Deficiency Signs And Symptoms

Due to the widespread availability of vitamin E in the food chain, it is generally accepted that primary vitamin E deficiency does not occur. However, deficiency has been reported in low birth weight infants given infant formula or cows' milk with low vitamin E levels, and in some intestinal malabsorption syndromes such as cystic fibrosis. Genetic abnormalities in alpha-tocopherol transport protein also result in vitamin E deficiency (Shils et al 1999).

Ultimately, it is tissue uptake, local oxidative stress levels and polyunsaturated fat content that influence whether symptoms of deficiency develop.

Symptoms of deficiency tend to be vague and difficult to diagnose due to the nutrient's widespread actions, but the following signs and symptoms have been reported in humans (FAO/WHO 2002, Meydani & Hayes 2003).

• Haemolytic anaemia.

• Immunological abnormalities.

• Neurological disturbances (e.g. peripheral neuropathies).

• Platelet dysfunction.

• Leakage of muscle enzymes such as creatine kinase and pyruvate kinase into plasma.

• Increased levels of lipid peroxidation products in plasma. MAIN ACTIONS

Vitamin E is an electron donor (reducing agent or antioxidant), and many of its biochemical and molecular functions can be accounted for by this function. It is involved in many biochemical processes in the body, but its most important biological function is that of an antioxidant and working within the antioxidant network. ANTIOXIDANT

Vitamin E is considered to be the most important and potent lipid-soluble antioxidant. It prevents free radical damage to the PUFAs within the phospholipid layer of each cell membrane and oxidation of LDL. It has been estimated that for every 1000-2000 molecules of phospholipid, one molecule of vitamin E is present for antioxidant defence (Sen & Packer 2000).

This is achieved by reacting with free radical molecules and forming a tocopheroxyl radical, which then leaves the cell membrane. Upon entering the aqueous environment outside the membrane, it reacts with vitamin C (or other hydrogen donors such as glutathione) to become reduced and, therefore, regenerated (Vatassery 1987). In this way, vitamin E activity is influenced by what has been called the'antioxidant network', which restores vitamin E to its unoxidised state, ready to act as an antioxidant many times over (see Clinical note below for more information).

Taking a larger perspective, the collective antioxidant action at each cell membrane protects the body's tissues and organs from undue oxidative stress. Prolonged and/or excessive exposure to free radicals has been implicated in many conditions, such as cardiovascular disease, cancer initiation and promotion, degenerative diseases, and ageing in general (FAO/WHO 2002).

Clinical note — Free radicals, antioxidant recycling and the antioxidant network

Oxygen-containing free radicals (such as the hydroxyl radical, superoxide anion radical, hydrogen peroxide, oxygen singlet and nitric oxide radical) are highly reactive species, capable of damaging biologically important molecules such as

DNA, proteins, carbohydrates and lipids. Antioxidants can break the destructive cascade of reactions initiated by free radicals by converting them into harmless derivatives.

The term 'oxidative stress' refers to an imbalance of free radicals over antioxidants. Both endogenous and exogenous antioxidants work in a synergistic way to avoid this situation, but antioxidants such as vitamin E become oxidised themselves during this process. Other antioxidants, such as ubiquinone, ascorbate and glutathione, are then involved in recycling vitamin E back to its unoxidised state, allowing it to continue neutralising free radical molecules (Sen & Packer 2000). When these other antioxidants become oxidised in turn, they are also regenerated to their antioxidant forms by yet others such as alpha-lipoic acid and cysteine. In this way, the recycling of various antioxidants occurs in an orchestrated manner.

In the body, the antioxidant network comprises four parts that work together to provide a continuous defence against free radical damage (De Vita et al 2006).

• Enzymes that destroy or detoxify common oxidants (e.g. catalase, glutathione peroxidase, which needs selenium).

• Antioxidant vitamins, notably vitamins E and C, and coenzyme Q10, which are continuously recycled, as discussed earlier.

• Dietary antioxidants or phytochemicals (e.g. carotenoids, polyphenols and allyl sulfides).

• Proteins that sequester iron and copper so that free forms do not exist in the body.

The antioxidant network provides a basis for recommending combinations of foods and antioxidant nutrients to provide maximal benefits rather than single entities in high doses.

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