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Vitamin E activity was first identified as a dietary factor essential for reproduction in the rat. It is now known that this vitamin has a far wider range of functions in the body than its role in fertility. It interacts with selenium-containing glutathione peroxidase to prevent the oxidative breakdown of tissue membranes associated with the hydroperoxides of polyunsaturated fatty acids. Relationships with other factors such as stress and vitamin C, have been proposed. The symptoms of deficiency of vitamin E vary according to species. With so many variables it is difficult to estimate the optimum allowances of the vitamin for the many types of livestock diets. These problems are discussed and the calculation of allowances of vitamin E in rations for both monogastric and ruminant animals is explained.
Vet Rec 1987 Dec 05
PMID:Vitamin E. 332 99

A review summarizing the voltammetric literature of the liposoluble vitamins A, D, E and K in organic solvents containing supporting electrolyte is presented. Electrochemical studies that were performed by attaching the vitamins to electrode surfaces and performing voltammetric scans in aqueous solutions are also summarized. Vitamins A (retinol and retinal) and D (cholecaliferol and ergocalciferol) undergo chemically irreversible voltammetric oxidation processes in organic solvents to form complicated or unknown compounds that cannot be electrochemically converted back to the starting materials. In contrast to vitamins A and D, vitamins E and K undergo chemically reversible electron-transfer processes that are often coupled to proton-transfer reactions. Vitamin E (a phenol) is voltammetrically oxidized in aprotic organic solvents in a -2e(-)/-H(+) process to form a diamagnetic cation, which is unusually long-lived compared to the analogous cations produced during the oxidation of other phenols. In an aqueous environment, vitamin E is electrochemically oxidized to the hydroquinone in a chemically irreversible -2e(-) process. In low moisture content aprotic solvents, vitamin K (a quinone) is reduced in two one-electron chemically reversible steps to form first a radical anion (semiquinone, at E(1)) and then at more negative potentials a dianion is formed (at E(2)). The dianion is especially prone to strong hydrogen-bonding interactions with trace water present in the organic solvents, resulting in a shift in the formal reduction potential of E(2) to more positive potentials as more water is added to the solvent.
Chem Rec 2012 Feb
PMID:Voltammetry of the liposoluble vitamins (A, D, E and K) in organic solvents. 2212 Nov 21

Methylmercury (MeHg) is an environmental contaminant that is found in many ecosystems. Many studies reported that MeHg toxicity is accompanied by increased lipid peroxidation that may lead to oxidative damage to DNA, RNA, and proteins. Vitamin E is considered as the most effective antioxidant preventing lipid peroxidation. The aim of this study was to evaluate the effects of MeHg exposure during pregnancy on the development of the appendicular skeleton in rat fetuses and whether vitamin E administration could reduce this toxicity. Positively mated adult female Sprague-Dawley rats were used and divided into the following experimental groups: control group, received only deionized water, and four MeHg treated groups received 1 mg of MeHg/kg/d, 2 mg of MeHg/kg/d, 1 mg of MeHg/kg/d plus 150 mg of vitamin E/kg/d, and 2 mg of MeHg/kg/d, plus 150 mg of vitamin E/kg/d starting from Day 0 of gestation. On Day 20 of gestation, the fetuses from the pregnant rats were extracted and the fetal growth parameters were evaluated. Skeletal evaluation of ossification of both fore- and hind-limbs, and coxal bones were undertaken. Results showed that treatment with MeHg caused adverse effects on fetal growth parameters and ossification of the bones. The coadministration of vitamin E with MeHg revealed an improvement in these parameters. These results suggest that vitamin E may ameliorate some aspects of MeHg developmental toxicity. The underlying and human health implications warrant further investigations.
Anat Rec (Hoboken) 2012 Jun
PMID:The prenatal toxic effect of methylmercury on the development of the appendicular skeleton of rat fetuses and the protective role of vitamin E. 2254 41