Burke KE, et al. 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.

ABSTRACT

This study investigates whether supplementation with topical RRR-alpha-tocopherol (Eol), topical RRR-alpha-tocopheryl succinate, and oral RRR-alpha-tocopheryl acetate can reduce the incidence of acute and chronic damage to the skin (i.e., sunburn and pigmentation and skin cancer, respectively) induced by ultraviolet (UV) irradiation to mice. Groups of twenty Skh:2 female hairless pigmented mice were treated with 1) lotion vehicle, 2) 5% Eol lotion, 3) 5% topical RRR-alpha-tocopheryl succinate lotion, or 4) lotion vehicle and oral RRR-alpha-tocopheryl acetate. Within each group, 15 mice were exposed to 0.24 J/cm2 of UV-B radiation three times per week. The animals’ weights and food intakes were monitored, and the vitamin E concentrations of skin, liver, and adipose tissue were measured to determine whether the topical Eol resulted in significant tissue levels. Skin pigmentation was scored, and the total number of clinically detectable skin tumors per animal was counted weekly. Results showed that the skin concentrations of Eol, as well as levels in the adipose tissue, were increased after topical application. Mice treated with each form of vitamin E showed no signs of toxicity and had significantly less acute and chronic skin damage induced by UV irradiation, as indicated by reduced inflammation and pigmentation and by later onset and lesser incidence of skin cancer. https://www.ncbi.nlm.nih.gov/pubmed/11341050

Lambert EM, et al. Yellow nail syndrome in three siblings: A randomized double-blind trial of topical Vitamin E. Pediatric Dermatology. 2006;23(4):390-395.

ABSTRACT

Abstract: Yellow nail syndrome is an uncommon disorder characterized by dystrophic nails, lymphedema, and respiratory disease. It has rarely been reported in children and this is the first report of congenital yellow nails in siblings. The purpose of this study was to determine whether topical vitamin E applied to the nail plates and periungual skin would affect the growth rate or appearance of the fingernails in patients with congenital yellow nail syndrome. This study was the first trial of a treatment for this entity in children and the largest randomized double blind trial to date. We found that vitamin E solution had no significant effect (p = 0.84) on fingernail growth or the global appearance score (p = 1.0) when compared with placebo. The average growth rates and global assessment scores improved and onycholysis and onychomadesis decreased from baseline with both vitamin E and placebo treatment, although these were not primary end points of the study. Topical vitamin E did not result in a statistically significant improvement when compared with oil alone for the treatment of the nails in our three patients with yellow nail syndrome. However, it is interesting and perhaps clinically useful that both vitamin E and placebo oil improved the condition of the nails. http://onlinelibrary.wiley.com/doi/10.1111/j.1525-1470.2006.00251.x/full

Placzek M, 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):304-7.

ABSTRACT

DNA damage caused by ultraviolet (UV) irradiation is considered the main etiologic factor contributing to the development of skin cancer. Systemic or topical application of antioxidants has been suggested as a protective measure against UV-induced skin damage. We investigated the effect of long-term oral administration of a combination of the antioxidants ascorbic acid (vitamin C) and D-alpha-tocopherol (vitamin E) in human volunteers on UVB-induced epidermal damage. The intake of vitamins C and E for a period of 3 mo significantly reduced the sunburn reaction to UVB irradiation. Detection of thymine dimers in the skin using a specific antibody revealed a significant increase of this type of DNA damage following UVB exposure. After 3 mo of antioxidant administration, significantly less thymine dimers were induced by the UVB challenge, suggesting that antioxidant treatment protected against DNA damage. https://www.ncbi.nlm.nih.gov/pubmed/15675947

Eberlein-Konig B, et al. Protective effect against sunburn of combined systemic ascorbic acid and d-alpha-tocopherol (Vitamin E). J Am Acad Dermatol. 1998;38(1):45-8.

ABSTRACT

BACKGROUND: UV radiation causes acute adverse effects like sunburn, photosensitivity reactions, or immunologic suppression, as well as long-term sequelae like photoaging or malignant skin tumors. UV radiation induces tissues to produce reactive oxygen species, eicosanoids and cytokines. Inhibition of these mediators might reduce skin damage. Antioxidants such as ascorbic acid and d-alpha-tocopherol have been found to be photoprotective in some in vitro studies and animal experiments.

OBJECTIVE: Our purpose was to assess the protective effect of systemic vitamins C and E against sunburn in human beings.

METHODS: In a double-blind placebo-controlled study, each of 10 subjects took daily either 2 gm of ascorbic acid (vitamin C) combined with 1000 IU of d-alpha-tocopherol (vitamin E) or placebo. The sunburn reaction before and after 8 days of treatment was assessed by determination of the threshold UV dose for eliciting sunburn (minimal erythema dose [MED]) and by measuring the cutaneous blood flow of skin irradiated with incremental UV doses against that of non irradiated skin.

RESULTS: The median MED of those taking vitamins increased from 80 to 96.5 mJ/cm2 (p < 0.01), whereas it declined from 80 to 68.5 mJ/cm2 in the placebo group. Cutaneous blood flow changed significantly (p < 0.05) for most irradiation doses with decreases in those given vitamins and increases in the placebo group.

CONCLUSION: Combined vitamins C and E reduce the sunburn reaction, which might indicate a consequent reduced risk for later sequelae of UV-induced skin damage. The increase of sunburn reactivity in the placebo group could be related to “priming” by the previous UV exposure. https://www.ncbi.nlm.nih.gov/pubmed/9448204