Reference from the joint report of FAO/WHO expert consultation on Human Vitamins and Minerals verbatim.
Nutrients with radical-quenching properties
Vitamins C and E are the principal nutrients which possess radical-quenching properties. Both are powerful antioxidants, and the most important difference between these two compounds stems from their different solubility in biologic fluids. Vitamin C is water soluble and is therefore especially found in the aqueous fractions of the cell and in body fluids whereas vitamin E is highly lipophilic and is found in membranes and lipoproteins.
Vitamin E
33. Burton, G.W. & Ingold, K.U. 1984. B-carotene: an unusual type of lipid antioxidant. Science, 224: 569-573.
46. Burton, G.W. & Ingold, K.U. 1981. Autoxidation of biological molecules. 1. The antioxidant activity of vitamin E and related chain-breaking phenolic antioxidants in vitro. J. Am. Chem. Soc., 103: 6472-6477.
Vitamin E falls into the class of conventional antioxidants which are generally phenols or aromatic amines (see Chapter 9). In the case of the four tocopherols that together constitute vitamin E, the initial step involves a very rapid transfer of phenolic hydrogen to the recipient free radical with the formation of a phenoxyl radical from vitamin E. The phenoxyl radical is resonance stabilised and is relatively unreactive towards lipid or oxygen. It does not therefore continue the chain (33, 46).
47. Kornbrust, D.J. & Mavis, R.D. 1979. Relative susceptibility of microsomes from lung, heart, liver, kidney, brain and testes to lipid peroxidation: correlation with vitamin E content. Lipids, 15:315-322.
31. Packer, J.E., Slater, T.F. & Willson, R.L. 1979. Direct observations of a free radical interaction between vitamin E and vitamin C. Nature, 278: 737-738.
32. Niki, E., Tsuchiya, J., Tanimura, R. & Kamiya, Y. 1982. Regeneration of vitamin E from α-chromanoxyl radical by glutathione and vitamin C. Chem. Lett., 27: 798-792.
48. Wefers, H. & Sies, H. 1988. The protection by ascorbate and glutathione against microsomal lipid peroxidation is dependent on vitamin E. Eur. J. Biochem., 174: 353-357.
49. McCay, P.B. 1985. Vitamin E: Interactions with free radicals and ascorbate. Annu. Rev. Nutr., 5:323-340.
50. Sies, H. & Murphy, M.E. 1991. The role of tocopherols in the protection of biological systems against oxidative damage. Photochem. Photobiol., 8: 211-224.
However, the phenoxyl radical is no longer an antioxidant and to maintain the antioxidant properties of membranes, it must be recycled or repaired – that is, reconverted to vitamin E – because the amount of vitamin E present in membranes can be several thousand-fold less than the amount of potentially oxidizable substrate (47). Watersoluble vitamin C is the popular candidate for this role (31), but thiols and particularly GSH can also function in vitro (32, 48-50).
5. Halliwell, B. & Gutteridgem J.M.C. 1989. Free radicals in biology and medicine. 2nd ed. Oxford: Clarendon Press.
6. Ames, B.N. 1983. Dietary carcinogens and anticarcinogens, oxygen radicals and degenerative diseases. Science, 221: 1256-1264.
7. Moncada, S. & Higgs, E.A. 1993. Mechanisms of disease: the L-arginine-nitric oxide pathway. N. Engl. J. Med., 329: 2002-2012.
8. Fridovich, I. 1983. Superoxide radical: an endogenous toxicant. Annu. Rev. Pharmacol Toxicol., 23: 239-257.
46. Burton, G.W. & Ingold, K.U. 1981. Autoxidation of biological molecules. 1. The antioxidant activity of vitamin E and related chain-breaking phenolic antioxidants in vitro. J. Am. Chem. Soc., 103: 6472-6477.
There are eight possible isomers of vitamin E, but α-tocopherol (5,7,8 trimethyl tocol) is the most biologically important antioxidant in vivo (46). In plasma samples, more than 90 percent is present as α-tocopherol but there may be approximately 10 percent of γ-tocopherol.
31. Packer, J.E., Slater, T.F. & Willson, R.L. 1979. Direct observations of a free radical interaction between vitamin E and vitamin C. Nature, 278: 737-738.
In foods such as margarine and soy products the γ form may be predominant and palm oil products are rich in the tocotrienols. Vitamin E is found throughout the body in both cell and sub-cellular membranes. It is believed to be orientated with the quinol ring structure on the outer surface (i.e., in contact with the aqueous phase) to enable it to be maintained in its active reduced form by circulating reductants such as vitamin C (31).
47. Kornbrust, D.J. & Mavis, R.D. 1979. Relative susceptibility of microsomes from lung, heart, liver, kidney, brain and testes to lipid peroxidation: correlation with vitamin E content. Lipids, 15:315-322.
Within biologic membranes, vitamin E is believed to intercalate with phospholipids and provide protection to PUFAs. PUFAs are particularly susceptible to free radical–mediated oxidation because of their methylene-interrupted doublebond structure. The amount of PUFAs in the membrane far exceeds the amount of vitamin E, and the tocopherol-PUFAs ratios are highest in tissues where oxygen exposure is greatest and not necessarily where the PUFAs content is highest (47).
46. Burton, G.W. & Ingold, K.U. 1981. Autoxidation of biological molecules. 1. The antioxidant activity of vitamin E and related chain-breaking phenolic antioxidants in vitro. J. Am. Chem. Soc., 103: 6472-6477.
Oxidation of PUFAs leads to disturbances in membrane structure and function and is damaging to cell function. Vitamin E is highly efficient at preventing the autoxidation of lipid and it appears as if the primary, and possibly only, role in biologic tissues is to provide this function (46). Autoxidation of lipid is initiated by a free radical abstracting hydrogen from PUFA to form a lipid radical (reaction 6) which is followed by a rearrangement of the doublebond structure to form a conjugated diene. In vitro the presence of minute amounts of peroxides and transition metals will stimulate the formation of the initial radical.
Oxygen adds to the lipid radical to form a lipid peroxide (reaction 7) which then reacts with another lipid molecule to form a hydroperoxide and a new lipid radical (reaction 8). This process is shown in general terms below for the autoxidation of any organic molecule (RH), where the initial abstraction is caused by a hydroxyl radical (OH·).
Autoxidation or lipid peroxidation is represented by reactions 6 and 7. The process stops naturally when reaction between two radicals (reaction 9) occurs more frequently than does reaction 8.
The presence of the chain-breaking antioxidant, vitamin E (ArOH), reacts in place of RH shown in reaction 8 and donates the hydrogen from the chromanol ring to form the hydroperoxide (reaction 10). The vitamin E radical (ArO·, tocopheroxyl radical) which is formed is fairly stable and therefore stops autoxidation. Hydroperoxides formed by lipid peroxidation can be released from membrane phospholipids by phospholipase A2 and then degraded by GPx in the cell cytoplasm (see Chapter 15). or Selenium
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