a-Tocopherol transfer protein (aTTP), a product of the gene which causes familial isolated vitamin E deficiency, plays an important role in determining the plasma vitamin E level. We examined the structural characteristics of vitamin E analogs required for recognition by aTTP. Ligand specificity was assessed by evaluating the competition of non-labeled vitamin E analogs and a-[ 3 H|tocopherol for transfer between membranes in vitro. Relative affinities (/J/?/?-a-tocopherol = 100%) calculated from the degree of competition were as follows: ß-tocopherol, 38%; y-tocopherol, 9%; 5-tocopherol, 2%; a-tocopherol acetate, 2%; a-tocopherol quinone, 2%; SRRa-tocopherol, 11%; a-tocotrienol, 12%; trolox, 9%. Interestingly, there was a linear relationship between the relative affinity and the known biological activity obtained from the rat résorption-gestation assay. From these observations, we conclude that the affinity of vitamin E analogs for aTTP is one of the critical determinants of their biological activity. © 1997 Federation of European Biochemical Societies.
In this study, we investigated a change in the excretory content of 2,7,8-trimethyl-2(2'-carboxyethyl)-6-hydroxychroman (gamma-CEHC), a gamma-tocopherol (gamma-Toc) metabolite, in rat urine and bile by using a new high-performance liquid chromatography-electrochemical detection (HPLC-ECD) method. In this determination, CEHC [alpha- and gamma-CEHC, where alpha-CEHC = 2,5,7,8-tetramethyl-2(2'-carboxyethyl)-6-hydroxychroman] in the biological specimens were treated with 3 N methanolic HCl to hydrolyze conjugates and to promote esterification. The methylated samples were extracted by n-hexane/water (1:2). The analyses of the methyl esters of alpha-CEHC and gamma-CEHC were performed by an HPLC-ECD using an ODS-3 column at 35 degrees C. The mobile phase was acetonitrile/water (45:55, vol/vol) containing 50 mM sodium perchlorate. After rat urine and bile samples, respectively, were methylated as described above, methylated biliary metabolites were identified by liquid chromatography-mass spectrometry as methyl esters of gamma-CEHC. Furthermore, we examined the differences in the excretion of gamma-CEHC between rat urine and bile after an oral administration of gamma-Toc or alpha- + gamma-Toc by the above HPLC method. In the gamma-Toc group, each vitamin E-deficient rat was given 0.5 mL of a stripped corn oil preparation containing 10 mg of gamma-Toc. In the alpha- + gamma-Toc group, the rat was given 10 mg of alpha-Toc and 10 mg of gamma-Toc. The content of gamma-CEHC in rat urine from the alpha- + gamma-Toc group was increased more in comparison to the gamma-Toc group at 18-36 h after oral administration. Moreover, the content of gamma-CEHC in rat bile in the alpha- + gamma-Toc group was increased more in comparison to the gamma-Toc group at 6-18 h after oral administration. Therefore, we have suggested that gamma-CEHC was shifted mainly to urinary excretion after gamma-CEHC had been excreted into the bile. Furthermore, we assume that alpha-Toc may affect the metabolism of gamma-Toc to gamma-CEHC in the body.
We investigated changes in the concentrations of the stereoisomers of alpha-tocopherol in serum and lipoproteins in seven normal, healthy women aged 21-37 y who had received oral administration of natural and synthetic alpha-tocopheryl acetate. This study was conducted in three separate periods of 28 d each; there was a 3-mo washout period between each experimental period. During the first period the subjects were administered a daily dose of 100 mg RRR-alpha-tocopherol/d, whereas in the second and third periods 100 mg all-rac-alpha-tocopheryl acetate/d and 300 mg all-rac-alpha-tocopheryl acetate/d were given, respectively. Blood samples were collected 3 d before each treatment and 1, 3, 7, 14, and 28 d after treatment. alpha-Tocopherol stereoisomer concentrations in serum and lipoproteins (very-low-, low-, and high-density lipoproteins) were determined by the chiral HPLC method. The bioavailability of RRR-alpha-tocopherol was greater than that of all-rac-alpha-tocopheryl acetate. When bioavailability was estimated from the increase in the concentration of RRR- or all-rac-alpha-tocopherol in serum, bioavailability of RRR-alpha-tocopherol administered at 100 mg/d was not different from that of all-rac-alpha-tocopheryl acetate administered at 300 mg/d. 2R-Isomers and small amounts of 2S-isomers were detected in the serum lipoproteins of subjects administered all-rac-alpha-tocopheryl acetate.
2,7,8-Trimethyl-2-(  -carboxyethyl)-6-hydroxychroman ( ␥ -CEHC), a metabolite of ␥ -tocopherol and ␥ -tocotrienol, was identified as a new endogenous natriuretic factor. However, ␥ -tocopherol and ␥ -tocotrienol, both precursors of ␥ -CEHC, have never directly been observed to have natriuretic potency. Thus, we investigated whether ␥ -tocotrienol could cause natriuresis and diuresis in rats. The rats were divided into two groups that were given a control or a high-sodium diet for 4 weeks, and then subdivided into placebo and ␥ -tocotrienol subgroups given only corn oil-removed vitamin E and oil supplemented with ␥ -tocotrienol, respectively. After oral administration of three experimental doses, rat urine was collected and ␥ -CEHC, urine volume, sodium, and potassium content were determined. Only in rats given a high-NaCl diet did ␥ -tocotrienol accelerate and increase sodium excretion, showing no effect on potassium excretion. Sodium excretion in the high-NaCl group given ␥ -tocotrienol was 5.06 ؎ 2.70 g/day, and in the control group given ␥ -tocotrienol, 0.11 ؎ 0.06 g/day. Furthermore, ␥ -tocotrienol affected urine volume in the specific condition of high-NaCl body stores and ␥ -tocotrienol supplementation. In this study, we found that ␥ -tocotrienol, one of the natural vitamin E homologs, stimulates sodium excretion in vivo, suggesting that ␥ -tocotrienol possesses a hormone-like natriuretic function. -Saito, H., C. Kiyose, H. Yoshimura, T. Ueda, K. Kondo, and O. Igarashi. ␥ -Tocotrienol, a vitamin E homolog, is a natriuretic hormone precursor. J. Lipid Res. 2003. 44: 1530-1535.
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