E a-tocopherol

Vitamin E-deficiency diseases are well known among laboratory and farm animals and can be a considerable problem in animal husbandry. Thus, the vitamin was discovered because its absence from the diet causes pregnant female rats to resorb their foetuses [25], and male rats to suffer testicular degeneration [26]. In the rabbit muscular dystrophy occurs, and in sheep and cattle similar muscular degeneration also is the principle sign of vitamin E deficiency [27], In the chick given high levels of linoleic acid and no vitamin E an acute central nervous system lesion called encephalomalacia occurs 

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The unexpected role of vitamin E (a-tocopherol) in peroxidation of human low-density lipoprotein 99ACR27. 

Another approach to safer stabilization is to use a biological antioxidant such as vitamin E (a-tocopherol is the active form of vitamin E, AO-9, Table la). It is essentially a hindered phenol which acts as an effective chain breaking donor antioxidant, donating a hydrogen to ROO to yield a very stable tocopheroxyl radical, a-Tocopherol is a very effective melt stabilizer in polyolefins that offers high protection to the polymer at very low concentration [41], (Table 2). 

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.)...

Antioxidants Reducing agents, such as vitamins C (ascorbic acid) and E (a-tocopherol), which scavenge toxic free radicals generated by oxidative reactions in the cell. 

Vitamin E (a-tocopherol) is capable of acting as a radical trap which may inhibit radical reactions that could cause cell damage. 

The possible prooxidant effects of a major lipophilic antioxidant vitamin E (a-tocopherol) have already been discussed in Chapter 25. Yamashita et al. [82] showed that a-tocopherol induced extensive DNA damage including base modification and strand breakage in the... 

Another important characteristic of oxidative stress in thalassemia is LDL oxidative modification. Livrea et al. [388] showed that the concentration of hydroperoxides in LDL of thalassemia patients was equal to 22.60+ 12.84 nmol/mg LDL protein compared to 6.25 +3.04 nmol/mg in control LDL. These authors proposed that the enhanced LDL oxidation in thalassemia was connected with the depletion of vitamin E in LDL. Interestingly, these findings contradict the suggestion about the prooxidant role of vitamin E (a-tocopherol) in LDL oxidation (Chapter 25). It was proposed that LDL oxidation could be the origin of atherogenetic risk in thalassemic patients. 

E (a-tocopherol) Antioxidant in the hpid phase. Protects membrane lipids from peroxidation and helps prevent oxidation of LDL particles thought to be involved in atherosclerotic plaque formation... 

Antioxidants are compounds that inhibit autoxidation reactions by rapidly reacting with radical intermediates to form less-reactive radicals that are unable to continue the chain reaction. The chain reaction is effectively stopped, since the damaging radical becomes bound to the antioxidant. Thus, vitamin E (a-tocopherol) is used commercially to retard rancidity in fatty materials in food manufacturing. Its antioxidant effect is likely to arise by reaction with peroxyl radicals. These remove a hydrogen atom from the phenol group, generating a resonance-stabilized radical that does not propagate the radical reaction. Instead, it mops up further peroxyl radicals. In due course, the tocopheryl peroxide is hydrolysed to a-tocopherylquinone. 

Simvastatin, a conjugated alkene, can polymerise as a result of peroxyl radical addition. The peroxide-linked oligomers can be subsequently cleaved to produce epoxides, which in turn degrade to form ketones and alcohols [69]. Inclusion of vitamin E (a-tocopherol) into formulations was found to inhibit chain-oxidation of simvastatin, lovastatin and other structurally related statins. 

The correlation between the TEARS assay and MDA dnring oxidation of edible oils may be complicated by the presence of tocopherols (e.g. Vitamin E, 21) . An evaluation was carried of MDA, determined by an independent method , and TEARS as indices for direct oxygen uptake of edible oils and unsatnrated fatty acids. The linear increase of MDA and TEARS with oxygen consumption of soybean oil, in a closed vessel at 170 °C, stops when the latter value reaches 500 p.molL, when both MDA and TEARS start to decrease on further O2 consumption. The same process carried out at 40 °C, using 2,2 -azobis(2,4-dimethylvaleronitrile) (171) as initiator, shows linearity up to 1500 p,molL O2 consumption . A similar behavior is observed for nnsatnrated fatty acids snch as oleic, linoleic and linolenic acids . On the other hand, depletion of Vitamin E (a-tocopherol, 21) and its analogs y- and 5-tocopherol (172, 173) present in the oil show a linear dependence on O2 consumption of the oil, np to 1800 p,molL . This points to the consumption of these antioxidants, and especially 21, as a good index for the O2 uptake in oils at high temperature. The determination of the tocopherols is carried ont by HPLC-FLD (Xex = 295 nm, Ah = 325 nm) . ... 

Vitamin E a-Tocopherol Any of several tocopherol derivatives Antioxidant l... 

Vitamin E (a-tocopherol) has as its active form any of several tocopherol derivatives. It functions as an antioxidant. Vitamin E deficiency is rarely seen, but can lead to red blood cell fragility that leads to hemolytic anemia. It has no known toxicity. 

Plants are significant to the diet of humans and animals since they provide most of the essential nutrients and vitamins. Vitamins C (ascorbic acid), E (a-tocopherol) and K (phylloquinone) are biosynthesized by plants, while (3-carotene, the precursor of vitamin A and ergosterol, the precursor of vitamin D, are also secondary plant metabolites. These metabolites are used in folk medicine and for industrial purposes, as raw materials for pharmaceutical and other products [3]. On the other hand, plants may produce substances, which are toxic and/or irritant to man. 

Vitamin E (a-tocopherol) (fig. 10.26) was recognized in 1926 as an organic-soluble compound that prevented sterility in rats. The function of this vitamin still has not been clearly established. A favorite theory is that it is an antioxidant that prevents peroxidation of polyunsaturated fatty acids. Tocopherol certainly prevents peroxidation in vitro, and it can be replaced by other antioxidants. However, other antioxidants do not relieve all the symptoms of vitamin E deficiency. 

Heteropolyacids catalyze the condensation reaction in the synthesis of vitamin E (a-tocopherol acetate) as shown in Eq. (42) (362). 

Fig. 9.4 Chemical structures of cellular lipids that act as endogenous antioxidants. Choline plasmalogens (a) ethanolamine plasmalogens (b) ganglioside (c) and vitamin E (a-tocopherol) (d)...

Vitamin E [a-tocopherol) Men women 15 mg/d Antioxidant effects Hemorrhagic toxicity... 

Much has been said about the positive effects of vitamin E (a-tocopherol) on sexual performance and ability in humans. Unfortunately, there is little scientific rationale to substantiate such claims. The primary reasons for attributing a positive role in sexual performance to vitamin E come from experiments on vitamin E deficiency in laboratory animals. In such experiments the principal manifestation of this deficiency is infertility, although the reasons for this condition differ in males and females. In female rats there is no loss in ability to produce apparently healthy ova, nor is there any defect in the placenta or uterus. However, fetal death occurs shortly after the first week of embryonic life, and fetuses are reabsorbed. This situation can be prevented if vitamin E is administered any time up to day 5 or 6 of embryonic life. In the male rat the earliest observable effect of vitamin E deficiency is immobility of spermatozoa, with subsequent degeneration of the germinal epithelium. Secondary sex organs are not altered and sexual vigor is not diminished, but vigor may decrease if the deficiency continues. 

Another important field of application concerns food and beverages, especially wine, juices, and tea (A2, A11, A17, B4, K12, V7, Yl). The antioxidant components of food include vitamin E (a-tocopherol), vitamin A (retinoids), vitamin C (ascorbic acid), and also fi-carotene (provitamin A), other carotenoids (of which more than 600 compounds have been identified), flavonoids, simple phenols, and glucobrasicins (H3). Unfortunately, the TAC value of a food is not informative on the bioavailability of its antioxidants. It has been estimated that polyphenols are normally present in blood plasma at concentrations of 0.2-2 //M (PI). However, it has been demonstrated that feeding rats a quercetin-augmented diet can increase their plasma levels of quercetin and its metabolites up to 10-100 //M (M27), and transient increases in the concentration of plant-derived phenolic compounds can take place after ingestion of food and beverages, which may affect blood plasma TAC (see later). 

Vitamin E (a-tocopherol) is most abundantly available in wheat germ oil and in small quantities in cereals, nuts, spinach, and egg yolk. Deficiency of vitamin E normally does not occur. Large doses of vitamin E are used to reduce the toxicity of vitamin A. Prolonged use causes delay in wound healing but significant... 

To test the system a synthetic feed mixture of a-Tocopherol and a-Tocopherol acetate both of 98 % purity, were used. Vitamin E (a-Tocopherol) is one of the fat-soluble vitamins used as an antioxidant in the food, pharma and cosmetic industries. 

Hydrophobic protective systems include vitamin E, i.e. a-tocopherol which, as all chromanol compounds, is a free radical scavenger which yields a long-lived radical upon hydrogen abstraction, thereby interrupting the chain reaction [160]. This property is optimized in a-tocopherol (a-TH) which is a remarkable scavenger of peroxyl radicals in phospholipid membrane bilayers [161,162] ... 

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