Natural Foods Merchandiser

Block the sun with antioxidants

An application of sunscreen in the morning is becoming about as routine as wearing deodorant these days. And it?s not surprising. Skin cancer is the most rapidly increasing form of cancer in the United States, with 600,000 new cases reported each year.1 In 2003, it was estimated that skin cancer would claim the lives of approximately 9,800 Americans.2

As the largest organ of the human body, the skin is the first line of defense against myriad external forces, toxins and irritants. Today?s active lifestyles, which often include significant sun exposure, can stress the skin?s resources, leading to skin damage and premature aging.3,4 Additional protection is therefore needed against daily environmental assaults.

Sunlight, especially ultraviolet wavelengths, can induce the formation of reactive oxygen species, the most potent of which are free radicals (molecules with an unpaired electron, making them extremely reactive). Although the most damage occurs from free radicals, the other ROS—such as molecular oxygen, singlet oxygen and hydrogen peroxide, which are not free radicals per se—also create damage by initiating oxidative reactions. In addition, they also generate free-radical species.5 Together, all the ROS can damage constituent components of skin cells such as cellular organelles and important cellular molecules including deoxyribonucleic acid, ribonucleic acid, proteins, enzymes and lipids.6,7,8

The good news is that preliminary and ongoing research indicates antioxidants found in vitamins and botanicals can be added to sunscreens or be taken orally, creating a combination that can significantly boost the skin?s natural UV-filtering properties and enhance its ROS defenses.

Vitamin and mineral antioxidants
Vitamins C and E: Among the group of AOs, vitamins C (L-ascorbic acid) and E (composed of tocopherols and tocotrienols) are powerful skin protectors. Although each functions well separately, they strongly complement each other when used in combination. Taking these vitamins in an oral form, however, does not appear to consistently protect the skin—whereas when applied topically, they do. The reason may be that when taken orally, the physiologic processes necessary for absorption, solubility and transport limit the amount that can be delivered to the skin. Furthermore, topical application has the added advantage of directly targeting the AOs to the area of skin needing protection.

Virtually all plants and animals synthesize vitamin C. Humans, however, lack this ability. Thus, as with most vitamins, we have to get our vitamin C through diet.9 What?s more, UV exposure significantly depletes the skin?s vitamin C reserves. So if a person has low stores of vitamin C to begin with, UV makes them lower yet. In one study, pigs? skins suffered a 64 percent loss of vitamin C when irradiated for five days. In terms of protection, regular topical application of a 10 percent solution of vitamin C just 30 minutes before exposure reduced incidence of sunburn by one third.10 Such research has led to the widespread hypothesis that UV damage may be due in part to a depletion of the skin?s defenses by radiation.

Another study, this time on humans, found skin levels of vitamin C were maximized after applying a 15 percent solution for three days.11

And vitamin C also may even help with allergies. Topical vitamin C protected against UV-induced immunosuppression and maintained systemic tolerance to contact allergens in hairless mice.12

Unfortunately, vitamin C?s inherent instability makes it difficult to formulate into an acceptable composition for cosmetic use.13 More research is being conducted in this area.

For its part, vitamin E is the body?s major lipid-phase AO, preventing lipid peroxidation.14 The fat solubility of vitamin E makes it attractive for application to and absorption into skin. Several studies have documented photoprotective effects when vitamin E was topically applied to animal skin. In addition to protecting against UV-induced immunosuppression in mice,15 it further protected their skins against UV-induced lipid peroxidation by 50 percent.16 And the application of vitamin E to the backs of hairless mice immediately after UV irradiation reduced sunburn by 40 percent to 55 percent.17

Substantial experimental evidence reveals vitamins C and E act synergistically in suppressing sunburn reaction. Specifically, vitamin C protects vitamin E from the oxidation it undergoes during the process of ending ROS chain reactions. Thus, vitamin C actually regenerates vitamin E activity without the need for new supplies in the cell membrane.18 Furthermore, one study found that an oral combination of vitamins C and E in high doses—2 g of E and 3 g of C per day for 50 or more days—provided significant protection against sunburn in humans, whereas either vitamin alone was ineffective.19

Selenium: This trace mineral is required for at least two types of enzymes (glutathione peroxidase and thioredoxin reductase). It represents a significant portion of cellular defense against oxidative stress in mammals because these enzymes are vital to maintaining a stable reduction and oxidation balance in cells. Several cellular studies have demonstrated the protective effects of selenium for UV-induced damage, including DNA damage20 and lipid peroxidation.21 Oral sodium selenite protected hairless mice against sunburn and tanning. Topical application protected mice against UV-induced sunburn and skin cancer.22 There have been no relevant human studies to date.

Zinc: The skin is rich in zinc. The mineral binds to several molecules, affecting their conformation, stability and activity. Specifically, zinc serves as a catalyst for enzymes responsible for DNA replication, gene transcription and RNA and protein synthesis.23 Topical application of zinc salts to mouse skin reduced UV-induced sunburn. In addition, several studies on transgenic mice indicate that zinc induction in skin also protects against UV-induced immunosuppression.24

Plant antioxidants
Carotenoids: The carotenoids beta-carotene, lutein, lycopene and zeaxanthin are potent AOs found naturally in green leafy vegetables, carrots, corn and eggs. (See the article on lycopene, ?A Tomato a Day,? in The Natural Foods Merchandiser, March 2005, page 110.) Preliminary research indicates they can absorb, and thus filter out, UV radiation. In one recent human study, topically applied lycopene provided much greater protection against free radical-induced cutaneous cellular damage than vitamins C and E.25 These results indicate that more research is needed on topical carotenoid skin protection, as most studies have been confined to oral consumption.

Oral carotenoid intake from natural sources or supplements has been shown to significantly reduce susceptibility to sunburn.6 One 12-week study divided 36 adults into three groups of 12 that took daily doses of 24 mg beta-carotene from a natural source of Dunaliella salina algae; or a mixed-carotenoid supplement of 8 mg each of natural beta-carotene, lutein and lycopene; or a placebo. The results showed that after three months, the degree of sunburn was significantly less in the groups that took either form of supplementation.26

Silymarin: This is an extract of the milk thistle plant, Silybum marianum. Milk thistle belongs to the aster family (Asteraceae or Compositae) that includes daisies, thistles and artichokes. It contains three flavonoids found in the fruit, seeds and leaves of the plant—silybin (silibinin), silydianin and silychristine. Silybin is the main component (comprising 70 percent to 80 percent) and is thought to have the most biologic activity.5

Silymarin has strong AO effects. Topically, it has been shown to provide substantial protection against different stages of UV-induced carcinogenesis. The number and size of tumors induced by UV irradiation in the skin of hairless mice was reduced by 92 percent to 97 percent when a 9 mg extract solution of silymarin was applied before exposure. In this same trial, silymarin also inhibited UV-induced sunburn in short-term experiments, presumably as a result of its AO properties rather than sunblocking effects.27 (The silymarin appeared to strengthen skin tolerance, but didn?t shield the skin or block UV radiation per se.)

Soy is a rich source of flavonoids called isoflavones. One of the most plentiful isoflavones in soy is genistein, a powerful AO. Genistein is also in red clover. It has been found to provide protection from oxidative damage induced by UV radiation both in vitro and in vivo. Lotions made of 20 mmg genistein and the metabolites equol, isoquol and the related derivative dehydroequol (added to facilitate metabolic activity) applied to hairless mice had a potent ability to reduce inflammatory swelling reactions and the suppression of contact hypersensitivity induced by moderate doses of UV radiation. Specifically, these lotions reduced photosuppression of the immune system more than inflammation from sunburn, even when applied after exposure. Such AO compounds may thus have a future role as sun-protective cosmetic ingredients.27

Soy isoflavones also have potent anti-carcinogenic effects. In animal studies, oral soy or genistein protected against several cancers including bladder, breast, colon, liver, lung, prostate and skin.28,29 When administered topically, it inhibited skin tumor development by 60 percent to 75 percent in hairless mice.30

Tea polyphenols: Tea (Camellia sinensis) is a significant source of ROS-scavenging polyphenols, which comprise 30 percent to 35 percent of the leaf?s dry weight. During processing, tea leaves are progressively oxidized to produce green (unoxidized), oolong or black tea.5 Tea polyphenols have been widely studied for their anti-carcinogenic potential in animals. However, initial trials studying oral consumption of black tea have supported only minimal but statistically significant anti-carcinogenic skin protection in humans.31,32

Topical green tea, however, has shown strong anti-inflammatory effects in human skin, reducing sunburn reaction. A 3 mg application per 2.5 cm2 of skin surface before UV exposure significantly reduced inflammation, blocking the infiltration of leukocytes—infection-fighting white blood cells, the major source of ROS activity.33 Green tea polyphenols also protected human skin from UV-induced cell depletion,34 as well as, in mice, against immunosuppression.35

Preliminary research shows that AO oral supplementation and/or topical application are effective in enhancing the skin?s resistance against UV-induced sunburn and skin cancer. Due to the well-documented research relating skin damage to premature aging, AO?s are likely to help there as well. (Premature aging, commonly known as photoaging, is a process whereby collagen and elastin in the skin are reduced. If imperfectly repaired, this creates solar scars, constituting premature aging when accumulated over a lifetime.)

Together, all these positive initial results warrant further study, particularly with respect to the benefits of topical additives to cosmetics, lotions and sunscreens. Applying AOs directly to the skin provides the dual advantage of immediate protection and direct targeting of the affected areas.

Oral supplementation, while clearly advantageous, takes several weeks to build up in the skin, and the physiologic processes necessary for absorption, solubility and transport markedly limit the amount that can be delivered into skin, thereby providing only limited protection from high UV exposure.

While early results are very encouraging, they do not indicate that the use of oral and/or topical AOs is sufficient to replace the use of sunscreen and the avoidance of UV overexposure. Rather, they should be considered highly effective enhancers to sun protection.

Anna Soref is a freelance writer in Lafayette, Colo.

Natural Foods Merchandiser volume XXVI/number 4/p. 46, 48

1. University Extension, University of Missouri-Columbia, Agricultural Engineering Department. Don?t let the sun spot you. August 4, 2004. [Available at]
2. Centers for Disease Control. Skin cancer: preventing America?s most common cancer. 2003 Fact sheet. [Available at:]
3. Fuchs J, et al. Acute effects of near ultraviolet and visible light on cutaneous antioxidant system. Photochem Photobiol 1989;50:739-44.
4. Shindo Y, et al. Dose-response effects of acute ultraviolet irradiation on antioxidants and molecular markers of oxidation in murine epidermis and dermis. J Invest Dermatol 1994;102:470-5.
5. Pinnell, SR. Cutaneous photodamage, oxidative stress, and topical antioxidant protection. J Amer Acad Dermatology 2003;48:1-19.
6. Roberts R, Barnes H. Lutein. Part 1-natural support for healthy skin. Agrofood Industry Hi-Tech 2004;Sept/Oct:49-52.
7. Kochevar IE, et al. Photophysics, photochemistry, and photobiology. In: Freedberg IM, et al., editors Dermatology in general medicine, 5th ed.. New York: McGraw-Hill; 1999. 220-9.
8. Pathak MA, et al. Acute and chronic effects of the sun. In: Freedberg IM, et al., editors. Dermatology in general medicine, 5th ed. New York: McGraw-Hill 1999. 598-1607.
9. Nishikimi M, et al. Cloning and chromosomal mapping of the human nonfunctional gene for L-gulono-gamma-lactone oxidase, the enzyme for L-ascorbic acid biosynthesis missing in man. J Biol Chem 1994;269:13685-8.
10. Darr D, et al. Topical vitamin C protects porcine skin from ultraviolet radiation-induced damage. Br J Dermatol 1992;127:247-53.
11. Pinnell SR, et al. Topical L-ascorbic acid: percutaneous absorption studies. Dermatol Surg 2001;27:137-42.
12. Nakamura T, et al. Vitamin C abrogates the deleterious effects of UVB radiation on cutaneous immunity by a mechanism that does not depend on TNF-alpha. J Invest Dermatol 1997;109:20-4.
13. Levine M, et al. A new recommended dietary allowance of vitamin C for healthy young women. Proc Natl Acad Sci USA 2001;98:9842-6.
14. Packer L, et al. Molecular aspects of alphatocotrienol antioxidant action and cell signaling. J Nutr 2001;31(Suppl):369-73.
15. Steenvoorden DP, Beijersbergen VH. Protection against UV-induced systemic immunosuppression in mice by a single topical application of the antioxidant vitamins C and E. Int?l J Radiat Biol 1999;75:747-55.
16. Savini I, et al. Topical application of alpha-tocopherol modulates the antioxidant network and diminishes ultraviolet-induced oxidative damage in murine skin. Br J Dermatol 1998;138:207-15.
17. Trevithick J, et al. Topical tocopherol acetate reduces post-UVB, sunburn-associated erythema, edema and skin sensitivity in hairless mice. Arch Biochem Biophys 1992;296:575-82.
18. Chan AC. Partners in defense, vitamin E and vitamin C. Can J Physiol Pharmacol 1993;71:725-31.
19. 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;25:1006-12.
20. Emonet-Piccardi N, et al. Protective effects of antioxidants against UV-induced DNA damage in human skin fibroblasts in culture. Free Radic Res 1998;29:307-13.
21. Moysan A, et al. Effects of selenium on UVA-induced lipid peroxidation in cultured human skin fibroblasts. Skin Pharmacol Appl Skin Physiol 1995;8:139-48.
22. Emonet-Piccardi N, et al. The effects of topical and oral L-selenomethionine on pigmentation and skin cancer induced by ultraviolet irradiation. Nutr Cancer 1992;17:123-37.
23.Coleman JE. Zinc proteins: enzymes, storage proteins, transcription factors, and replication proteins. Ann Rev Biochem 1992;61:897-946.
24. Reeve VE, et al. Dietary zinc, photoimmunosuppression and metallothionein (MT). In: Klaassen C, editor. Metallothionein IV. Basel, Switzerland: Birkhauser Verlag 1999:445-9.
25. Andreassi M, et al. Antioxidant activity of topically applied lycopene. J Eur Acad Dermatol Venereol 2004;18(1):52-5.
26. Heinrich U, et al. Supplementation with beta-carotene or a similar amount of mixed carotenoids protects humans from UV-induced erythema, J Nutr 2003;133(1):98-101.
27. Widyarini S, et al. Isoflavonoid compounds from red clover (Trifolium pratense) protect from inflammation and immune suppression induced by UV radiation. Photochem Photobiol 2001;74:465-70.
28. Barnes S. Effect of genistein on in vitro and in vivo models of cancer. J Nutr 1995;125(Suppl):S777-83.
29. Pinnell SR. Cutaneous photodamage, oxidative stress, and topical antioxidant protection. J Amer Acad Dermatol 2003;48:1-19.
30. Wei H, et al. Isoflavone genistein inhibits the initiation and promotion of two-stage skin carcinogenesis in mice. Carcinogenesis 1998;19:1509-14.
31. Katiyar SK, Mukhtar H. Tea consumption and cancer. World Rev Nutr Diet 1996;79:154-84.
32. Hakim IA, et al. Tea intake and squamous cell carcinoma of the skin: influence of type of tea beverages. Cancer Epidemiol Biomarkers Prev 2000;9:727-31.
33. Katiyar SK, et al. Polyphenolic antioxidant epigallocatechin-3-gallate from green tea reduces UVB-induced inflammatory responses and infiltration of leukocytes in human skin. Photochem Photobiol 1999;69:14853.
34. Elmets CA, et al. Cutaneous photoprotection from ultraviolet injury by green tea polyphenols. J Am Acad Dermatol 2001;44:425-32.
35. Castronovo V, et al. Prevention of UV-induced immunosuppression in mice by the green tea polyphenol epigallocatechin-3-gallate may be associated with alterations in IL-10 and IL-12 production. Carcinogenesis 1999;20:2117-24.

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