Beta-Tocopherol

Differential inhibition by alpha- and beta-tocopherol of human erythroleukemia cell adhesion: role of integrins.[Pubmed:11390183]

Free Radic Biol Med. 2001 Jun 15;30(12):1381-9.

The effect of alpha- and Beta-Tocopherol on human erythroleukemia cell (HEL) adhesion induced by phorbol 12-myristate 13-acetate (PMA) has been studied. Adhesion induced by PMA stimulation was prevented by 44.5% by physiological concentrations of alpha-tocopherol. Under the same experimental conditions, Beta-Tocopherol, an analogue of alpha-tocopherol, produced 11% inhibition of adhesion. Cell response gradually increased from 0 to 24 h of alpha-tocopherol treatment. Only a slight time dependency of Beta-Tocopherol inhibition was observed. Another human erythroleukemia cell line (K562) and the human monocyte tumor cell line U937 showed 5.0 and 11.2% inhibition, respectively. Similar to alpha-tocopherol, the protein kinase C inhibitor, Calphostin C, and the MAPK inhibitor, PD98059, prevented PMA-induced cell adhesion. An inhibition of ERK-1 phosphorylation was observed for alpha-tocopherol only in HEL, implying that MAP kinase pathway is involved in this cell line. Fluorescence-activated cell sorting (FACS), by using various integrin-specific monoclonal antibodies, has shown that alpha (1-6), beta1, and alphav integrins are less expressed at the cell surface after alpha-tocopherol treatment. Beta-Tocopherol treatment was less effective.

Dietary beta-tocopherol and linoleic acid, serum insulin, and waist circumference predict circulating sex hormone-binding globulin in premenopausal women.[Pubmed:19339706]

J Nutr. 2009 Jun;139(6):1135-42.

Reduced levels of circulating sex hormone-binding globulin (SHBG) are implicated in the etiology of sex steroid-related pathologies and the metabolic syndrome. Dietary correlates of serum SHBG remain unclear and were studied in a convenient cross-sectional sample of healthy 30- to 40-y-old women (n = 255). By univariate analyses, serum SHBG correlated negatively with several indices of the metabolic syndrome, such as BMI, waist circumference, hip circumference (r = -0.36 to -0.44; P < 0.0001), fasting serum insulin (r = -0.41; P < 0.0001), serum triglycerides (r = -0.27; P < 0.0001), serum glucose (r = -0.23; P < 0.001), and plasma testosterone (r = -0.19; P = 0.002). Serum SHBG correlated positively with serum HDL-cholesterol (r = 0.33; P < 0.0001), plasma progesterone (r = 0.17; P = 0.007), and dietary intake of Beta-Tocopherol (r = 0.17; P = 0.006), and negatively with that of fructose (r = -0.13; P = 0.04). Principal component analysis (PCA) extracted 12 nutrient factors with eigenvalues > 1.0 from 54 nutrients and vitamins in food records. Multivariate regression analyses showed that the PCA-extracted nutrient factor most heavily loaded with Beta-Tocopherol and linoleic acid (P = 0.03) was an independent positive predictor of serum SHBG. When individual nutrients were the predictor variables, Beta-Tocopherol (P = 0.002), but not other tocopherols or fatty acids (including linoleic acid), was an independent positive predictor of serum SHBG. Circulating insulin (P = 0.02) and waist circumference (P = 0.002), but not serum lipids, were negative independent predictors of SHBG in all regression models. Additional studies are needed in women of other age groups and men to determine whether consumption of foods rich in Beta-Tocopherol and/or linoleic acid may increase serum SHBG concentrations and may thereby decrease the risk for metabolic syndrome and reproductive organ cancer.