Vitamin E , oxidation

Skinner, W. A. Vitamin E oxidation with free radical initiators Azobis(isobutyronitrile). Biochem. Biophys. Res. Commurt. 1964, 15, 469 472. 

Japanese publications report that vitamin E can be used elfectively in the treatment of facial pigmentation. It inhibits tyrosinase indirectly by inhibiting its hydroxylase activity. It also acts by limiting the oxidative phases required in the first stages of the transformation of tyrosine into indole derivatives. Vitamin E oxidizes easily, and more stable derivatives than pure a-tocopherol have to be used in cosmetic preparations. Tocopheryl acetate is one of the more stable derivatives of vitamin E. Tocopheryl ferulate is also frequently used. 

Recently P450 4F11 has also been shown to be a catalyst of Further research has also shown a role in vitamin E oxidation [1635],... 

Tutem et al. (1997) reported another spectrophotometric method for vitamin E (a-tocopherol) in pharmaceutical preparations using copper(II)-neocuproine reagent in neutral medium, that is, ammonium acetate buffer (pH 7, 0.1 mol/E) and obeyed Beer s law between 2.4 x 10 and 9 x 10 mol/E a-tocopherol with a correlation coefficient (R ) of 0.996. The absorbance of the copper(I)-neocuproine complex as a result of vitamin E oxidation was stabilized after 30 min (monitored at 450 nm against the reagent blank) and was stable for at least a further 90 min. 

They are widely distributed in vegetable lipids, and in the body fat of animals, though animals cannot synthesize them. They have vitamin E activity and can protect unsaturated lipids against oxidation. Four are found naturally ... 

The pharmaceutical industry employs ozone in organic reactions to produce peroxides as germicides in skin lotions, for the oxidation of intermediates for bacteriostats, and in the synthesis of steroids (qv) such as cortisone (see Disinfectants and antiseptics). Vitamin E can be prepared by ozonation of trimethyUiydroquinone. 

The total antioxidant activity of teas and tea polyphenols in aqueous phase oxidation reactions has been deterrnined using an assay based on oxidation of 2,2 -azinobis-(3-ethylbenzothiazoline-sulfonate) (ABTS) by peroxyl radicals (114—117). Black and green tea extracts (2500 ppm) were found to be 8—12 times more effective antioxidants than a 1-mAf solution of the water-soluble form of vitamin E, Trolox. The most potent antioxidants of the tea flavonoids were found to be epicatechin gallate and epigallocatechin gallate. A 1-mAf solution of these flavanols were found respectively to be 4.9 and 4.8 times more potent than a 1-mAf solution of Trolox in scavenging an ABT radical cation. 

Vitamin E can also act as an antioxidant (qv) in animals and humans alone or in combination with vitamin C (qv). Both are good free-radical scavengers with the vitamin C acting to preserve the levels of vitamin E (35). Vitamin E in turn can preserve the levels of vitamin A in animals (13). It has been shown that vitamin E reduces the incidence of cardiovascular disease (36—39). This most likely results from the antioxidant property of the vitamin which inhibits the oxidation of low density Hpoproteins (LDLs) (40—42). The formation of the oxidized LDLs is considered important in decreasing the incidence of cardiovascular disease (43). 

AH formulations of vitamin E must show low acidity, and contain not more than 0.004% heavy metals (reported as Pb) and not more than 10 ppm Pb. Eormulations that contain RRR-a-tocopherol must have a specific rotation of +24 ° for the oxidation product with alkaline potassium ferricyanide. 

P450 Mono-oxygenase System Reactive Oxygene Species Oxidative Stress Vitamin C Vitamin E... 

It has been proposed that the development of the complications of diabetes mellitus may be linked to oxidative stress and therefore might be attenuated by antioxidants such as vitamin E. Furthermore, it is discussed that glucose-induced vascular dysfunction in diabetes can be reduced by vitamin E treatment due to the inactivation of PKC. Cardiovascular complications are among the leading causes of death in diabetics. In addition, a postulated protective effect of vitamin E (antioxidants) on fasting plasma glucose in type 2 diabetic patients is also mentioned but could not be confirmed in a recently published triple-blind, placebo-controlled clinical trial [3]. To our knowledge, up to now no clinical intervention trials have tested directly whether vitamin E can ameliorate the complication of diabetes. 

Heinecke JW (2001) Is the emperor wearing clothes Clinical trials of vitamin E and the LDL oxidation hypothesis. Arterioscler Thromb Vase Biol 21 1261—1264... 

Encouraged by the short synthesis of K vitamins, the chromium-mediated benzannulation was extended to the synthesis of vitamin E 68 [59]. The problem of imperfect regioselectivity of alkyne incorporation - which did not hamper the approach to vitamin K due to the final oxidation to the quinone - was tackled by demethylation of both regioisomeric hydroquinone monomethyl ethers 67 to give the unprotected hydroquinone. Subsequent ring closure yielded a-tocopherol (vitamin E) 68 (Scheme 39). 

Vitamin E is added to some food products as a nutrient, but it is better known for its antioxidant properties, which protect oils and fats from oxidation. 

Ubiquinone or Q (coenjyme Q) (Figure 12-5) finks the flavoproteins to cytochrome h, the member of the cytochrome chain of lowest redox potential. Q exists in the oxidized quinone or reduced quinol form under aerobic or anaerobic conditions, respectively. The structure of Q is very similar to that of vitamin K and vitamin E (Chapter 45) and of plastoquinone, found in chloroplasts. Q acts as a mobile component of the respiratory chain that collects reducing equivalents from the more fixed flavoprotein complexes and passes them on to the cytochromes. 

Figure 45-6. Interaction and synergism between antioxidant systems operating in the lipid phase (membranes) of the cell and the aqueous phase (cytosol). (R-,free radical PUFA-00-, peroxyl free radical of polyunsaturated fatty acid in membrane phospholipid PUFA-OOH, hydroperoxy polyunsaturated fatty acid in membrane phospholipid released as hydroperoxy free fatty acid into cytosol by the action of phospholipase Aj PUFA-OH, hydroxy polyunsaturated fatty acid TocOH, vitamin E (a-tocopherol) TocO, free radical of a-tocopherol Se, selenium GSH, reduced glutathione GS-SG, oxidized glutathione, which is returned to the reduced state after reaction with NADPH catalyzed by glutathione reductase PUFA-H, polyunsaturated fatty acid.)...

More recently, large human intervention trials were undertaken with P-carotene alone, or in combination with non-dietary amounts of vitamin E. These trials were undertaken because of promising animal studies that suggested that these antioxidants could offer chemo-preventive action against oxidative stress. The results, which are summarised in Table 11.1, were disappointing. Although the study population in two of the studies (ATBC and CARET)... 

Under aqueous conditions, flavonoids and their glycosides will also reduce oxidants other than peroxyl radicals and may have a role in protecting membranal systems against pro-oxidants such as metal ions and activated oxygen species in the aqueous phase. Rate constants for reduction of superoxide anion show flavonoids to be more efficient than the water-soluble vitamin E analogue trolox (Jovanovic et al, 1994), see Table 16.1. 

NIKI E, SAITO T, KAWAKAMI A and KAMIYA Y (1984) Inhibition of oxidation of methyl linoleate by vitamin E and vitamin C, J Biol Chem, 259, 4177-82. 

Nonaqueous Systems In nonaqueous (nonpolar) solvent systems, nitrosatlon also proceeds. In these solvents, alpha-tocopherol acts as a lipid soluble blocking agent in much the same fashion as ascorbic acid functions in the aqueous phase. Alpha-tocopherol reacts with a nitrosating agent and reduces it to nitric oxide. At the same time, alpha-tocopherol is oxidized to tocoquinone, which is the first oxidation product of vitamin E and also a normal metabolite in vivo. 

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