ree radicals, most commonly coming from oxygen, are molecules containing one or more unpaired electrons in their atomic orbitals, which gives the molecule a considerable about of reactivity. These reactive free-radicals can cause damage, known as oxidative stress, to cellular lipids, proteins or DNA when there is an overproduction of free-radicals and a deficiency of antioxidants1. This oxidative stress will inhibit the normal function of the cell and their constituents and has been linked to various human diseases, including cancer, Alzheimer's, and cardiovascular diseases, and the ageing process1, 2.
Vitamin E as an Antioxidant
Vitamin E is a fat-soluble vitamin that has non-enzymatic antioxidant activity i.e. it can eliminate free radicals, however, it is only synthesised in plants so it is a very important dietary requirement for humans, as we cannot produce our own3.
|Figure 1: Action of an Antioxidant on a Free Radical
Tocopherols and tocotrienols (grouped as chromanols), the compounds in vitamin E, are well known for their effective inhibition of lipid oxidation in biological species.
Their antioxidant activity comes from their ability to donate their phenolic hydrogens to lipid free-radicals (see figure 1)3; alpha (α) tocopherol is the most powerful donator of hydrogen with the highest bioavailibilty, out of the four tocopherol families (alpha, beta, gamma and delta) therefore, vitamin E is often referred to simply as α-tocopherol1, 3.
Vitamin E has a key role reacting with the lipid radicals produced in the lipid peroxidation chain reaction, in which one lipid molecule after another becomes oxidised to the maximum extent to form a lipid peroxide (a lipid molecule containing one or more oxygen-oxygen bonds). The polyunsaturated fatty acids in biological cell membranes are very susceptible to peroxidation4. Vitamin E is a highly
|Figure 2: Lipid Peroxidation
efficient antioxidant as, after it has been oxidized and before it has been decomposed for waste, it can be re-reduced i.e. recycled by ascorbic acid and glutathione5.
Lipid peroxidation consists of three separate phases: initiation, propagation and termination (see figure 2). Initiation occurs when a small number of radicals, usually from oxygen, can abstract hydrogen from lipid molecules to yield lipid free radicals. Propagation is the chain reaction phase. The lipid free radical can react with an oxygen molecule to form lipid peroxyl radicals. This peroxyl radical can then react with the original substrate; a process that is repeated until the substrate runs out. Termination occurs when substrate is depleted and the remaining radicals combine unpaired electrons to form a non-radical product4. By this point damage will have already been done to the cellular membrane. Vitamin E and other antioxidants can also initiate the termination phase by donating hydrogen atoms to the unpaired electrons of the free radicals before they can combine with the original substrate2, 4 (see Fiigures 1 and 2).
With increasing concerns about the potential adverse effects of the damage caused and the adverse effects of lipid peroxidation in cellular membranes and links to human disease, there has been an increase in the number of studies investigating the effects of vitamin E supplementation.
Vitamin E Supplementation Studies
Vitamin E supplementation studies have shown mixed results; some studies have shown that vitamin E has no effect on lipid peroxidation, even when more than one indicator of lipid peroxidation was measured3. However, other research has shown that, when using breath pentane as an indicator of lipid oxidation, daily supplementation of 1000UI of vitamin E daily for 10 days significantly reduced the excretion of breath pentane in healthy adults consuming a normal balanced diet. This seems to suggest that vitamin E supplementation can reduce lipid peroxide concentrations, assumingly controlling lipid peroxidation in cell membranes5.
Research suggests that free radicals originating from oxygen molecules are involved in the initiation and progression of cancer. Because of its antioxidant properties research has linked of vitamin E with a reduced risk of developing various cancers5. A study of Nigerian patients with prostate cancer showed that they had serum levels of vitamin E that were significantly lower than in cancer-free participants6.
The majority of supplementation studies have been carried out on the α-tocopherol family of vitamin E so little is known about the other forms: beta, delta and gamma-tocopherol, as the liver preferentially resecretes only alpha-tocopherol via the hepatic alpha-tocopherol transfer protein; the liver metabolizes and excretes the other vitamin E forms7.
Taking a Vitamin E Supplements
Humans do not produce their own vitamin E; plants are the only organisms that can synthesise their own vitamin E, so humans must get their recommended daily amount (15mg/day8) from their diet. Good sources of vitamin E include: nuts, seeds and vegetable oils, green leafy vegetables and fortified cereals9.
Severe deficiencies in vitamin E, which can cause instability in red blood cells, are rare and are often limited to the elderly, premature infants or in individuals with fat malabsorption10. However, many adults, particularly women10, do not meet the daily requirements for vitamin E intake and may benefit from adding a vitamin E supplement to their diet.
Dietary deficiencies in vitamin E and its beneficial actions as an antioxidant means that vitamin E is often taken alone as an anti-ageing supplement or combined with other compounds with anti-ageing compounds. As before beginning any drug or supplementing regime consult with your doctor especially if you have any specific allergies, particularly to vitamin E, are breastfeeding or are currently pregnant.
Additionally, check with your doctor over any other medications you are taking as vitamin E has the potential to interact with some drugs and medications. Vitamin E can interact with anticoagulant medications, such as Warfarin and as a result increase the risk of bleeding. This vitamin also interacts with the cholesterol-lowering drugs, Simvastatin and Niacin, and the weight loss drug Orlistat. Additionally oncologists advise against the use of antioxidant supplements during chemotherapy and radiotherapy, as they may reduce the effctiveness by inhibiting cellular oxidative damage in cancerous cells11.
Side Effects Of Vitamin E
Side effects of vitamin E supplementation can include allergic reactions, such as rashes or hives, which highlights the importance of consulting with your doctor before beginning treatment. Other side effects include nausea, vomiting, diarrhoea and stomach pains and if any of these persist cease treatment immediately and consult a physician.
There are no adverse effects of consuming vitamin E in food, but if more than the recommended amount of supplementation is ingested it can cause haemorrhaging, interrupt blood coagulation and inhibit platelet agreggation11, so take all supplements with care.
about unsaturated acids
1.) Valko, M., Libfritz, D., Moncol, J., Cronin, M. T. D., Mazur, M., Tesler, J. (2007) Free radicals and antioxidants in normal physiological functions and human disease The International Journal of Biochemistry and Cell Biology Vol. 39: 44-84
2.) Kamal-Eldin, A., Appleqvist, L. (1996) The chemistry and antioxidant properties of tocopherols and tocotrienols Lipids Vol. 31, No. 7: 671-701
3.) Meagher, E. A., Barry, O. P., Lawson, J. A., Rokach, J., Fitzgerald, G. A. (2001) Effects of vitamin E in lipid peroxidation in healthy persons JAMA Vol. 285, No. 9: 1178-1182.
4.) Cai, Z. (2005) Lipid peroxidation Encyclopedia of Toxicology Vol. 2: 730-734.
5.) Packer, L. (1991) Protective role of vitamin E in biological systems American Journal of Clinical Nutrition Vol. 53: 1050S-1055S
6.) Adaramoye, O. A., Akinloye, O., Olatunji, I. K. (2010) Trace elements and vitamin E status in Nigerian patients with prostate cancer Afr Health Sci Vol. 10, No. 1: 2-8
7.) Traber, M. G. (2007) Vitamin E regulatory mechanisms. Annu Rev Nutr Vol. 27:347-62
8.) Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes: Vitamin C, Vitamin E, Selenium, and Carotenoids. Washington, DC: National Academy Press, 2000.
9.) U.S. Department of Agriculture, Agricultural Research Service. USDA National Nutrient Database for Standard Reference, Release 16-1, 2004. http://www.ars.usda.gov/ba/bhnrc/ndl
10.) Murphy, S. P., Subar, A. F., Block, G. (1990) Vitamin E intakes and sources in the United States American Journal of Clinical Nutrition Vol. 52: 361-367.
11.) Office of Dietary Supplements: National Institute of Health: Dietary Fact Sheet: Vitamin E Updated 12/15/2009 .
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