kinase Signaling System; Mitogen-Activated Protein Kinase 1; Neurons; Neuroprotective Agents; Oxidative Stress; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-bcl-2; Rats; Tocotrienols; Up-Regulation; Vitamin E