Figure 28.13 • Antioxidant mechanisms of a- and y-tocopherols. (R1, H, or CH3; R2, Phytyl.)
functions of the vitamin is preventing the oxidation of lipids, particularly unsaturated fatty acids. Through this antioxidant effect, a-tocopherol plays an important role in protecting cell membranes made of lipids and LDLs. The a-tocopherol donates its electrons to the free radicals to neutralize them, thus protecting the cellular lipids from oxidative damage. In this process, a-tocopherol loses its antioxidant capacity by forming the a-tocoquinone (Fig. 28.13). It is generally accepted that other antioxidants like vitamin C or glutathione can restore vitamin E from its single electron oxidation state, tocopherol radical. Although several reports suggested that once it is fully oxidized to the toco-quinone form, it will not be regenerated back to vitamin E, reports are also available showing that it can be regenerated back in presence of glutathione according to the mechanism shown in Figure 28.14.9394
Figure 28.14 • Interconversion of a-tocopherol and a-tocoquinone.
Because of the methylation level, which enhances the nucleophilicity and reactivity of the 6-OH group, the a-isoforms of both tocopherol and tocotrienol are the most potent antioxidants among all the vitamin E family. Although a-tocotrienol is believed to be a more potent antioxidant than the a-tocopherol for many factors (e.g., higher recycling efficiency, more uniform distribution within the microsomal membrane bilayer and more efficient interaction with lipid free radicals) misleading results have been demonstrated because of the high affinity of a-TTP for a-tocopherol. a-Tocopherol is biologically the most important isoform because of its high affinity for a-TTP, which results in high bioavailability and bioactivity.95
Biochemical functions of the vitamin E family are diverse and may include actions other than their well-documented antioxidant activities. a-Tocopherol not only strongly inhibits platelet and other cell adhesion but also inhibits cell proliferation, protein kinase C, 5-lipooxygenase, and phospholipase A2 and activates protein phosphatase 2A and diacylglycerol kinase, which are unrelated to its antioxidant activity. These actions reflect the specific interactions of a-tocopherol with enzymes, structural proteins, lipids, and transcription factors. y-Tocopherol and CEHC metabolic products of vitamin E exhibit many other functions including anti-inflammatory, anti-neoplastic, natriuretic, and also cardioprotective functions.96 During the last 5 years, interest in the action of to-cotrienols has increased with the inclusion of a substantial amount of vitamin E research directed toward that of a-tocotrienol. Numerous unique biochemical functions of a-to-cotrienol have been discovered that include prevention of inducible neurodegeneration by regulating specific mediators of cell death, hypocholesterolemic effects by suppressing 3-hydroxy-3-methyl-glutaryl-CoA (HCG-CoA) reductase activity, and protection against stroke. It has also been reported that tocotrienols, but not tocopherols, suppress the growth of breast cancer cells.96
The diseases caused by vitamin E deficiency in animals are not well correlated with that in human. The sterility in rats and nutritional muscular dystropies in other lower animal including monkeys, rabbits, lambs, and chicks are well documented. Reversible neurological disorders in humans and hemolytic anemia in premature infants because of vitamin E deficiency have been seen.
The antioxidant function does not explain all the biochemical abnormalities caused by vitamin E deficiency. Moreover, vitamin E is not the only in vivo antioxidant. Two enzyme systems, glutathione reductase and o-phenylenediamine peroxidase, also function in this capacity.97 It has been postulated that vitamin E has a role in the regulation of protein synthesis. Other actions of this vitamin have also been investigated, for example, effects on muscle creatine kinase and liver xanthine oxidase. Vitamin E deficiency leads to an increase in the turnover of creatine kinase. Vitamin E-deficient animals also exhibit increased liver xanthine oxidase activity, which is because of increased de novo synthesis.97
Although it has been difficult to establish clinical correlates of vitamin E deficiency in humans, Bieri and Farrell97 have summarized some useful generalizations and conclusions. These workers noted that the infant, especially the premature infant, is susceptible to tocopherol deficiency because of ineffective transfer of the vitamin from placenta to fetus and that growth in infants requires greater availability of the vitamin. In adults, the tocopherol storage depots provide adequate availability that is not readily depleted, but intestinal malabsorption syndromes, when persistent, can lead to depletion of the storage depots. Children with cystic fi-brosis suffer from severe vitamin E deficiency caused by malabsorption. Tropical sprue, celiac disease, gastrointestinal resections, hepatic cirrhosis, biliary obstruction, and excessive ingestion of mineral oil may also cause long-term malabsorption.
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