See the Skin Health Overview article


Vitamin E is a fat-soluble antioxidant that is essential for the maintenance of healthy skin. Naturally occurring vitamin E is not a single compound; instead, vitamin E is a group of molecules with related structures, some of which may have unique properties in skin. Vitamin E is also found as vitamin E conjugates that increase stability but require cellular metabolism for activation. Vitamin E is normally provided to the skin through the sebum. Topical application can also supply the skin with vitamin E and may provide specific vitamin E forms that are not available from the diet. As an antioxidant, vitamin E primarily reacts with reactive oxygen species. In addition, vitamin E can also absorb the energy from ultraviolet (UV) light. Thus, it plays important roles in photoprotection, preventing UV-induced free radical damage to skin. Vitamin E may also have related anti-inflammatory roles in the skin. Other roles of vitamin E in the skin are poorly understood because research is limited. This article discusses the roles of vitamin E in the skin and summarizes the current knowledge about vitamin E in skin health.

Forms of vitamin E

The term “vitamin E” does not refer to a single molecule but to two classes of molecules with similar structures and antioxidant properties, comprising a family of eight substances. Tocopherols are the most abundant form of vitamin E in the body, consisting of four different forms (α-, β-, γ-, and δ-tocopherol). Tocotrienols, which are found in the body to a lesser extent, also exist in four different forms (α-, β-, γ-, and δ-tocotrienol). Although tocopherols and tocotrienols are available from the diet, α-tocopherol is the primary form of vitamin E found and maintained in the body, due to the specificity of a transport protein for α-tocopherol (see the article on Vitamin E).

Naturally occurring vitamin E is usually labeled as “natural” or “d” vitamin E, while synthetic vitamin E is a mixture of eight isomeric forms, usually labeled “all-rac” or “dl.” Tocopherols and tocotrienols are also available as ester derivatives that increase molecular stability upon exposure to heat, light, and air. Conjugated vitamin E molecules are typically used in dietary supplements; the esterified molecule is removed by cellular metabolism in the intestine. However, metabolism of vitamin E conjugates in skin is low; therefore, the availability of unesterified or “free” vitamin E from cutaneous application of conjugates may be limited (see Topical application).

Content and availability

Vitamin E is the most abundant lipophilic antioxidant found in human skin (1, 2). In humans, levels of vitamin E in the epidermis are higher than the dermis (1). Although the predominant form of vitamin E in skin of unsupplemented individuals is α-tocopherol, skin may also contain measurable amounts of γ-tocopherol (3) and other diet-derived tocopherols and tocotrienols (4).

Vitamin E first accumulates in the sebaceous glands before it is delivered to the skin surface through sebum (5, 6). Following oral ingestion, it takes at least seven days before the vitamin E content of sebum is altered (5, 7). There are no transport proteins specific for vitamin E in the skin. Sebum is secreted to the surface of the stratum corneum, where it concentrates in the lipid-rich extracellular matrix of this layer (3). Due to its lipophilic nature, vitamin E can also penetrate into all underlying layers of skin (8). Skin vitamin E levels are higher in individuals with increased sebum production, as well as in skin types that naturally produce more sebum (e.g., “oily’ skin on the face vs. drier skin on the arm) (1, 8).

Exposures to UV light (3, 9, 10) or ozone (6, 11, 12) lower the vitamin E content in skin, primarily in the stratum corneum. Vitamin E concentrations in the human epidermis also decline with age (1). Since epidermal structure changes with age (13), this may be due to increased UV penetration of this layer.

Topical application

Topical application of vitamin E has been used in a wide variety of forms throughout history, ranging from the application of oils to the skin surface to the use of modern cosmetic formulations. Just as sebum provides a delivery mechanism for vitamin E to the stratum corneum, topical applications of vitamin E permeate the epidermis and dermis (14, 15). The rate of percutaneous vitamin E absorption and factors that influence its penetration are largely unknown in humans, with a large range of concentrations and times used in various studies. It is generally assumed that solutions with vitamin E concentrations as low as 0.1% can increase vitamin E levels in the skin (16). Interestingly, vitamin E levels in the dermis increase greatly after topical application, likely accumulating in the sebaceous glands (15). However, although it is increased after topical delivery, the concentration of vitamin E in the dermis is lower than in the stratum corneum. Skin supplied only with dietary vitamin E primarily contains α- and γ-tocopherol (3, 7, 8); by contrast, skin supplied with synthetic vitamin E topically can contain a mixture of different tocopherols and/or tocotrienols (10, 15). In terms of penetration and absorption following topical application, tocotrienols and tocopherols accumulate in skin at varying rates, but the mechanisms governing these differences are unclear (15).

After topical application, vitamin E accumulates not only in cell membranes but also in the extracellular lipid matrix of the stratum corneum, where vitamin E contributes to antioxidant defenses. However, much of a topically applied dose of vitamin E alone will be destroyed in the skin following exposure to UV light (10). This suggests that although vitamin E is working as an antioxidant, it is unstable on its own and easily lost from the skin. Thus, improving the stability of topical applications with vitamin E is important. Products containing both vitamin C and vitamin E have shown greater efficacy in photoprotection than either antioxidant alone (see Photoprotection).

The stability of topical vitamin E solutions may also be increased by the use of vitamin E conjugates. These vitamin E derivatives are usually commercially produced esters of tocopherol (although tocotrienol esters have been formulated) that are resistant to oxidation but can still penetrate the skin layers. Vitamin E conjugates, however, do not have antioxidant functions. To be effective, the molecule conjugated to vitamin E must be removed by enzymes within a cell. Since the stratum corneum contains metabolically inactive cells and the remaining layers of the epidermis and dermis may contain a large volume of extracellular proteins, it is unclear how efficiently ester conjugates are converted to “free” vitamin E in skin. Depending on the compound and the model system used, the effectiveness of these formulations can vary greatly (16-20), and studies often do not compare the application of vitamin E conjugates to the application of unmodified vitamin E molecules.

Because vitamin E can absorb UV light to produce free radicals (see Photoprotection), there is the possibility that heavy sunlight exposure after topical application can cause skin reactions. However, concentrations of vitamin E between 0.1%-1.0% are generally considered safe and effective to increase vitamin E levels in the skin, but higher levels of α-tocopherol have been used with no apparent side effects (16). On the other hand, studies of dose-dependent vitamin E accumulation and effectiveness in skin protection are lacking. Some forms of vitamin E, especially ester conjugates, have led to adverse reactions in the skin, including allergic contact dermatitis and erythema. Although such reactions may be due to oxidation by-products, the emulsion creams used for topical delivery of compounds may also contribute to the observed effects (21).


Vitamin E deficiency may affect skin function, but there is little evidence from human studies. Vitamin E deficiency in rats has been reported to cause skin ulcerations (22) and changes in skin collagen cross-linking (23, 24), but the underlying cause of these effects is unknown.

Functions in Healthy Skin


The primary role of vitamin E in the skin is to prevent damage induced by free radicals and reactive oxygen species; therefore, the use of vitamin E in the prevention of UV-induced damage has been extensively studied. Although molecules in the vitamin E family can absorb light in the UVB spectrum, the “sunscreen” activity of vitamin E is considered limited since it cannot absorb UVA light or light in higher wavelengths of the UVB spectrum (25). Thus, the primary photoprotective effect of vitamin E is attributed to its role as a lipid-soluble antioxidant.

Many studies in cell culture models (in vitro studies) have found protective effects of vitamin E molecules on skin cells (26-28), but these models do not recreate the complex structure of skin tissues. Therefore, in vivo studies are needed.

Studies using orally administered vitamin E have reported mixed results on its photoprotective potential. An early study of vitamin E supplementation in hairless mice found no effect of dietary α-tocopherol acetate on UV-induced carcinogenesis (29). Three other mouse studies reported inhibition of UV-induced tumors in mice fed α-tocopherol acetate (30-32), but one of these studies utilized vitamin E doses that were toxic to animals when combined with the UV treatment (30). Another study in mice found a reduction of UV-induced DNA damage with dietary α-tocopherol acetate, but no effects on other free radical damage were observed in the skin (33). One human study reported that subjects taking 400 IU/day of α-tocopherol had reduced UV-induced lipid peroxidation in the skin but concluded there was no overall photoprotective effect (34). This was supported by another human study that found that 400 IU/day of α-tocopherol for six months provided no meaningful protection to skin (35). Furthermore, multiple human studies have shown no effect of vitamin E on the prevention or development of skin cancers (36, 37).

In contrast to oral supplementation with α-tocopherol alone, multiple studies have found that the combination of vitamin C and vitamin E protects the skin against UV damage. Human subjects orally co-supplemented with vitamins C and E show increased Minimal Erythemal Dose (MED), a measure of photoprotection from UV light in skin (38, 39). The combination of the two vitamins was associated with lower amounts of DNA damage after UV exposure (40). Results of another study suggest a mixture of tocopherols and tocotrienols may be superior to α-tocopherol alone, as the mixture showed reduced sunburn reactions and tumor incidence after UV exposure in mice (41). However, further trials with dietary tocotrienol/tocopherol mixtures are needed in human subjects.

Topical application of vitamin E is generally effective for increasing photoprotection of the skin. In rodent models, the application of α-tocopherol or α-tocopherol acetate before UV exposure reduces UV-induced skin damage by reducing lipid peroxidation (33, 42-44), limiting DNA damage (33, 45-47), and reducing the many chemical and structural changes to skin after UV exposure (14, 48-50). Vitamin E topical applications have also been shown to reduce UV-induced tumor formation in multiple mouse studies (14, 31, 51) and to reduce the effects of photo-activated toxins in the skin (52-55). Topical application of vitamin E also reduces the effects of UV radiation when applied after the initial exposure. In mice, α-tocopherol acetate prevents some of the erythema, edema, skin swelling, and skin thickening if applied immediately after UV exposure (49, 50). A similar effect has been shown in rabbits, where applying α-tocopherol to skin immediately after UV increased the MED (56). While the greatest effect was seen when vitamin E was applied immediately after UV exposure, one study showed a significant effect of application eight hours after the insult (49). In human subjects, the use of vitamin E on skin lowers peroxidation of skin surface lipids (57), decreases erythema (58, 59), and limits immune cell activation after UV exposure (60).

Like oral supplementation with vitamin C and vitamin E, topical preparations with both vitamins have also been successful. Together, the application of these antioxidants to the skin of animals before UV exposure has been shown to decrease sunburned cells (61, 62), decrease DNA damage (61, 63), inhibit erythema (61, 64), and decrease skin pigmentation after UV exposure (64). Similar effects have been seen in human subjects (65-67).

While a majority of studies have found benefit of topical α-tocopherol, there is much less evidence for the activity of esters of vitamin E in photoprotection (57). As described above, vitamin E esters require cellular metabolism to produce “free” vitamin E. Thus, topical use of vitamin E esters may provide only limited benefit or may require a delay after administration to provide significant UV protection.

Anti-inflammatory effects

Vitamin E has been considered an anti-inflammatory agent in the skin, as several studies have supported its prevention of inflammatory damage after UV exposure. As mentioned above, topical vitamin E can reduce UV-induced skin swelling, skin thickness, erythema, and edema — all signs of skin inflammation. In cultured keratinocytes, α-tocopherol and γ-tocotrienol have been shown to decrease inflammatory prostaglandin synthesis, interleukin production, and the induction of cyclooxygenase-2 (COX-2) and NADPH oxidase by UV light (68-70), as well as limit inflammatory responses to lipid hydroperoxide exposure (71). In mice, dietary γ-tocotrienol suppresses UV-induced COX-2 expression in the skin (70). Furthermore, topical application of α-tocopherol acetate or a γ-tocopherol derivative inhibited the induction of COX-2 and nitric oxide synthase (iNOS) following UV exposure (72). In vitro studies have shown similar anti-inflammatory effects of α- and γ-tocopherol on immune cells (73-75).

Many of these anti-inflammatory effects of vitamin E supplementation have been reported in combination with its photoprotective effects, making it difficult to distinguish an anti-inflammatory action from an antioxidant action that would prevent inflammation from initially occurring. Despite these limitations, there are many reports of vitamin E being used successfully in chronic inflammatory skin conditions, either alone (76, 77) or in combination with vitamin C (78) or vitamin D (79), thus suggesting a true anti-inflammatory action.

Wound healing

As mentioned above, skin lesions have been reported in rats suffering from vitamin E deficiency, although their origin is unclear. Vitamin E levels decrease rapidly at the site of a cutaneous wound, along with other skin antioxidants, such as vitamin C or glutathione (80). Since skin antioxidants slowly increase during normal wound healing, these observations have stimulated additional studies on the effect of vitamin E on the wound healing process. However, no studies have demonstrated a positive effect of vitamin E supplementation on wound repair in normal skin. Studies have shown that α-tocopherol supplementation decreases wound closure time in diabetic mice, but no effects have been observed in normal mice (81, 82). Vitamin E increases the breaking strength of wounds pre-treated with ionizing radiation (83), but this is likely due to antioxidant functions at the wound site akin to a photoprotective effect. In contrast, intramuscular injection of α-tocopherol acetate in rats has been suggested to decrease collagen synthesis and inhibit wound repair (84).

In humans, studies with topical α-tocopherol have either found no effects on wound healing or appearance or have found negative effects on the appearance of scar tissue (85, 86). However, these studies are complicated by a high number of skin reactions to the vitamin E preparations, possibly due to uncontrolled formation of tocopherol radicals in the solutions used. Despite these results, vitamin E, along with zinc and vitamin C, is included in oral therapies for pressure ulcers (bed sores) and burns (87, 88).

Other functions

There is limited information concerning the effects of vitamin E supplementation on photodamage, which is commonly observed as skin wrinkling. Although vitamin E can protect mice exposed to UV from excessive skin wrinkling, this is a photoprotective effect rather than treatment of pre-existing wrinkles. Other reports using vitamin E to treat photodamage or reduce wrinkles are poorly controlled studies or unpublished observations (89, 90). An analysis of the dietary intake of Japanese women showed no correlation between vitamin E consumption and skin wrinkling (91).

Vitamin E and oils containing tocopherols or tocotrienols have been reported to have moisturizing properties, but data supporting these roles are limited. Cross-sectional studies have shown no association between vitamin E consumption and skin hydration in healthy men and women (91, 92). However, two small studies have shown topical application of vitamin E can improve skin water-binding capacity after two to four weeks of use (93, 94). Long-term studies with topical vitamin E are needed to establish if these moisturizing effects can be sustained.

Environmental pollutants like ozone can decrease vitamin E levels in the skin (6, 11, 12) and lead to free radical damage that may compound the effects of UV exposure (12). Although not well studied, topical applications of vitamin E may reduce pollution-related free radical damage (11).


Vitamin E is an integral part of the skin’s antioxidant defenses, primarily providing protection against UV radiation and other free radicals that may come in contact with the epidermis. Oral supplementation with only vitamin E may not provide adequate protection for the skin, and co-supplementation of vitamin E and vitamin C may be warranted to effectively increase the photoprotection of skin through the diet. However, topical vitamin E seems to be an effective mechanism for both delivery to the skin and providing a photoprotective effect. Additional anti-inflammatory effects of topical vitamin E have been seen in the skin, although more studies are needed to determine if vitamin E primarily works as a free-radical scavenger or can have other effects on inflammatory signaling. Vitamin E is available commercially as a variety of synthetic derivatives, but the limited cellular metabolism in skin layers makes the use of such products problematic. Use of unesterified vitamin E, similar to that found in natural sources, has provided the most consistent data concerning its topical efficacy. The vitamin E family consists of eight different tocopherols and tocotrienols, and it will be important for future studies to determine if one or more of these molecules can have unique effects on skin function.

Authors and Reviewers

Written in February 2012 by:
Alexander J. Michels, Ph.D.
Linus Pauling Institute
Oregon State University

Reviewed in February 2012 by:
Maret G. Traber, Ph.D.
Professor of Nutrition
Helen P. Rumbel Professor for Micronutrient Research
Linus Pauling Institute
Oregon State University

This article was underwritten, in part, by a grant from Neutrogena Corporation, Los Angeles, California.

Copyright 2012-2024  Linus Pauling Institute


1.  Rhie G, Shin MH, Seo JY, et al. Aging- and photoaging-dependent changes of enzymic and nonenzymic antioxidants in the epidermis and dermis of human skin in vivo. J Invest Dermatol. 2001;117(5):1212-1217.  (PubMed)

2.  Shindo Y, Witt E, Han D, Epstein W, Packer L. Enzymic and non-enzymic antioxidants in epidermis and dermis of human skin. J Invest Dermatol. 1994;102(1):122-124.  (PubMed)

3.  Thiele JJ, Traber MG, Packer L. Depletion of human stratum corneum vitamin E: an early and sensitive in vivo marker of UV induced photo-oxidation. J Invest Dermatol. 1998;110(5):756-761.  (PubMed)

4.  Ikeda S, Toyoshima K, Yamashita K. Dietary sesame seeds elevate alpha- and gamma-tocotrienol concentrations in skin and adipose tissue of rats fed the tocotrienol-rich fraction extracted from palm oil. J Nutr. 2001;131(11):2892-2897.  (PubMed)

5.  Ekanayake-Mudiyanselage S, Kraemer K, Thiele JJ. Oral supplementation with all-Rac- and RRR-alpha-tocopherol increases vitamin E levels in human sebum after a latency period of 14-21 days. Ann N Y Acad Sci. 2004;1031:184-194.  (PubMed)

6.  Weber SU, Thiele JJ, Cross CE, Packer L. Vitamin C, uric acid, and glutathione gradients in murine stratum corneum and their susceptibility to ozone exposure. J Invest Dermatol. 1999;113(6):1128-1132.  (PubMed)

7.  Vaule H, Leonard SW, Traber MG. Vitamin E delivery to human skin: studies using deuterated alpha-tocopherol measured by APCI LC-MS. Free Radic Biol Med. 2004;36(4):456-463.  (PubMed)

8.  Thiele JJ, Weber SU, Packer L. Sebaceous gland secretion is a major physiologic route of vitamin E delivery to skin. J Invest Dermatol. 1999;113(6):1006-1010.  (PubMed)

9.  Shindo Y, Witt E, Han D, Packer L. Dose-response effects of acute ultraviolet irradiation on antioxidants and molecular markers of oxidation in murine epidermis and dermis. J Invest Dermatol. 1994;102(4):470-475.  (PubMed)

10.  Weber C, Podda M, Rallis M, Thiele JJ, Traber MG, Packer L. Efficacy of topically applied tocopherols and tocotrienols in protection of murine skin from oxidative damage induced by UV-irradiation. Free Radic Biol Med. 1997;22(5):761-769.  (PubMed)

11.  Thiele JJ, Traber MG, Podda M, Tsang K, Cross CE, Packer L. Ozone depletes tocopherols and tocotrienols topically applied to murine skin. FEBS Lett. 1997;401(2-3):167-170.  (PubMed)

12.  Valacchi G, Weber SU, Luu C, Cross CE, Packer L. Ozone potentiates vitamin E depletion by ultraviolet radiation in the murine stratum corneum. FEBS Lett. 2000;466(1):165-168.  (PubMed)

13.  Baumann L. Skin ageing and its treatment. J Pathol. 2007;211(2):241-251.  (PubMed)

14.  Bissett DL, Chatterjee R, Hannon DP. Photoprotective effect of superoxide-scavenging antioxidants against ultraviolet radiation-induced chronic skin damage in the hairless mouse. Photodermatol Photoimmunol Photomed. 1990;7(2):56-62.  (PubMed)

15.  Traber MG, Rallis M, Podda M, Weber C, Maibach HI, Packer L. Penetration and distribution of alpha-tocopherol, alpha- or gamma-tocotrienols applied individually onto murine skin. Lipids. 1998;33(1):87-91.  (PubMed)

16.  Thiele JJ, Ekanayake-Mudiyanselage S. Vitamin E in human skin: organ-specific physiology and considerations for its use in dermatology. Mol Aspects Med. 2007;28(5-6):646-667.  (PubMed)

17.  Nada A, Krishnaiah YS, Zaghloul AA, Khattab I. In vitro and in vivo Permeation of Vitamin E and Vitamin E Acetate from Cosmetic Formulations. Med Princ Pract. 2011;20(6):509-513.  (PubMed)

18.  Alberts DS, Goldman R, Xu MJ, et al. Disposition and metabolism of topically administered alpha-tocopherol acetate: a common ingredient of commercially available sunscreens and cosmetics. Nutr Cancer. 1996;26(2):193-201.  (PubMed)

19.  Mavon A, Raufast V, Redoules D. Skin absorption and metabolism of a new vitamin E prodrug, delta-tocopherol-glucoside: in vitro evaluation in human skin models. J Control Release. 2004;100(2):221-231.  (PubMed)

20.  Marra F, Ostacolo C, Laneri S, et al. Synthesis, hydrolysis, and skin retention of amino acid esters of alpha-tocopherol. J Pharm Sci. 2009;98(7):2364-2376.  (PubMed)

21.  Kosari P, Alikhan A, Sockolov M, Feldman SR. Vitamin E and allergic contact dermatitis. Dermatitis. 2010;21(3):148-153.  (PubMed)

22.  Machlin LJ, Filipski R, Nelson J, Horn LR, Brin M. Effects of a prolonged vitamin E deficiency in the rat. J Nutr. 1977;107(7):1200-1208.  (PubMed)

23.  Brown RG, Button GM, Smith JT. Effect of vitamin E deficiency on collagen metabolism in the rat's skin. J Nutr. 1967;91(1):99-106.  (PubMed)

24.  Igarashi A, Uzuka M, Nakajima K. The effects of vitamin E deficiency on rat skin. Br J Dermatol. 1989;121(1):43-49.  (PubMed)

25.  Kagan V, Witt E, Goldman R, Scita G, Packer L. Ultraviolet light-induced generation of vitamin E radicals and their recycling. A possible photosensitizing effect of vitamin E in skin. Free Radic Res Commun. 1992;16(1):51-64.  (PubMed)

26.  Kondo S, Mamada A, Yamaguchi J, Fukuro S. Protective effect of dl-alpha-tocopherol on the cytotoxicity of ultraviolet B against human skin fibroblasts in vitro. Photodermatol Photoimmunol Photomed. 1990;7(4):173-177.  (PubMed)

27.  Jin GH, Liu Y, Jin SZ, Liu XD, Liu SZ. UVB induced oxidative stress in human keratinocytes and protective effect of antioxidant agents. Radiat Environ Biophys. 2007;46(1):61-68.  (PubMed)

28.  Stewart MS, Cameron GS, Pence BC. Antioxidant nutrients protect against UVB-induced oxidative damage to DNA of mouse keratinocytes in culture. J Invest Dermatol. 1996;106(5):1086-1089.  (PubMed)

29.  Pauling L, Willoughby R, Reynolds R, Blaisdell BE, Lawson S. Incidence of squamous cell carcinoma in hairless mice irradiated with ultraviolet light in relation to intake of ascorbic acid (vitamin C) and of D, L-alpha-tocopheryl acetate (vitamin E). Int J Vitam Nutr Res Suppl. 1982;23:53-82.  (PubMed)

30.  Gerrish KE, Gensler HL. Prevention of photocarcinogenesis by dietary vitamin E. Nutr Cancer. 1993;19(2):125-133.  (PubMed)

31.  Burke KE, Clive J, Combs GF, Jr., Nakamura RM. Effects of topical L-selenomethionine with topical and oral vitamin E on pigmentation and skin cancer induced by ultraviolet irradiation in Skh:2 hairless mice. J Am Acad Dermatol. 2003;49(3):458-472.  (PubMed)

32.  Burke KE, Clive J, Combs GF, Jr., Commisso J, Keen CL, Nakamura RM. Effects of topical and oral vitamin E on pigmentation and skin cancer induced by ultraviolet irradiation in Skh:2 hairless mice. Nutr Cancer. 2000;38(1):87-97.  (PubMed)

33.  Record IR, Dreosti IE, Konstantinopoulos M, Buckley RA. The influence of topical and systemic vitamin E on ultraviolet light-induced skin damage in hairless mice. Nutr Cancer. 1991;16(3-4):219-225.  (PubMed)

34.  McArdle F, Rhodes LE, Parslew RA, et al. Effects of oral vitamin E and beta-carotene supplementation on ultraviolet radiation-induced oxidative stress in human skin. Am J Clin Nutr. 2004;80(5):1270-1275.  (PubMed)

35.  Werninghaus K, Meydani M, Bhawan J, Margolis R, Blumberg JB, Gilchrest BA. Evaluation of the photoprotective effect of oral vitamin E supplementation. Arch Dermatol. 1994;130(10):1257-1261.  (PubMed)

36.  van der Pols JC, Heinen MM, Hughes MC, Ibiebele TI, Marks GC, Green AC. Serum antioxidants and skin cancer risk: an 8-year community-based follow-up study. Cancer Epidemiol Biomarkers Prev. 2009;18(4):1167-1173.  (PubMed)

37.  McNaughton SA, Marks GC, Green AC. Role of dietary factors in the development of basal cell cancer and squamous cell cancer of the skin. Cancer Epidemiol Biomarkers Prev. 2005;14(7):1596-1607.  (PubMed)

38.  Eberlein-Konig B, Placzek M, Przybilla B. Protective effect against sunburn of combined systemic ascorbic acid (vitamin C) and d-alpha-tocopherol (vitamin E). J Am Acad Dermatol. 1998;38(1):45-48.  (PubMed)

39.  Fuchs J, Kern H. Modulation of UV-light-induced skin inflammation by D-alpha-tocopherol and L-ascorbic acid: a clinical study using solar simulated radiation. Free Radic Biol Med. 1998;25(9):1006-1012.  (PubMed)

40.  Placzek M, Gaube S, Kerkmann U, et al. Ultraviolet B-induced DNA damage in human epidermis is modified by the antioxidants ascorbic acid and D-alpha-tocopherol. J Invest Dermatol. 2005;124(2):304-307.  (PubMed)

41.  Yamada Y, Obayashi M, Ishikawa T, Kiso Y, Ono Y, Yamashita K. Dietary tocotrienol reduces UVB-induced skin damage and sesamin enhances tocotrienol effects in hairless mice. J Nutr Sci Vitaminol (Tokyo). 2008;54(2):117-123.  (PubMed)

42.  Lopez-Torres M, Thiele JJ, Shindo Y, Han D, Packer L. Topical application of alpha-tocopherol modulates the antioxidant network and diminishes ultraviolet-induced oxidative damage in murine skin. Br J Dermatol. 1998;138(2):207-215.  (PubMed)

43.  Saral Y, Uyar B, Ayar A, Naziroglu M. Protective effects of topical alpha-tocopherol acetate on UVB irradiation in guinea pigs: importance of free radicals. Physiol Res. 2002;51(3):285-290.  (PubMed)

44.  Yuen KS, Halliday GM. alpha-Tocopherol, an inhibitor of epidermal lipid peroxidation, prevents ultraviolet radiation from suppressing the skin immune system. Photochem Photobiol. 1997;65(3):587-592.  (PubMed)

45.  Chen W, Barthelman M, Martinez J, Alberts D, Gensler HL. Inhibition of cyclobutane pyrimidine dimer formation in epidermal p53 gene of UV-irradiated mice by alpha-tocopherol. Nutr Cancer. 1997;29(3):205-211.  (PubMed)

46.  McVean M, Liebler DC. Inhibition of UVB induced DNA photodamage in mouse epidermis by topically applied alpha-tocopherol. Carcinogenesis. 1997;18(8):1617-1622.  (PubMed)

47.  McVean M, Liebler DC. Prevention of DNA photodamage by vitamin E compounds and sunscreens: roles of ultraviolet absorbance and cellular uptake. Mol Carcinog. 1999;24(3):169-176.  (PubMed)

48.  Ritter EF, Axelrod M, Minn KW, et al. Modulation of ultraviolet light-induced epidermal damage: beneficial effects of tocopherol. Plast Reconstr Surg. 1997;100(4):973-980.  (PubMed)

49.  Trevithick JR, Shum DT, Redae S, et al. Reduction of sunburn damage to skin by topical application of vitamin E acetate following exposure to ultraviolet B radiation: effect of delaying application or of reducing concentration of vitamin E acetate applied. Scanning Microsc. 1993;7(4):1269-1281.  (PubMed)

50.  Trevithick JR, Xiong H, Lee S, et al. Topical tocopherol acetate reduces post-UVB, sunburn-associated erythema, edema, and skin sensitivity in hairless mice. Arch Biochem Biophys. 1992;296(2):575-582.  (PubMed)

51.  Gensler HL, Aickin M, Peng YM, Xu M. Importance of the form of topical vitamin E for prevention of photocarcinogenesis. Nutr Cancer. 1996;26(2):183-191.  (PubMed)

52.  Beijersbergen van Henegouwen GM, Junginger HE, de Vries H. Hydrolysis of RRR-alpha-tocopheryl acetate (vitamin E acetate) in the skin and its UV protecting activity (an in vivo study with the rat). J Photochem Photobiol B. 1995;29(1):45-51.  (PubMed)

53.  Schoonderwoerd SA, Beijersbergen van Henegouwen GM, Persons KC. Effect of alpha-tocopherol and di-butyl-hydroxytoluene (BHT) on UV-A-induced photobinding of 8-methoxypsoralen to Wistar rat epidermal biomacromolecules in vivo. Arch Toxicol. 1991;65(6):490-494.  (PubMed)

54.  Slaga TJ, Bracken WM. The effects of antioxidants on skin tumor initiation and aryl hydrocarbon hydroxylase. Cancer Res. 1977;37(6):1631-1635.  (PubMed)

55.  Potapenko A, Abijev GA, Pistsov M, et al. PUVA-induced erythema and changes in mechanoelectrical properties of skin. Inhibition by tocopherols. Arch Dermatol Res. 1984;276(1):12-16.  (PubMed)

56.  Roshchupkin DI, Pistsov MY, Potapenko AY. Inhibition of ultraviolet light-induced erythema by antioxidants. Arch Dermatol Res. 1979;266(1):91-94.  (PubMed)

57.  Thiele JJ, Hsieh SN, Ekanayake-Mudiyanselage S. Vitamin E: critical review of its current use in cosmetic and clinical dermatology. Dermatol Surg. 2005;31(7 Pt 2):805-813; discussion 813.  (PubMed)

58.  Zhai H, Behnam S, Villarama CD, Arens-Corell M, Choi MJ, Maibach HI. Evaluation of the antioxidant capacity and preventive effects of a topical emulsion and its vehicle control on the skin response to UV exposure. Skin Pharmacol Physiol. 2005;18(6):288-293.  (PubMed)

59.  Montenegro L, Bonina F, Rigano L, Giogilli S, Sirigu S. Protective effect evaluation of free radical scavengers on UVB induced human cutaneous erythema by skin reflectance spectrophotometry. Int J Cosmet Sci. 1995;17(3):91-103.  (PubMed)

60.  Chung JH, Seo JY, Lee MK, et al. Ultraviolet modulation of human macrophage metalloelastase in human skin in vivo. J Invest Dermatol. 2002;119(2):507-512.  (PubMed)

61.  Lin JY, Selim MA, Shea CR, et al. UV photoprotection by combination topical antioxidants vitamin C and vitamin E. J Am Acad Dermatol. 2003;48(6):866-874.  (PubMed)

62.  Darr D, Dunston S, Faust H, Pinnell S. Effectiveness of antioxidants (vitamin C and E) with and without sunscreens as topical photoprotectants. Acta Derm Venereol. 1996;76(4):264-268.  (PubMed)

63.  Lin FH, Lin JY, Gupta RD, et al. Ferulic acid stabilizes a solution of vitamins C and E and doubles its photoprotection of skin. J Invest Dermatol. 2005;125(4):826-832.  (PubMed)

64.  Quevedo WC, Jr., Holstein TJ, Dyckman J, McDonald CJ, Isaacson EL. Inhibition of UVR-induced tanning and immunosuppression by topical applications of vitamins C and E to the skin of hairless (hr/hr) mice. Pigment Cell Res. 2000;13(2):89-98.  (PubMed)

65.  Dreher F, Gabard B, Schwindt DA, Maibach HI. Topical melatonin in combination with vitamins E and C protects skin from ultraviolet-induced erythema: a human study in vivo. Br J Dermatol. 1998;139(2):332-339.  (PubMed)

66.  Quevedo WC, Jr., Holstein TJ, Dyckman J, McDonald CJ. The responses of the human epidermal melanocyte system to chronic erythemal doses of UVR in skin protected by topical applications of a combination of vitamins C and E. Pigment Cell Res. 2000;13(3):190-192.  (PubMed)

67.  Murray JC, Burch JA, Streilein RD, Iannacchione MA, Hall RP, Pinnell SR. A topical antioxidant solution containing vitamins C and E stabilized by ferulic acid provides protection for human skin against damage caused by ultraviolet irradiation. J Am Acad Dermatol. 2008;59(3):418-425.  (PubMed)

68.  Wu S, Gao J, Dinh QT, Chen C, Fimmel S. IL-8 production and AP-1 transactivation induced by UVA in human keratinocytes: roles of D-alpha-tocopherol. Mol Immunol. 2008;45(8):2288-2296.  (PubMed)

69.  Kato E, Sasaki Y, Takahashi N. Sodium dl-alpha-tocopheryl-6-O-phosphate inhibits PGE(2) production in keratinocytes induced by UVB, IL-1beta and peroxidants. Bioorg Med Chem. 2011;19(21):6348-6355.  (PubMed)

70.  Shibata A, Nakagawa K, Kawakami Y, Tsuzuki T, Miyazawa T. Suppression of gamma-tocotrienol on UVB induced inflammation in HaCaT keratinocytes and HR-1 hairless mice via inflammatory mediators multiple signaling. J Agric Food Chem. 2010;58(11):7013-7020.  (PubMed)

71.  Nakagawa K, Shibata A, Maruko T, et al. gamma-Tocotrienol reduces squalene hydroperoxide-induced inflammatory responses in HaCaT keratinocytes. Lipids. 2010;45(9):833-841.  (PubMed)

72.  Yoshida E, Watanabe T, Takata J, Yamazaki A, Karube Y, Kobayashi S. Topical application of a novel, hydrophilic gamma-tocopherol derivative reduces photo-inflammation in mice skin. J Invest Dermatol. 2006;126(7):1633-1640.  (PubMed)

73.  Meydani SN, Barklund MP, Liu S, et al. Vitamin E supplementation enhances cell-mediated immunity in healthy elderly subjects. Am J Clin Nutr. 1990;52(3):557-563.  (PubMed)

74.  Han SN, Meydani SN. Impact of vitamin E on immune function and its clinical implications. Expert Rev Clin Immunol. 2006;2(4):561-567.  (PubMed)

75.  Jiang Q, Ames BN. Gamma-tocopherol, but not alpha-tocopherol, decreases proinflammatory eicosanoids and inflammation damage in rats. FASEB J. 2003;17(8):816-822.  (PubMed)

76.  Tsoureli-Nikita E, Hercogova J, Lotti T, Menchini G. Evaluation of dietary intake of vitamin E in the treatment of atopic dermatitis: a study of the clinical course and evaluation of the immunoglobulin E serum levels. Int J Dermatol. 2002;41(3):146-150.  (PubMed)

77.  Keller KL, Fenske NA. Uses of vitamins A, C, and E and related compounds in dermatology: a review. J Am Acad Dermatol. 1998;39(4 Pt 1):611-625.  (PubMed)

78.  Hayakawa R, Ueda H, Nozaki T, et al. Effects of combination treatment with vitamins E and C on chloasma and pigmented contact dermatitis. A double blind controlled clinical trial. Acta Vitaminol Enzymol. 1981;3(1):31-38.  (PubMed)

79.  Javanbakht MH, Keshavarz SA, Djalali M, et al. Randomized controlled trial using vitamins E and D supplementation in atopic dermatitis. J Dermatolog Treat. 2011;22(3):144-150.  (PubMed)

80.  Shukla A, Rasik AM, Patnaik GK. Depletion of reduced glutathione, ascorbic acid, vitamin E and antioxidant defence enzymes in a healing cutaneous wound. Free Radic Res. 1997;26(2):93-101.  (PubMed)

81.  Musalmah M, Nizrana MY, Fairuz AH, et al. Comparative effects of palm vitamin E and alpha-tocopherol on healing and wound tissue antioxidant enzyme levels in diabetic rats. Lipids. 2005;40(6):575-580.  (PubMed)

82.  Musalmah M, Fairuz AH, Gapor MT, Ngah WZ. Effect of vitamin E on plasma malondialdehyde, antioxidant enzyme levels and the rates of wound closures during wound healing in normal and diabetic rats. Asia Pac J Clin Nutr. 2002;11 Suppl 7:S448-451.  (PubMed)

83.  Taren DL, Chvapil M, Weber CW. Increasing the breaking strength of wounds exposed to preoperative irradiation using vitamin E supplementation. Int J Vitam Nutr Res. 1987;57(2):133-137.  (PubMed)

84.  Ehrlich HP, Tarver H, Hunt TK. Inhibitory effects of vitamin E on collagen synthesis and wound repair. Ann Surg. 1972;175(2):235-240.  (PubMed)

85.  Baumann LS, Spencer J. The effects of topical vitamin E on the cosmetic appearance of scars. Dermatol Surg. 1999;25(4):311-315.  (PubMed)

86.  Jenkins M, Alexander JW, MacMillan BG, Waymack JP, Kopcha R. Failure of topical steroids and vitamin E to reduce postoperative scar formation following reconstructive surgery. J Burn Care Rehabil. 1986;7(4):309-312.  (PubMed)

87.  Ellinger S, Stehle P. Efficacy of vitamin supplementation in situations with wound healing disorders: results from clinical intervention studies. Curr Opin Clin Nutr Metab Care. 2009;12(6):588-595.  (PubMed)

88.  Barbosa E, Faintuch J, Machado Moreira EA, et al. Supplementation of vitamin E, vitamin C, and zinc attenuates oxidative stress in burned children: a randomized, double-blind, placebo-controlled pilot study. J Burn Care Res. 2009;30(5):859-866.  (PubMed)

89.  Passi S, De Pita O, Grandinetti M, Simotti C, Littarru GP. The combined use of oral and topical lipophilic antioxidants increases their levels both in sebum and stratum corneum. Biofactors. 2003;18(1-4):289-297.  (PubMed)

90.  Burke KE. Photodamage of the skin: protection and reversal with topical antioxidants. J Cosmet Dermatol. 2004;3(3):149-155.  (PubMed)

91.  Nagata C, Nakamura K, Wada K, et al. Association of dietary fat, vegetables and antioxidant micronutrients with skin ageing in Japanese women. Br J Nutr. 2010;103(10):1493-1498.  (PubMed)

92.  Boelsma E, van de Vijver LP, Goldbohm RA, Klopping-Ketelaars IA, Hendriks HF, Roza L. Human skin condition and its associations with nutrient concentrations in serum and diet. Am J Clin Nutr. 2003;77(2):348-355.  (PubMed)

93.  Gehring W, Fluhr J, Gloor M. Influence of vitamin E acetate on stratum corneum hydration. Arzneimittelforschung. 1998;48(7):772-775.  (PubMed)

94.  Gonullu U, Sensoy D, Uner M, Yener G, Altinkurt T. Comparing the moisturizing effects of ascorbic acid and calcium ascorbate against that of tocopherol in emulsions. J Cosmet Sci. 2006;57(6):465-473.  (PubMed)