D-a-Tocopherol Concentrate

Ammonium Hydroxide DL-a-Tocopherol D-a-Tocopherol Concentrate Tocopherols Concentrate, Mixed D-a-Tocopheryl Acetate DL-a-Tocopheryl Acetate D-a-Tocopheryl Acetate Concentrate D-a-Tocopheryl Acid Succinate... 

TASINATO A D, BOISCOBOINIK D, BARTOLI G M, MARONi p and Azzi A (1995) d-a-tocopherol inhibition of vascular smooth muscle cell proliferation occurs at physiological concentrations, correlates with protein kinase C inhibition, and is independent of its ntioydd ait xo eriie% Proceedings National Academy Sciences USA 92, 12190-4. 

Studies of the metabolism of vitamin E were triggered by the observations of Alaupovic and coworkers [126, 127]. When " [Cj-D-a-tocopherol-5-methyl was administered to rats or pigs and attempts were made to detect metabolic derivatives, two compounds were separated by chromatography. One of the compounds is " [C]-D-a-tocopherol quinone the other is either a dimer or a trimer of a-tocopherol. The dimer and trimer are terminal oxidation products of a-tocopherol and are excreted in the bile. a-Tocopherol quinone can be converted to a-hydroquinone. a-Tocopherol hydroquinone may be esterified in liver and eliminated in the feces after concentration in the bile and excretion in the intestine, or it may be oxidized in the kidney to a-tocopheronic acid, which may be converted into an a-tocopheronolactone conjugate, which is excreted in the urine. In conclusion, vitamin E is excreted as such in the urine or the bile after conversion to a dimer or a trimer, in the form of a conjugated hydroxy-quinone or tocopheronic acid (see Fig. 4-43). 

Vitamin E, or D-a-tocopherol, is the primary anti-oxidant in the blood. Because it is fat soluble, it is concentrated in the most vulnerable spot, the cell membrane, where it scavenges free radicals before they can get into the cell. 

The most concentrated sources of vitamin E are vegetables oils, but these contain no fiber. On the other hand, nuts such as almonds and hazel nuts are sources of dietary fiber as well as vitamin E, thus improving their health benefits. Furthermore, the vitamine E in almonds and hazel nuts is almost all in the D-a-tocopherol, or biologically active and natural form. 

Kennedy, D.G., P.B. Young, W.J. Blanchflower, J. M. Scott, D.G. Weir, A.M. Molloy and S. Kennedy, 1994. Cobalt-vitamin Bj2 deficiency causes lipid accumulation, lipid peroxidation and decreased a-tocopherol concentrations in the liver of sheep. Intemat. J. Vit. Nutr. Res. 64, 270-276. 

CONCENTRATIONS OF PLASMA RETINOL (1, NG/ML), LUTEIN (2, NG/ML), ZEAXANTHIN (3, NG/ ML), CANTHAXANTHIN (4, NG/ML) AND a-TOCOPHEROL (5, /xG/ML) IN CONTROL AND EXPERIMENTAL GREEN IGUANAS AFTER INGESTING DIETS SUPPLEMENTED WITH DIFFERENT CAROTENOIDS (80 MG/KG DIET) FOR 28 DAYS (MEAN S.D N = 5)... 

Dunkley, W. L., Franke, A. A. and Robb, J. 1968B. Tocopherol concentration and oxidative stability of milk from cows fed supplements of d- or dl-o-tocopheryl acetate. J. Dairy Sci, 51, 531-534. 

Procedure Transfer an accurately measured volume of the Test Solution, equivalent to about 100 mg of a-tocopherol, into a separator, and add 200 mL of water. Extract first with 75 mL, then with two 25-mL portions of ether, and combine the ether extracts in another separator. Add 20 mL of a 10% solution of potassium ferricyanide in a 1 125 sodium hydroxide solution to the ether solution, and shake for 3 min. Wash the ether solution with four 50-mL portions of water, discard the washings, and dry over anhydrous sodium sulfate. Evaporate the dried ether solution on a water bath under reduced pressure or in an atmosphere of nitrogen until about 7 or 8 mL remain, and then complete the evaporation, removing the last traces of ether without the application of heat. Immediately dissolve the residue in 5.0 mL of isooctane, and determine the optical rotation. Calculate the optical rotation [see Optical (Specific) Rotation, Appendix IIB], using as c the concentration of D-a-Tocopheryl Acetate, as determined in the Assay (above), in 100 mL of solution. 

Liposomes are prepared by sequential filter extrusion of the lipid/drug mixtures. The basic composition for the preparation of 5.0 mL liposomes is 1.0 g soy phophatidylcholine (SPC, L. Meyer GmbH, Hamburg, Germany), 125 mg cholesterol (Fluka, Buchs, Switzerland) (see Note 1), 6 mg D,L-a-tocopherol (Merck, Darmstadt, Germany) and the lipophilic drug at concentrations of 1-10 mg/mL. 

About one tenth of the total amount of vitamin E produced is semi-synthetic, isomerically pure (2R,4 K,8 R)-a-tocopherol (RRR-3) which is used almost exclusively in human applications (mainly pharma). This product, originating from natural sources, is obtained from soya deodorizer distillates (SDD). Vegetable oils refined on a large scale are the major sources of vitamin E compounds [26-28]. The deodorizer distillate, originally a waste stream, contains considerable amounts (up to 10%) of a-, [I-, y- and b-tocopherols (RRR-3 to RRR-6) which are isolated by several separation methods. To increase the value of the vitamin E concentrate of mixed tocopherols obtained from SDD, the lower (I-, y- and d-homologues (RRR-4 to RRR-6, content ca. 90%) have to be transformed subsequently into the biologically more active a-tocopherol (RRR-3, only ca. 5% in the original mixture) by permethylation reactions. Permethylations are performed by chloro-, amino-, or hydroxymethylation reactions to provide functionalized alkylated intermediates, which are reductively converted into RRR-3 (Fig. 3) [29]. 

Inhibitors and anticarcinogens more potent in their effect against PAHs than the saturated hydrocarbon fraction in mouse skin carcinogenesis were identified in CSC (phytosterols, a-tocopherol, duvanediols, D-limonene) Their concentrations relative to that of the PAHs are far in excess of that required to elicit anticarcinogenesis. 

Pastori M, Pfander H, Boscoboinik D, Azzi A. Lycopene in association with a7/)7)a-tocopherol inhibits at physiological concentrations proliferation of prostate carcinoma cells. Biochem Biophys Res Gommun 1998 250 582-585. 

Supplementation of Finnish smokers with 50mg/d of synthetic a-tocopherol for 6 years was associated with a 34% decrease in prostate cancer incidence, and p-carotene (50mg on alternate days) supplementation of male physicians with low baseline seram p-carotene concentrations for 12 years was associated with a 32% decrease in prostate cancer incidence. These data may indicate that men with low intake or increased destruction of these compounds, e.g., through oxidative stress, represent subgroups that could benefit from supplementation. 

Lycopene in combination with vitamin E or vitamin D has been reported to potentiate inhibition of cancer cell growth. A synergistic effect was observed when physiologically relevant concentrations of a-tocopherol and lycopene were studied in various prostate cancer cell lines. Lycopene, in itself, was not a potent inhibitor of prostate carcinoma cell proliferation however, up to 90% growth inhibition was reported with the a-tocopherol and lycopene combined treatment. This synergistic effect was not shared by p-tocopherol, ascorbic acid, or probucol, indicating a nonantioxidant mechanism to be the basis of the finding. 

Krukovsky et al. (1949) reported that milk with higher concentrations of a-tocopherol was more resistant to development of oxidized flavors than milk with lower tocopherol concentrations. The authors noted that oxidative stability of milk was greater in summer than in winter and that this was likely related to seasonal differences in the tocopherol content of feed. Erickson et al. (1964) reported that within milk, a-tocopherol was primarily associated with the milk fat globule membrane. The milk of control cows and cows supplemented with d-a-tocopheryl acetate was equally resistant to copper-induced (5 ppm) off-flavors. Milk from treated animals did, however, demonstrate partial resistance to off-flavors induced by 1 ppm copper. Nicholson et al. (1991) reported that improvement in... 

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