I. Bogdan Allemann, MD; L. Baumann, MD

Cosmetic Medicine and Research Institute, Miller School of Medicine, University of Miami, Miami Beach, FL, USA


The formation of free radicals is a widely accepted pivotal mechanism leading to skin aging. Free radicals are highly reactive molecules with unpaired electrons that can directly damage various cellular structural membranes, lipids, proteins, and DNA. The damaging effects of these reactive oxygen species are induced internally during normal metabolism and externally through various oxidative stresses. The production of free radicals increases with age, while the endogenous defense mechanisms that counter them decrease. This imbalance leads to the progressive damage of cellular structures, and thus, results in accelerated aging. Antioxidants are substances that can provide protection from endogenous and exogenous oxidative stresses by scavenging free radicals. Topical antioxidants are available in multivariate combinations through over-the-counter skin care products that are aimed at preventing the clinical signs of photoaging.

Key Words:
antioxidants, photoaging, topical treatments, skin aging

Skin aging is a complex process involving various genetic, environmental, and hormonal mechanisms. One can differentiate between intrinsic, chronologic aging and extrinsic, “environmental” aging; both processes occur in conjunction with the other and are superimposed on each other. Free radicals play a central role in the course of both intrinsic and extrinsic aging. During the chronologic aging process, free radicals are formed naturally through normal human metabolism, whereas, in the extrinsic aging process, they are produced by exogenous factors, such as UV exposure, cigarette smoking, and alcohol consumption. At least 50% of UV-induced damage to the skin is estimated to be attributable to the UV-induced formation of free radicals.1 Harman, et al. first proposed this “free radical theory of aging” in 1956, and today it is one of the most widely accepted theories used to explain the cause of aging.2

Free radicals are highly reactive molecules with an odd number of electrons that are generated from oxygen;3 they can damage various cellular structures, such as DNA, proteins, and cellular membranes. In addition, free radicals may lead to inflammation, which seems to play an additional role in skin aging.4

The body possesses endogenous defense mechanisms, such as antioxidative enzymes (superoxide dismutase, catalase, glutathione peroxidase) and nonenzymatic antioxidative molecules (vitamin E, vitamin C, glutathione, ubiquinone), protecting it from free radicals by reducing and neutralizing them.5 Some of these antioxidant defense mechanisms can be inhibited by ultraviolet (UV) light.6 Moreover, as part of the natural aging process endogenous defense mechanisms decrease, while the production of reactive oxygen species increases, resulting in accelerated skin aging.

It is intuitive to hypothesize that the topical application of antioxidants may neutralize some of the resulting free radicals, and consequently lessen or prevent the signs of aging skin. At present, topical antioxidants are marketed to prevent aging and UV-induced skin damage, as well as to treat wrinkles and erythema due to inflammation (e.g., post laser resurfacing). However, currently, only vitamin C can actually treat wrinkles by influencing collagen formation through a mechanism other than antioxidation. For other products, their ability to improve wrinkles is either due to swelling or hydrating effects, or to other formulary constituents, such as retinol and vitamin C. Hence, antioxidants can prevent wrinkles, but not treat them.

For topically administered antioxidants to be effective in preventing skin aging, a couple of considerations should be made when formulating them:

  • Product stabilization is crucial. Because antioxidants are very unstable, they may become oxidized and inactive before reaching the target.
  • They must be properly absorbed into the skin, reach their target tissue in the active form, and remain there long enough to exert the desired effects.

Many antioxidants have been used for centuries in ancient and modern cultures around the world for various diseases.7 In addition to their antioxidant activity, most of them possess numerous other biologic properties, e.g., they can be anticarcinogenic and anti-inflammatory. This article will discuss antioxidants that are currently marketed in cosmetic formulations and will focus on their antioxidant activities.

Vitamin E

Vitamin E (tocopherol) is a lipid-soluble antioxidant that is present in the skin and found in various foods, such as vegetables, seeds, and meat.8 There are 8 active isoforms that are grouped into tocopherols and tocotrienols. Of the 4 tocopherols (á-, â-, ã- and ä-), á-tocopherol (AT) has the highest activity. In animals, a topical application of á-tocopherol has been shown to exert photoprotective effects by reducing the number of sunburn cells,9 reducing ultraviolet B (UVB)-induced damage,10 and inhibiting photocarcinogenesis.11 In humans, tocopherol 5%-8% cream that was applied to the face improved signs of photoaging when compared with placebo.12 Furthermore, application of vitamin E (5%) to human skin under light-tight occlusion 24 hours before UV treatment was shown to inhibit human macrophage metalloelastase, a member of the matrix metalloproteinase family involved in the degradation of elastin.13

Newer studies suggest that the combined application of various antioxidants can increase their potency when compared with 1 antioxidant alone, and consequently can provide superior photoprotection, as has been shown for the combination of vitamins E and C.14 Topical application of vitamin E has been linked with various cutaneous side-effects, including contact dermatitis.15-17

Coenzyme Q10

Coenzyme Q10 (CoQ10), or ubiquinone, is a fat-soluble antioxidant that is found in all human cells as a component of the respiratory chain, as well as in food, e.g., fish and shellfish. Up to 95% of the body’s energy requirements seem to be provided by CoQ10.18 In vitro studies showed that CoQ10 suppressed the expression of collagenase following ultraviolet A (UVA) irradiation.19 In human skin, few studies exist on the topical effect of CoQ10. Nevertheless, CoQ10 is a popular topical antioxidant included in several over-the-counter (OTC) cosmetic products. No side-effects with topical application of CoQ10 have been reported to date.


The synthetic analog of coenzyme Q10 is called idebenone, which has been demonstrated to be stronger than CoQ10 and other well known antioxidants.20 In humans, a study with a topical skin care formulation containing idebenone showed positive effects on photodamaged skin (i.e., reduction in skin roughness/dryness, reduction in fine lines/wrinkles).21 However, the effects on wrinkles were most likely due to hydration or skin irritation. There is 1 report of contact dermatitis attributed to idebenone 0.5% in a cream.22

However, the authors have seen many patients who developed contact dermatitis from skin care products containing idebenone.


Lycopene, a powerful antioxidant, is a carotenoid found in red fruits and vegetables. It is, in fact, responsible for their red color.23 Its chemopreventive effects against photo-induced tumors have been proven in mouse models.24 Despite very little clinical data, lycopene is included in various skin care products.

Vitamin C

In humans vitamin C (ascorbic acid) can be obtained solely from food, such as citrus fruits. Sunlight and environmental pollution can deplete vitamin C present in the epidermis25 and because vitamin C is a potent antioxidant, enhancing its levels in the skin seems reasonable. Vitamin C predominantly exists in its reduced form, ascorbic acid. Its oxidized form, dehydro-L-ascorbic acid can be found in trace quantities and can revert back to ascorbic acid. However, if the lactone ring irreversibly opens, diketogulonic acid is formed, which is no longer active. This happens when vitamin C preparations are oxidized, rendering them ineffective and useless.26 Thus, vitamin C preparations should be kept in airtight, light-resistant containers to avoid exposure to UV rays or the air.

Topical vitamin C as a photoprotectant has been studied in vitro and in vivo, demonstrating its effects in preventing sun damage by reducing sunburn cells and decreasing erythema when exposed to both UVA and UVB irradiation.27 The addition of topical vitamin C to either a UVA or UVB sunscreen was shown to improve sun protection when compared with sunscreen alone.28 Furthermore, adding topical vitamin C to “after–sun” products has been shown to scavenge UV-induced reactive oxygen species.29

Ascorbate is required for collagen synthesis30 and the addition of ascorbic acid increases collagen production in human skin fibroblasts.31 At the same time it may reduce production of elastin by an unknown mechanism.32 Two studies in humans have shown an improvement in the appearance of wrinkles upon topical application of vitamin C.33,34 However, more clinical trials are necessary to unravel all the effects of vitamin C on skin and aging. Thus, vitamin C preparations are useful in preventing or lessening the detrimental effects of UV radiation. Some patients experience minimal discomfort (stinging and mild irritation) from topical application.

Green Tea

Green tea is a very popular beverage as well as an antioxidant, that is extracted from the plant Camellia sinensis. There are 4 major polyphenolic catechins, of which Epigallocatechin 3-gallate (EGCG) is the most abundant and biologically active. The green tea polyphenols (GTP) possess not only antioxidant activity, but they also act as anti-inflammatory and anticarcinogenic agents. GTP can be administered either orally or topically.35 With various in vitro and in vivo studies, green tea is probably the most studied antioxidant. In vivo topical application of GTPs has been shown to suppress chemo- and photocarcinogenesis in mice,36 and prevent UV-induced oxidative damage and induction of matrix metalloproteinases.37 In human skin, GTPs reduced UV-induced erythema, the number of sunburn cells, immunosuppression, and DNA-damage.38 In spite of the limited data in humans, there are numerous OTC products containing green tea, and using them every morning for photoprotection in combination with a sunscreen makes sense. As with most of the antioxidants, no controlled clinical trials exist and the concentration of phenols in the various products is not standardized.


Silymarin, derived from the milk thistle plant, Silybum marianum, is a natural polyphenolic flavonoid. Its main component silybin (silibinin), is considered to be the most biologically active with strong antioxidant properties.39 In vivo studies have shown photoprotective effects with topically applied silybin prior to, or immediately after, UV irradiation.40 Thus, there is reasonable evidence to include the compound into sunscreens.


CoffeeBerry® (VDF FutureCeuticals) is the proprietary name for an antioxidant extracted from the fruit of the coffee plant Coffea arabica. It has been shown to be a stronger antioxidant than green tea, pomegranate extract, vitamins C and E.41 It contains polyphenols, which are well known for their antioxidant properties.42 In 2007, a product containing CoffeeBerry® polyphenols 1% (Revaléskin™, Stiefel Laboratories) was launched. The company claims that its use over a 6-week period can result in significant improvement of hyperpigmentation, fine lines, wrinkles, and overall appearance. Furthermore, there have been no reports of irritation by patients with sensitive skin. However, further prospective, randomized and controlled human studies assessing the antioxidant effects of topical preparations containing CoffeeBerry® extract are needed.


The antioxidant resveratrol is a polyphenolic phytoalexin compound that is found in grapes, nuts, fruits, and red wine, among others.43 In vitro and in vivo studies have shown that, when topically applied, resveratrol protects against UVB-mediated cutaneous damage and inhibits UVB-mediated oxidative stress.44-46 The effect of resveratrol on human skin and photoaging remains to be examined. It is included in a few products that claim to have antiaging benefits.

Grape Seed

Grape seed is extracted from Vitis vinifera and is rich in proanthocyanidins, which belong to the flavonoid family. Proanthocyanidins are potent antioxidants with strong free radical scavenging activities.47 Grape seed extract has been shown to be an even stronger scavenger of free radicals than vitamins C and E.48 A possible antioxidant mechanism of photoprotection by grape seed proanthocyanidins (GSP) was suggested by Mittal, et al.49 GSP was shown to inhibit the depletion of antioxidant defense components induced by UVB,50 and topical application of grape seed extract seems to enhance the sun protection factor in humans.43 It is included in topical cosmetic formulations for antiaging purposes.


Pomegranate extracts can be obtained from various parts of the fruit Punica granatum, such as the juice, seed, and peel. In particular, the phenolic components have potent antioxidant activity.51 Topical application of the peel extract was shown to restore catalase, peroxidase, and superoxide dismutase enzyme activities in vivo.52 The fruit extract has been shown to ameliorate UVA-mediated damages,53 and protect against the adverse effects of UVB radiation in vitro.54 Pomegranate extract is available in various skin care products.


Genistein is an isoflavone derived from soybeans with the capacity to inhibit UV-induced oxidative DNA damage.55 Genistein, either topically applied or orally supplemented, was shown to effectively protect human skin against UVB-induced skin photodamage.56,57 It is included in various products such as facial moisturizers, sunscreens, and other skin care formulations that claim to provide anti-aging effects.


Pycnogenol can be extracted from the French maritime pine (Pinus pinaster). It contains flavonoids and phenolic compounds, which act as potent free-radical scavengers. Immunosuppression and a reduction of the inflammatory sunburn reaction were observed in mice after topical application of pycnogenol 0.05%–0.2%.58 The potential of pycnogenol to provide photoprotection for humans has been investigated for oral supplementation, showing that a significantly elevated UV radiation level was necessary in order to reach 1 minimal erythema dose.59


Niacinamide, or nicotinamide, is the biologically active amide of vitamin B3. Besides its antioxidant activity, it has also been shown to exhibit anti-inflammatory, depigmenting, and immunomodulant properties. The use of niacinamide has been shown to improve the texture and tone of the skin, and reduce fine lines, wrinkles, and hyperpigmentation.60 Topical niacinamide is well tolerated and can be found in various skin care products.


The use of topically applied antioxidants seems promising; however, there is a paucity of controlled clinical trials in humans examining the role of antioxidants in preventing or decelerating skin aging. Thus, further experimental data needs to be generated. Current research suggests that combinations of different antioxidants seem to have synergistic effects and, thus, better efficacy, when compared with 1 antioxidant used alone.61,62 Also, some data suggest that a cumulative or additive benefit can be derived from using oral and topical antioxidant products in combination.63,64 In spite of the lack of data, millions of dollars are spent annually on these products worldwide. At this point, it is important to understand that these agents are harmless when applied topically, but the exact efficacy of these products is currently unknown.


  1. Black HS. Potential involvement of free radical reactions in ultraviolet light-mediated cutaneous damage. Photochem Photobiol 46(2):213-21 (1987 Aug).
  2. Harman D. Aging: a theory based on free radical and radiation chemistry. J Gerontol 11(3):298-300 (1956 Jul).
  3. Werninghaus K. The role of antioxidants in reducing photodamage. In: Gilchrest B (Ed.). Photodamage. London: Blackwell Science, pp. 249 (1995).
  4. Greenstock CL. Free radicals, aging, and degenerative diseases. New York:Alan R. Liss (1986).
  5. Shindo Y, Witt E, Han D, et al. Enzymic and non-enzymic antioxidants in epidermis and dermis of human skin. J Invest Dermatol 102(1):122-4 (1994 Jan).
  6. Fuchs J, Huflejt ME, Rothfuss LM, et al. Impairment of enzymic and nonenzymic antioxidants in skin by UVB irradiation. J Invest Dermatol 93(6):769-73 (1989 Dec).
  7. Langley P. Why a pomegranate? BMJ 321(7269):1153-4 (2000 Nov).
  8. Nachbar F, Korting HC. The role of vitamin E in normal and damaged skin. J Mol Med 73(1):7-17 (1995 Jan).
  9. Darr D, Combs S, Dunston S, et al. Topical vitamin C protects porcine skin from ultraviolet radiation-induced damage. Br J Dermatol 127(3):247-53 (1992 Sep).
  10. 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 296(2):575-82 (1992 Aug).
  11. Gensler HL, Magdaleno M. Topical vitamin E inhibition of immunosuppression and tumorigenesis induced by ultraviolet irradiation. Nutr Cancer 15(2):97-106 (1991).
  12. Mayer P. The effects of vitamin E on the skin. Cosmet Toiletries 108:99 (1993).
  13. Chung JH, Seo JY, Lee MK, et al. Ultraviolet modulation of 13. human macrophage metalloelastase in human skin in vivo. J Invest Dermatol 119(2):507-12 (2002 Aug).
  14. Lin JY, Selim MA, Shea CR, et al. UV photoprotection by combination topical antioxidants vitamin C and vitamin E. J Am Acad Dermatol 48(6):866-74 (2003 Jun).
  15. Jenkins M, Alexander JW, MacMillan BG, et al. Failure of topical steroids and vitamin E to reduce postoperative scar formation following reconstructive surgery. J Burn Care Rehabil 7(4):309-12 (1986 Jul-Aug).
  16. Perrenoud D, Homberger HP, Auderset PC, et al. An epidemic outbreak of papular and follicular contact dermatitis to tocopheryl linoleate in cosmetics. Swiss Contact Dermatitis Research Group. Dermatology 189(3):225-33 (1994).
  17. Hunter D, Frumkin A. Adverse reactions to vitamin E and aloe vera preparations after dermabrasion and chemical peel. Cutis 47(3):193-6 (1991 Mar).
  18. Ernster L, Dallner G. Biochemical, physiological and medical aspects of ubiquinone function. Biochim Biophys Acta 1271(1):195-204 (1995 May).
  19. Hoppe U, Bergemann J, Diembeck W, et al. Coenzyme Q10, a cutaneous antioxidant and energizer. Biofactors 9(2-4):371-8 (1999).
  20. McDaniel DH, Neudecker BA, Dinardo JC, et al. Idebenone: a new antioxidant-Part I. Relative assessment of oxidativie stress protection capacity compared to commonly know antioxidants. J Cosmet Dermatol 4(1):10–7 (2005 Jan).
  21. 21. assessment in photodamaged skin of 0.5% and 1.0% idebenone. J Cosmet Dermatol 4(3):167-73 (2005 Sep).
  22. Sasseville D, Moreau L, Al-Sowaidi M. Allergic contact dermatitis to idebenone used as an antioxidant in an anti-wrinkle cream. Contact Dermatitis 56(2):117-8 (2007 Feb).
  23. Britton G. Structure and properties of carotenoids in relation to function. FASEB J 9(15):1551-8 (1995 Dec).
  24. Fazekas Z, Gao D, Saladi RN, et al. Protective effects of lycopene against ultraviolet B–induced photodamage. Nutr Cancer 47(2):181-7 (2003).
  25. Thiele JJ, Traber MG, Tsange KG, et al. In vivo exposure to ozone depletes vitamins C and E and induces lipid peroxidation in epidermal layers of murine skin. Free Radic Biol Med 23(3):385–91 (1997).
  26. Mclauren S. Nutrition and wound healing. Wound Care 1:45 (1992).
  27. Gilchrest B (Ed.). Photodamage. London:Blackwell Science (1995).
  28. Darr D, Dunston S, Faust H, et al. Effectiveness of antioxidants (vitamin C and E) with and without sunscreens as topical photoprotectants. Acta Derm Venereol 76(4):264-8 (1996 Jul).
  29. Cabelli DE, Bielski BH. Kinetics and mechanism for the oxidation of ascorbic acid/ascorbate by HO2/O2 radicals: a pulse radiolysis and stopped flow photolysis study. J Phys Chem 87:1805 (1983).
  30. Kivirikko KI, Myllyla R. Post-translational processing of procollagens. Ann NY Acad Sci 460:187-201 (1985).
  31. Geesin JC, Darr D, Kaufman R, et al. Ascorbic acid specifically increases type I and type III procollagen messenger RNA levels in human skin fibroblast. J Invest Dermatol 90(4):420-4 (1988 Apr).
  32. Davidson JM, LuValle PA, Zoia O, et al. Ascorbate differentially regulates elastin and collagen biosynthesis in vascular smooth muscle cells and skin fibroblasts by pretranslational mechanisms. J Biol Chem 272(1):345-52 (1997 Jan).
  33. Traikovich SS. Use of topical ascorbic acid and its effects on photodamaged skin topography. Arch Otolaryngol Head Neck Surg 125(10):1091-8 (1999 Oct).
  34. Humbert PG, Haftek M, Creidi P, et al. Topical ascorbic acid in photoaged skin. Clinical topographical and ultrastructural evaluation: double-blind study vs. placebo. Exp Dermatol 12(3):237-44 (2003 Jun).
  35. Katiyar SK, Ahmad N, Mukhtar H. Green tea and skin. Arch Dermatol 136(8):989-94 (2000 Aug).
  36. Wang ZY, Agarwal R, Bickers DR, et al. Protection against ultraviolet B radiation-induced photocarcinogenesis in hairless mice by green tea polyphenols. Carcinogenesis 12(8):1527-30 (1991 Aug).
  37. Vayalil PK, Mittal A, Hara Y, et al. Green tea polyphenols 37. prevent ultraviolet light-induced oxidative damage and matrix metalloproteinases expression in mouse skin. J Invest Dermatol 122(6):1480-7 (2004 Jun).
  38. Elmets CA, Singh D, Tubesing K, et al. Cutaneous photoprotection from ultraviolet injury by green tea polyphenols. J Am Acad Dermatol 44(3):425-32 (2001 Mar).
  39. Svobodová A, Psotová J, Walterová D. Natural phenolics in the prevention of UV-induced skin damage. A review. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub 147(2):137-45 (2003 Dec).
  40. Dhanalakshmi S, Mallikarjuna GU, Singh RP, et al. Silibinin prevents ultraviolet radiation-caused skin damages in SKH-1 hairless mice via a decrease in thymine dimmer positive cells and an up-regulation of p53-p21/Cip 1 in epidermis. Carcinogenesis 25(8):1459-65 (2004 Aug).
  41. Farris P. Idebenone, green tea, and CoffeeBerry41. ® extract: new and innovative antioxidants. Dermatol Ther 20(5):322-9 (2007 Sep-Oct).
  42. 42. biological effects and potential molecular targets. Histol Histopathol 23(4):487-96 (2008 Apr).
  43. Afaq F, Adhami VM, Ahmad N. Prevention of short-term ultraviolet B radiation-mediated damages by resveratrol in SKH-1 hairless mice. Toxicol Appl Pharmacol 186(1):28-37 (2003 Jan).
  44. Aziz MH, Afaq F, Ahmad N. Prevention of ultraviolet-B radiation damage by resveratrol in mouse skin is mediated via modulation in survivin. Photochem Photobiol 81(1):25-31 (2005 Jan-Feb).
  45. Aziz MH, Reagan-Shaw S, Wu J, et al. Chemoprevention of skin cancer by grape constituent resveratrol: relevance to human disease? FASEB J 19(9):1193-5 (2005 Jul).
  46. Adhami VM, Afaq F, Ahmad N. Suppression of ultraviolet B exposure-mediated activation of NF-kappaB in normal human keratinocytes by resveratrol. Neoplasia 5(1):74-82 (2003 Jan-Feb).
  47. Vinson JA, Dabbagh YA, Serry MM, et al. Plant flavonoids, especially tea flavonols, are powerful antioxidants using an in vitro oxidation model for heart disease. J Agric Food Chem 43:2800-2 (1995).
  48. Bagchi D, Bagchi M, Stohs SJ, et al. Free radicals and grape seed proanthocyanidin extract: importance in human health and disease prevention. Toxicology 148(2-3):187-97 (2000 Aug).
  49. Mittal A, Elmets CA, Katiyar SK. Dietary feeding of proanthocyanidins from grape seeds prevents photocarcinogenesis in SKH-1 hairless mice: relationship to decreased fat and lipid peroxidation. Carcinogenesis 24(8):1379-88 (2003 Aug).
  50. Mantena SK, Katiyar SK. Grape seed proanthocyanidins inhibit UV-radiation-induced oxidative stress and activation of MAPK and NF-kappaB signaling in human epidermal keratinocytes. Free Radic Biol Med. 40(9):1603-14 (2006 May).
  51. Gil MI, Tomás-Barberán FA, Hess-Pierce B, et al. Antioxidant activity of pomegranate juice and its relationship with phenolic composition and processing. J Agric Food Chem 48(10):4581-9 (2000 Oct).
  52. Chidambara Murthy KN, Jayaprakasha GK, Singh RP. Studie s on antioxidant activity of pomegranate (Punica granatum) peel extract using in vivo models. J Agric Food Chem 50(17):4791-5 (2000 Oct).
  53. Syed DN, Malik A, Hadi N, et al. Photochemopreventive effect of pomegranate fruit extract on UVA-mediated activation of cellular pathways in normal human epidermal keratinocytes. Photochem Photobiol 82(2):398-405 (2006 Mar-Apr).
  54. modulates UV-B-mediated phosphorylation of mitogen-activated protein kinases and activation of nuclear factor kappa B in normal human epidermal keratinocytes paragraph sign. Photochem Photobiol 81(1):38-45 (2005 Jan-Feb).
  55. Wei H, Cai Q, Rahn RO. Inhibition of UV light- and Fenton reaction-induced oxidative DNA damage by the soybean isoflavone genistein. Carcinogenesis 17:73-7 (1996).
  56. Wei H, Saladi R, Lu Y, et al. Isoflavone genistein: photoprotection and clinical implications in dermatology. J Nutr 133(11 Suppl 1):3811S-3819S (2003 Nov).
  57. Maziere C, Dantin F, Dubois F, et al. Biphasic effect of UVA radiation on STAT1 activity and tyrosine phosphorylation in cultured human keratinocytes. Free Radic Biol Med 28(9):1430-7 (2000 May).
  58. Sime S, Reeve VE. Protection from inflammation, immunosuppression and carcinogenesis induced by UV radiation in mice by topical Pycnogenol. Photochem Photobiol 79(2):193-8 (2004 Feb).
  59. Saliou C, Rimbach G, Moini H, et al. Solar ultraviolet-induced erythema in human skin and nuclear factor-kappa-B-dependent gene expression in keratinocytes are modulated by a French maritime pine bark extract. Free Radic Biol Med 30(2):154-60 (2001 Jan).
  60. Bissett DL, Oblong JE, Berge CA. Niacinamide: a B vitamin that improves aging facial skin appearance. Dermatol Surg 31(7 Pt 2):860-5 (2005 Jul).
  61. Cho HS, Lee MH, Lee JW, et al. Anti-wrinkling effects of the mixture of vitamin C, vitamin E, pycnogenol and evening primrose oil, and molecular mechanisms on hairless mouse skin caused by chronic ultraviolet B irradiation. Photodermatol Photoimmunol Photomed; 23(5):155-62 (2007 Oct).
  62. Lin FH, Lin JY, Gupta RD, et al. Ferulic acid stabilizes a solution of vitamins A and E and doubles its photoprotection of skin. J Invest Dermatol 125(4):826-32 (2005 Oct).
  63. Greul AK, Grundmann JU, Heinrich F, et al. Photoprotection of UV-irradiated human skin: an antioxidative combination of vitamins E and C, carotenoids, selenium and proanthocyanidins. Skin Pharmacol Appl Skin Physiol 15(5):307-15 (2002 Sep-Oct).
  64. Passi S, De Pita O, Grandinetti M, et al. The combined use of oral and topical lipophilic antioxidants increases their levels both in sebum and stratum corneum. Biofactors 18(1-4):289-97 (2003).