Vitamin E

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The α-tocopherol form of vitamin E.

Vitamin E is the collective name for a set of 8 related α-, β-, γ-, and δ-tocopherols and the corresponding four tocotrienols, which are fat-soluble vitamins with antioxidant properties.[1][2] Of these, α-tocopherol (also written as alpha-tocopherol) has been most studied as it has the highest bioavailability.[3]

It has been claimed that α-tocopherol is the most important lipid-soluble antioxidant, and that it protects cell membranes from oxidation by reacting with lipid radicals produced in the lipid peroxidation chain reaction.[1][4] This would remove the free radical intermediates and prevent the oxidation reaction from continuing. The oxidised α-tocopheroxyl radicals produced in this process may be recycled back to the active reduced form through reduction by other antioxidants, such as ascorbate, retinol or ubiquinol.[5] However, the importance of the antioxidant properties of this molecule at the concentrations present in the body is not clear and it is possible that the reason why vitamin E is required in the diet is unrelated to its ability to act as an antioxidant.[6]. Other forms of vitamin E have their own unique properties. For example, γ-tocopherol (also written as gamma-tocopherol) is a nucleophile that may react with electrophilic mutagens[3]; and the tocotrienols having specialized roles in protecting neurons from damage[7], cancer prevention[8] and cholesterol reduction[9]by inhibiting the activity of HMG-CoA reductase[16-1];δ-tocotrienol blocks processing of sterol regulatory element‐binding proteins (SREBPs)[16-1].However, the roles and importance of all of the various forms of vitamin E are presently unclear,[10][11] and it has even been suggested that the most important function of vitamin E is as a signaling molecule, and that it has no significant role in antioxidant metabolism.[12][13]

Most studies about vitamin E have supplemented using only the synthetic alpha-tocopherol, but doing so leads to reduced serum gamma- and delta-tocopherol concentrations. Moreover, a 2007 clinical study involving synthetic alpha-tocopherol concluded that supplementation did not reduce the risk of major cardiovascular events in middle aged and older men[14]. For more info, read article tocopherol.


[edit] Food sources of Vitamin E

Particularly high levels of vitamin E can be found in the following foods:[15]

[edit] Vitamin E to prevent prostate cancer study discontinued

There have been some theories that Vitamin E, especially when coupled with selenium, may reduce the risk of prostate cancer[16] by 30 percent.[17] However, the Selenium and Vitamin E Cancer Prevention Trial, ("SELECT"), run from 2004 to 2008, found that vitamin E, whether taken alone or in combination with selenium, did not prevent prostate cancer.[18] The SELECT study was discontinued after independent reviewers determined that there was no benefit to the 35,000 men who were the subject of the study. [16]

[edit] Congenital heart defects

Vitamin E has been linked to congenital heart defects.[19] It thus might be wise to discourage its use in pregnant women.

[edit] References

  1. ^ a b Herrera E, Barbas C (2001). "Vitamin E: action, metabolism and perspectives". J Physiol Biochem 57 (2): 43 – 56. PMID 11579997. 
  2. ^ Packer L, Weber SU, Rimbach G (01 Feb 2001). "Molecular aspects of alpha-tocotrienol antioxidant action and cell signalling". J. Nutr. 131 (2): 369S–73S. PMID 11160563. 
  3. ^ a b Brigelius-Flohé R, Traber M (01 Jul 1999). "Vitamin E: function and metabolism". Faseb J 13 (10): 1145 – 55. PMID 10385606. 
  4. ^ Traber MG, Atkinson J (2007). "Vitamin E, antioxidant and nothing more". Free Radic. Biol. Med. 43 (1): 4–15. doi:10.1016/j.freeradbiomed.2007.03.024. PMID 17561088. 
  5. ^ Wang X, Quinn P (1999). "Vitamin E and its function in membranes". Prog Lipid Res 38 (4): 309 – 36. doi:10.1016/S0163-7827(99)00008-9. PMID 10793887. 
  6. ^ Brigelius-Flohé R (2009). "Vitamin E: The shrew waiting to be tamed". Free Radic. Biol. Med. 46 (5): 543–554. doi:10.1016/j.freeradbiomed.2008.12.007. PMID 19133328. 
  7. ^ Sen C, Khanna S, Roy S (2006). "Tocotrienols: Vitamin E beyond tocopherols". Life Sci 78 (18): 2088 – 98. doi:10.1016/j.lfs.2005.12.001. PMID 16458936. 
  8. ^ Malafa MP (2008). "New insights and gains in pancreatic cancer". Cancer Control 15 (4): 276-277. 
  9. ^ Das, S., I. Lekli, et al. (2008). "Cardioprotection with palm oil tocotrienols: comparision of different isomers.". Am J Physiol Heart Circ Physiol 294 (2): 970-978. 
  10. ^ Brigelius-Flohé R, Davies KJ (2007). "Is vitamin E an antioxidant, a regulator of signal transduction and gene expression, or a 'junk' food? Comments on the two accompanying papers: "Molecular mechanism of alpha-tocopherol action" by A. Azzi and "Vitamin E, antioxidant and nothing more" by M. Traber and J. Atkinson". Free Radic. Biol. Med. 43 (1): 2–3. PMID 17561087. 
  11. ^ Atkinson J, Epand RF, Epand RM (2007). "Tocopherols and tocotrienols in membranes: A critical review". Free Radic. Biol. Med. 44 (5): 739–764. doi:10.1016/j.freeradbiomed.2007.11.010. PMID 18160049. 
  12. ^ Azzi A (2007). "Molecular mechanism of alpha-tocopherol action". Free Radic. Biol. Med. 43 (1): 16–21. doi:10.1016/j.freeradbiomed.2007.03.013. PMID 17561089. 
  13. ^ Zingg JM, Azzi A (2004). "Non-antioxidant activities of vitamin E". Curr. Med. Chem. 11 (9): 1113–33. PMID 15134510. 
  14. ^ Sesso, H.D., et al (2008). "Vitamins E and C in the Prevention of Cardiovascular Disease in Men: The Physicians' Health Study II Randomized Controlled Trial". JAMA 300 (18): 2123-2133. doi:10.1001/jama.2008.600. 
  15. ^ USDA National Nutrient Database
  16. ^ a b American Cancer Society, Vitamin E, updated Oct. 27, 2008
  17. ^ National Cancer Institute, The SELECT Prostate Cancer Prevention Trial, Oct. 27, 2008
  18. ^ National Cancer Institute, Selenium and Vitamin E Cancer Prevention Trial (SELECT), Oct. 31, 2008
  19. ^ Smedts HP, de Vries JH, Rakhshandehroo M, et al (February 2009). "High maternal vitamin E intake by diet or supplements is associated with congenital heart defects in the offspring". BJOG 116 (3): 416–23. doi:10.1111/j.1471-0528.2008.01957.x. PMID 19187374. 

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