Disease relevance of BETA-TOCOPHEROL

• The effect of alpha- and beta-tocopherol on human erythroleukemia cell (HEL) adhesion induced by phorbol 12-myristate 13-acetate (PMA) has been studied [1].

High impact information on BETA-TOCOPHEROL

• In vitro, the activity of PKC from monocytes was inhibited by alpha-tocopherol in a specific manner compared with that of beta-tocopherol or Trolox(R) [2].
• Differential inhibition by alpha- and beta-tocopherol of human erythroleukemia cell adhesion: role of integrins [1].
• Also, a similar antioxidant, beta-tocopherol, had no effect on IL-1 beta release [3].
• The addition of vitamin C and alpha- or beta-tocopherol to the culture medium prevented the induction of VEGF and VEGFR-2 expression by HC-LDL, both at mRNA and protein levels [4].
• We examined the hypothesis that VEGF and VEGF receptor-2 (VEGFR-2) expression is upregulated in apoE-/- and, since it could be driven by oxidative stress, tested whether dietary supplementation with vitamins C and E could downregulate it.Two-month-old apoE-/- received vitamin C combined with alpha- or beta-tocopherol for 4 weeks [5].

Biological context of BETA-TOCOPHEROL

• The m locus was epistatic to the d locus-the d locus had no effect in m (+) m (+) and m (+) m individuals, but significantly increased beta-tocopherol percentages in m m individuals [6].
• Apoptosis was also decreased by beta-tocopherol or intracellular radical scavengers, but these suppressive effects were less than those of alpha-tocopherol [7].
• Both enzymes converted delta- and gamma- into beta- and alpha-tocopherol, respectively, but beta-tocopherol was not accepted as a substrate, pointing to a specific methylation at the C(5)-position of the tocopherol aromatic head group [8].
• Alpha-tocopherol, but not beta-tocopherol, inhibited smooth muscle cell proliferation and protein kinase C in a dose-dependent manner, at concentrations ranging from 10 to 50 microM [9].
• The effect of alpha-tocopherol and beta-tocopherol on protein kinase C activity and gene expression suggest a cause-to-effect relationship [10].

Anatomical context of BETA-TOCOPHEROL

• By differential display analysis it has been found that several genes of smooth muscle cells are differentially transcribed in the presence of alpha-tocopherol but not beta-tocopherol [11].
• Rat and human vascular smooth muscle cell proliferation is specifically sensitive to alpha-tocopherol, but not beta-tocopherol [12].
• Alpha-tocopherol but not beta-tocopherol inhibits thrombin-induced PKC activation and endothelin secretion in endothelial cells [13].
• Lower levels of the primary antioxidants, alpha- and beta-tocopherol, and glutathione (GSH) in PHS mitochondria confirmed the presence of oxidative stress [14].
• In HeLa cells no inhibition by alpha-tocopherol or beta-tocopherol of protein kinase C activity and cell proliferation was observed [10].

Associations of BETA-TOCOPHEROL with other chemical compounds

• When eight human volunteers (age range 30-60) were given 1200 IU of all-rac-alpha-tocopherol daily for 8 wk, plasma gamma-tocopherol and beta-tocopherol decreased in all subjects [15].
• The results allow the antioxidant hierarchy to be established: alpha-tocopherol > lycopene approximately beta-tocopherol approximately gamma-tocopherol > beta-carotene > zeaxanthin approximately delta-tocopherol > lutein > echinenone >> canthaxanthin approximately beta-apo-8'-carotenal > astaxanthin [16].

Gene context of BETA-TOCOPHEROL

• The antioxidants beta-tocopherol and N-acetylcysteine did not induce CTGF gene expression, suggesting a nonantioxidant mechanism for alpha-tocopherol action [17].
• At a gene level alpha-tocopherol but not beta-tocopherol induces a transient activation of alpha-tropomyosin gene transcription and protein expression [12].

References