Vitamin E

More than other tissues, the skin is exposed to various aggressive effects of the environment. Chemical and physical agents, such as ultraviolet (UV) light, ozone, heavy metals, and many others, cause permanent stress to the outermost cell layers of the skin. In particular, regular and excessive exposure to UV light induces damage and disease in the tissue. The skin becomes wrinkled, appears older, the immune system is weakened, and, more seriously, skin cancer can develop.

Up to 20% of the solar UVB impinging on the skin reaches the viable cells of the epidermis, and about 10% penetrates to the dermis [1]. An even higher portion of UVA and visible light can reach the dermis. The interaction of UV light with various skin components results in the formation of free radicals.

The skin has enzymatic and nonenzymatic antioxidant systems. These work to prevent the formation of free radicals, which can harm the integrity of the cell structures and with it the normal function of the skin. One nonenzymatic antioxidant is vitamin E.

Chemically, vitamin E (tocopherol) (Fig. 1) is a chromanol derivative. It consists of two functional units, a chromane ring bearing a phenolic OH group and a branched side chain. The hydrocarbon chain is necessary for the proper orientation of tocopherol at its site of activity, whereas the chromanol part provides the antioxidant properties.

Vitamin E has a protector function. It is considered to be essential for the stabilization of biological membranes, particularly those containing large amounts of polyunsatu-rated fatty acids. Cell membrane lipids in the skin are under constant attack from free radicals formed both in the course of normal biological reactions as well as, in particular, by various external factors. Free radicals can take electrons from membrane lipids, which leads to the impairment of the membranes on one side. On the other side, new free radicals are then formed that continue the destructive work.

Vitamin E is considered the major free-radical chain-breaking antioxidant in membranes. It inactivates peroxyl radicals in the vicinity of the membranes and thus inhibits the propagation of lipid peroxidation. Vitamin E loses thereby its antioxidant power and itself becomes a low-energy radical. This tocopheryl radical is, however, unable to attack other molecules and thus initiate a new free-radical chain reaction. In a next step, the tocopheryl radical gets back its antioxidant properties: it is regenerated by a redox system to the active tocopherol.

Although lost antioxidants are continuously replaced and regenerated, oxidative stress, such as excessive exposure to UV light, can overwhelm the natural cutaneous anti-oxidant capacity and harm the insufficiently protected tissue. A great number of studies performed during the past 15 to 20 years deal with this problem, and some of them with the role of vitamin E in this process. Investigations include studies on the consequences of low levels of vitamin E in the skin, the influence of external factors on vitamin E concentration, and the possible use of topical vitamin E in the form of tocopherol or its ester vitamin E acetate to reduce or even prevent possible damage to the skin.

In an animal study by Igarashi, low levels of vitamin E increased lipid peroxide levels. Rats deficient in vitamin E showed significantly higher peroxide concentrations than normal animals. UV irradiation of the deficient animals led to a further significant increase [2]. Khettab applied vitamin E to the skin of hairless mice before UV irradiation and observed a reduction in epidermal lipid peroxidation compared with control [3].

Kondo examined the protective effect of vitamin E on UVB damage in human skin fibroblasts in vitro. He found a significant difference in surviving fibroblasts in the presence of 100 and 1000 |g a-tocopherol per mL culture fluid. The results suggest that vitamin E protects human skin fibroblasts against the cytotoxic effects of UVB [4].

Interesting is the result of a study performed by Lopez-Torres et al., in which they investigated the effects of topical tocopherol on epidermal and dermal antioxidants and their ability to prevent UV-induced oxidative damage. Topically applied tocopherol to hairless mice in vivo increased dermal superoxide dismutase activity by 30% and protected epidermal glutathione peroxidase and superoxide dismutase from depletion after UV irradiation. Total and reduced glutathione levels in the epidermis were also increased, as were dermal vitamin C levels. The investigators conclude that topical administration of a-tocopherol protects cutaneous tissues against oxidative damage induced by UV irradiation [5].

Application of pure vitamin E acetate to the skin of hairless mice immediately after UVB irradiation reduced sunbum symptoms such as erythema, skin sensitivity, and skin swelling in a study carried out by Trevithick et al. [6]. Reduced erythema formation after UV irradiation was also reported by Roshchupkin [7] and Pathak [8].

In a human skin model, antioxidant depletion as a result of UV light exposure was shown by Podda [9]. Ubiquinol and ubiquinone in particular, as well as a-tocopherol to a lesser extent, were susceptible and decreased with higher UV light intensities to virtually non detectable levels. Partial impairment of the cutaneous antioxidant defense system, including vitamin E, by UV light was also observed by Fuchs [10].

Clement-Lacroix et al. tested the protector effect of vitamin E on immune suppression in human epidermal cells in vitro. Cultured cells preincubated with or without vitamin E were irradiated with UVA light. The investigators could show that incubation of cell cultures with vitamin E before irradiation partially protected the cells from the immuno-suppressive effects of UVA radiation [11]. Finally, Weiser [12] and Miyamoto [13] have shown wound-healing properties of topical vitamin E acetate.

Vitamin E is used in cosmetics for everyday use to strengthen the natural antioxidant potency of the skin and thus to better cope with oxidative stress. Most of the scientific background for the topical use of vitamin E stems from observations in context with UV light. Vitamin E is often used, therefore, in suncare products for improvement of the protection achieved with the sun filters. Even high SPF factors still allow the penetration of some UV light onto and into the skin. Whereas the sun filters absorb or reflect most of the rays on the surface of the skin, vitamin E acts on the inside and reduces the risk of damage that could be caused by rays passing through the sun filter barrier. Vitamin E helps, therefore, in the prevention of symptoms caused by UV-induced skin damage such as wrinkling and irregular pigmentation.

In nature, Vitamin E appears as tocopherols, of which the alpha form has the highest biological potency. The unesterified form is present in wheat germ oil and other vegetable oils that are used in cosmetics as sources of Vitamin E. Most often used is dl-alpha tocoph-eryl acetate, because this ester is less prone to oxidation than free tocopherol. In the skin, vitamin E acetate is bioconverted into the biologically active antioxidant tocopherol [14,15].

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