See the Skin Health Overview article


The antioxidant properties of vitamin C (ascorbic acid) and its role in collagen synthesis make vitamin C a vital molecule for skin health. Dietary and topical ascorbic acid have beneficial effects on skin cells, and some studies have shown that vitamin C may help prevent and treat ultraviolet (UV)-induced photodamage. However, the effects of vitamin C in the skin are not well understood due to limited research. This article discusses the potential roles of vitamin C in the skin and summarizes the current knowledge about vitamin C in skin health.

Content and availability

Vitamin C is a normal skin constituent that is found at high levels in both the dermis and epidermis (1, 2). The vitamin C content of the epidermis is higher than the dermis, although the vitamin C concentrations in both layers are approximately equal to that of other water-soluble antioxidants, including uric acid and glutathione (2-4). Aging, however, causes a decline in vitamin C content in both the epidermis and dermis (2). Excessive exposures to UV light or pollutants (e.g., cigarette smoke and ozone) may also lower vitamin C content, primarily in the epidermis (4-6).

Vitamin C in the skin is normally transported from the bloodstream. Transport proteins specific for ascorbic acid are found on cells in all layers of the skin (7). Keratinocytes have a high capacity for vitamin C transport, possibly to compensate for limited vascularization of the epidermis (7, 8). Oral supplementation with vitamin C effectively increases vitamin C levels in the skin (9, 10). However, when plasma vitamin C levels are saturated, skin vitamin C concentrations no longer increase. Optimum skin concentrations of the vitamin are not yet known.

Topical application

Vitamin C can be provided to the skin through topical application. The stratum corneum is the primary obstacle to efficient vitamin C absorption from external sources (11); removal of the stratum corneum by laser, chemical, or mechanical methods enhances absorption (12). Although similar studies are still required for humans, studies in laboratory animals show that percutaneous vitamin C absorption greatly depends on pH. Preparations with a pH below 4.0 aid in transport by promoting the uncharged form of vitamin C, ascorbic acid (11). Although concentrations of vitamin C up to 30% have been used for animal studies, maximal absorption was achieved with a 20% vitamin C solution, with higher concentrations showing lower absorption (11). Topical application of ascorbic acid will cross the epidermis into the underlying dermal layers.

The stability of vitamin C in topical solutions is a concern, as exposures to air, heat, and/or light may slowly degrade vitamin C. Although the natural form of vitamin C, ascorbic acid, is the most effective for topical administration (11), it is the least stable in solution. However, stable synthetic derivatives, such as ascorbate phosphate, are considered to have limited permeability (11) and function in skin (13, 14). Another stable lipid-soluble derivative, ascorbyl palmitate, also has limited absorption (11), and one in vitro study with cultured skin cells found that the administration of ascorbyl palmitate had some toxic effects (15). Yet, the stability of topical vitamin C solutions may be increased by the addition of other antioxidant compounds (16-19).

Human studies with subjects using topically applied solutions of 0.6%-10.0% vitamin C or its synthetic derivatives have not reported adverse effects (14, 19-27).


Symptoms of vitamin C deficiency (knowns as scurvy) appear once plasma concentrations of ascorbic acid drop below 10 micromolar (μM), a level that can be prevented by consuming as little as 10 mg of ascorbic acid daily (28). Cutaneous manifestations of scurvy result from declines in collagen synthesis, leading to disruption of connective tissue and fragility of blood vessels. Early symptoms in the skin include a thickening of the stratum corneum and spots of small subcutaneous bleeding (29, 30). As scurvy progresses, wound healing is impaired due to the loss of mature collagen, which allows wounds to remain open (31, 32). Skin lesions caused by vitamin C deficiency are remediated by an adequate intake of vitamin C.

Functions in Healthy Skin


Vitamin C limits the damage induced by ultraviolet (UV) light exposure. Vitamin C is not a “sunscreen” because it does not absorb light in the UVA or UVB spectrum. Rather, the antioxidant activity of vitamin C protects against UV-induced damage caused by free radicals (33). Vitamin C transport proteins are increased in keratinocytes in response to UV light, suggesting an increased need for vitamin C uptake for adequate protection (7, 8).

UV light decreases vitamin C content of skin, an effect that is dependent on the intensity and duration of UV exposure (4, 6, 34). In cultured keratinocytes, the addition of vitamin C reduces UV-related DNA damage and lipid peroxidation, limits the release of pro-inflammatory cytokines, and protects against apoptosis (35, 36). Vitamin C also modulates redox-sensitive cell signaling in cultured skin cells and consequently increases cell survival following UV exposure (37, 38).

In two rodent studies, addition of ascorbic acid to the diet reduced the size and number of dermal neoplasms and skin tumors induced by chronic UV exposure (39, 40). To date, no other studies with UV exposure and oral ascorbic acid supplementation in animal models have been published.

In two human studies, oral vitamin C supplementation alone did not significantly increase Minimal Erythemal Dose (MED), a measure of photoprotection from UV light in skin (9, 10). Overall, limited data suggest that vitamin C consumption alone provides insufficient antioxidant protection against UV irradiation. However, multiple studies have found that oral supplementation with a combination of vitamin C and vitamin E effectively increases MED and decreases erythema-induced blood flow to damaged areas of skin (41, 42). Thus, interactions between the two antioxidant vitamins may be necessary to achieve UV protection by dietary means.

Topical application of vitamin C, alone or in combination with other compounds, may result in greater photoprotection than oral supplementation because of the more direct route of administration. In one mouse study, topical application of ascorbic acid delayed the effects of chronic high-dose UVB exposure on the skin, including a reduction in skin wrinkling and the development of skin tumors (13). In pig models, topical application of vitamin C reduced the number of sunburned cells, decreased erythema response, and reduced DNA damage induced by UVA exposure (18, 33). Topically applied combinations of vitamin C and vitamin E are more effective in preventing photodamage than either vitamin alone. In particular, this combination of antioxidant vitamins decreased the immunosuppressive effects of UV exposure (43), increased MED, and decreased cell damage (16, 18, 44).

Limited human studies are available on photoprotection by topical application of vitamin C. Although topical ascorbic acid reduces radicals in UV-exposed human skin (45), only one study examined its effect on UV-induced erythemal response; this study reported no significant benefit of topical vitamin C (24). Like animal research, human studies using combinations of vitamin C and vitamin E have documented UV protective effects (17, 19, 24).


The accumulation of oxidative damage to proteins is a distinguishing feature of both photodamage (photoaging) and intrinsic aging; such oxidative damage can lead to changes in skin structure. In addition to its antioxidant functions, vitamin C regulates the synthesis of the structural protein collagen. The role of vitamin C in the hydroxylation of collagen molecules is well characterized (46). Hydroxylation of collagen is necessary for its extracellular stability and support of the epidermis.

In cell culture models, vitamin C supplementation has many beneficial effects in combating photodamage. Specifically, vitamin C has been shown to stabilize collagen mRNA, thus increasing collagen protein synthesis for repair of the damaged skin (47). This occurs concurrently with a decrease in elastin production; the elastin protein is often overproduced in response to photodamage (48). Vitamin C also increases the proliferation rate of fibroblasts, a capacity that is decreased with age (49). Further, vitamin C stimulates DNA repair in cultured fibroblasts (50).

Human studies often assess skin health by changes in depth or number of wrinkles and by the individual’s perception of skin health. Two observational studies found that higher intakes of vitamin C from the diet were associated with better skin appearance, with notable decreases in skin wrinkling (51, 52). The use of vitamin C (3-10%) in topical applications for at least 12 weeks has been shown to decrease wrinkling (21, 23, 25, 27), reduce protein fiber damage (25), decrease apparent roughness of skin (21), and increase production of collagen (26, 27). Topical vitamin C has also been shown to reverse some of the age-related structural changes in the interface between the dermis and the epidermis (22). However, the effects of topical vitamin C are not apparent in all individuals, and interestingly, one study found that individuals with high dietary intakes of vitamin C showed no or little effect of a topical administration (26).

Wound healing

One of the distinctive features of scurvy is poor wound healing (31). Vitamin C levels decrease rapidly at a wound site (53, 54). Although inflammatory responses often increase free radicals at the site of injury and the presence of vitamin C may limit free radical damage, free radicals may play a complex role in the healing response that is not yet understood (54, 55). However, the increased demand for dermal collagen synthesis may increase utilization of vitamin C. Vitamin C may have additional roles in wound healing, for example, by promoting keratinocyte differentiation (50, 56), stimulating the formation of the epidermal barrier (57), and re-establishing the stratum corneum (58).

Studies on the effect of vitamin C supplementation on wound healing have reported somewhat mixed results. Data from laboratory animals and humans show that vitamin C deficiency results in poor wound healing, and vitamin C supplementation in deficient individuals shows significant benefits (31, 59-61). Although vitamin C levels appear to increase collagen synthesis and decrease inflammatory responses at the site of the wound, neither vitamin C supplementation (62-64) or increased plasma vitamin C status (55) increases wound closure time in otherwise healthy individuals. This suggests that vitamin C may only affect specific facets of the wound healing response. Topical ascorbic acid has not been properly evaluated prior to or during wound healing in humans.

Vitamin C is included in oral therapies for pressure ulcers (bed sores) and burns, along with vitamin E, zinc, and other nutritive factors (65-67).

Dry skin

Higher intakes of dietary vitamin C have been correlated with a decreased risk of dry skin (51), suggesting that ascorbic acid may have effects on trans-epidermal water loss (TEWL). In cell culture models, addition of vitamin C promotes the synthesis of barrier lipids, which would establish a functioning stratum corneum with low water permeability (58, 68). One study using topical vitamin C in human subjects correlated its use with decreased skin roughness (21). However, another study suggested vitamin C increased TEWL when applied to the skin (14). Thus, the effects of vitamin C on skin dryness are not clear.

Other functions

Environmental pollutants, such as ozone, can decrease vitamin C levels in the skin and lead to free radical damage (5). Smoking also leads to increased wrinkling and decreased collagen synthesis, which corresponds to a decline in plasma vitamin C levels (55); however, it is unclear if this correlates to lower vitamin C levels in skin. Topical ascorbic acid has not been evaluated against pollution-related damage.

Topical vitamin C may be useful against acne to reduce inflammatory lesions. However, studies have primarily focused on the use of sodium ascorbyl phosphate, a synthetic derivative that may be poorly absorbed by the skin (20, 69). Topical vitamin C may also have mild skin lightening effects that are caused by reductions in melanin production and melanin oxidation (70).


Vitamin C is an essential part of skin health both as a small molecular weight antioxidant and as a critical factor for collagen synthesis. Vitamin C contributes to photoprotection, decreases photodamage, and is needed for adequate wound healing. Oral supplementation with vitamin C may help prevent UV-induced damage, especially in combination with supplemental vitamin E. Dietary vitamin C may also provide photoprotection, but the extent of the protective effects will require additional research. Topical application of vitamin C appears to be an effective route for delivering ascorbic acid to the skin because ascorbic acid appears to be taken up readily at an acidic pH. Despite inconsistencies in vitamin C preparations and study design, the data suggest that vitamin C is most effective in protecting against damage induced by UV light and also has utility in the treatment of photodamage and/or skin wrinkling. Although vitamin C appears to benefit dry skin and may support wound healing, further research is needed to determine the effect of vitamin C on both. Lastly, the greatest effects of vitamin C supplementation are seen when it is combined with other micronutrients, such as vitamin E and zinc.

Authors and Reviewers

Written in September 2011 by:
Alexander J. Michels, Ph.D.
Linus Pauling Institute
Oregon State University

Reviewed in September 2011 by:
Zoe Diana Draelos, M.D.
Consulting Professor
Department of Dermatology
Duke University School of Medicine
Durham, NC

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

Copyright 2011-2024  Linus Pauling Institute


1.  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;102:122-124.  (PubMed)

2.  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;117:1212-1217.  (PubMed)

3.  Lopez-Torres M, Shindo Y, Packer L. Effect of age on antioxidants and molecular markers of oxidative damage in murine epidermis and dermis. J Invest Dermatol 1994;102:476-480.  (PubMed)

4.  Shindo Y, Witt E, Packer L. Antioxidant defense mechanisms in murine epidermis and dermis and their responses to ultraviolet light. J Invest Dermatol 1993;100:260-265.  (PubMed)

5.  Thiele JJ, Traber MG, Tsang K, Cross CE, Packer L. In vivo exposure to ozone depletes vitamins C and E and induces lipid peroxidation in epidermal layers of murine skin. Free Radic Biol Med 1997;23:385-391.  (PubMed)

6.  Podda M, Traber MG, Weber C, Yan LJ, Packer L. UV-irradiation depletes antioxidants and causes oxidative damage in a model of human skin. Free Radic Biol Med 1998;24:55-65.  (PubMed)

7.  Steiling H, Longet K, Moodycliffe A, et al. Sodium-dependent vitamin C transporter isoforms in skin: Distribution, kinetics, and effect of UVB-induced oxidative stress. Free Radic Biol Med 2007;43:752-762.  (PubMed)

8.  Kang JS, Kim HN, Jung da J, et al. Regulation of UVB-induced IL-8 and MCP-1 production in skin keratinocytes by increasing vitamin C uptake via the redistribution of SVCT-1 from the cytosol to the membrane. J Invest Dermatol 2007;127:698-706.  (PubMed)

9.  McArdle F, Rhodes LE, Parslew R, Jack CI, Friedmann PS, Jackson MJ. UVR-induced oxidative stress in human skin in vivo: effects of oral vitamin C supplementation. Free Radic Biol Med 2002;33:1355-1362.  (PubMed)

10.  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;25:1006-1012.  (PubMed)

11.  Pinnell SR, Yang H, Omar M, et al. Topical L-ascorbic acid: percutaneous absorption studies. Dermatol Surg 2001;27:137-142.  (PubMed)

12.  Lee WR, Shen SC, Kuo-Hsien W, Hu CH, Fang JY. Lasers and microdermabrasion enhance and control topical delivery of vitamin C. J Invest Dermatol 2003;121:1118-1125.  (PubMed)

13.  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;7:56-62.  (PubMed)

14.  Campos PM, Goncalves GM, Gaspar LR. In vitro antioxidant activity and in vivo efficacy of topical formulations containing vitamin C and its derivatives studied by non-invasive methods. Skin Res Technol 2008;14:376-380.  (PubMed)

15.  Meves A, Stock SN, Beyerle A, Pittelkow MR, Peus D. Vitamin C derivative ascorbyl palmitate promotes ultraviolet-B-induced lipid peroxidation and cytotoxicity in keratinocytes. J Invest Dermatol 2002;119:1103-1108.  (PubMed)

16.  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;125:826-832.  (PubMed)

17.  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;59:418-425.  (PubMed)

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

19.  Oresajo C, Stephens T, Hino PD, et al. Protective effects of a topical antioxidant mixture containing vitamin C, ferulic acid, and phloretin against ultraviolet-induced photodamage in human skin. J Cosmet Dermatol 2008;7:290-297.  (PubMed)

20.  Woolery-Lloyd H, Baumann L, Ikeno H. Sodium L-ascorbyl-2-phosphate 5% lotion for the treatment of acne vulgaris: a randomized, double-blind, controlled trial. J Cosmet Dermatol 2010;9:22-27.  (PubMed)

21.  Traikovich SS. Use of topical ascorbic acid and its effects on photodamaged skin topography. Arch Otolaryngol Head Neck Surg 1999;125:1091-1098.  (PubMed)

22.  Sauermann K, Jaspers S, Koop U, Wenck H. Topically applied vitamin C increases the density of dermal papillae in aged human skin. BMC Dermatol 2004;4:13.  (PubMed)

23.  Raschke T, Koop U, Dusing HJ, et al. Topical activity of ascorbic acid: from in vitro optimization to in vivo efficacy. Skin Pharmacol Physiol 2004;17:200-206.  (PubMed)

24.  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;139:332-339.  (PubMed)

25.  Humbert PG, Haftek M, Creidi P, et al. Topical ascorbic acid on photoaged skin. Clinical, topographical and ultrastructural evaluation: double-blind study vs. placebo. Exp Dermatol 2003;12:237-244.  (PubMed)

26.  Nusgens BV, Humbert P, Rougier A, et al. Topically applied vitamin C enhances the mRNA level of collagens I and III, their processing enzymes and tissue inhibitor of matrix metalloproteinase 1 in the human dermis. J Invest Dermatol 2001;116:853-859.  (PubMed)

27.  Fitzpatrick RE, Rostan EF. Double-blind, half-face study comparing topical vitamin C and vehicle for rejuvenation of photodamage. Dermatol Surg 2002;28:231-236.  (PubMed)

28.  Padayatty SJ, Katz A, Wang Y, et al. Vitamin C as an antioxidant: evaluation of its role in disease prevention. J Am Coll Nutr 2003;22:18-35.  (PubMed)

29.  Hodges RE, Hood J, Canham JE, Sauberlich HE, Baker EM. Clinical manifestations of ascorbic acid deficiency in man. Am J Clin Nutr 1971;24:432-443.  (PubMed)

30.  Hodges RE, Baker EM, Hood J, Sauberlich HE, March SC. Experimental scurvy in man. Am J Clin Nutr 1969;22:535-548.  (PubMed)

31.  Lind J. A Treatise on the Scurvy. In. London: A. Millar; 1753.

32.  Ross R, Benditt EP. Wound healing and collagen formation. II. Fine structure in experimental scurvy. J Cell Biol 1962;12:533-551.  (PubMed)

33.  Darr D, Combs S, Dunston S, Manning T, Pinnell S. Topical vitamin C protects porcine skin from ultraviolet radiation-induced damage. Br J Dermatol 1992;127:247-253.  (PubMed)

34.  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;102:470-475.  (PubMed)

35.  Tebbe B, Wu S, Geilen CC, Eberle J, Kodelja V, Orfanos CE. L-ascorbic acid inhibits UVA-induced lipid peroxidation and secretion of IL-1alpha and IL-6 in cultured human keratinocytes in vitro. J Invest Dermatol 1997;108:302-306.  (PubMed)

36.  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;106:1086-1089.  (PubMed)

37.  Savini I, D'Angelo I, Ranalli M, Melino G, Avigliano L. Ascorbic acid maintenance in HaCaT cells prevents radical formation and apoptosis by UV-B. Free Radic Biol Med 1999;26:1172-1180.  (PubMed)

38.  Nakamura T, Pinnell SR, Darr D, 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;109:20-24.  (PubMed)

39.  Dunham WB, Zuckerkandl E, Reynolds R, et al. Effects of intake of L-ascorbic acid on the incidence of dermal neoplasms induced in mice by ultraviolet light. Proc Natl Acad Sci U S A 1982;79:7532-7536.  (PubMed)

40.  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)

41.  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;124:304-307.  (PubMed)

42.  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;38:45-48.  (PubMed)

43.  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;13:89-98.  (PubMed)

44.  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;76:264-268.  (PubMed)

45.  Ou-Yang H, Stamatas G, Saliou C, Kollias N. A chemiluminescence study of UVA-induced oxidative stress in human skin in vivo. J Invest Dermatol 2004;122:1020-1029.  (PubMed)

46.  Peterkofsky B. Ascorbate requirement for hydroxylation and secretion of procollagen: relationship to inhibition of collagen synthesis in scurvy. Am J Clin Nutr 1991;54:1135S-1140S.  (PubMed)

47.  Geesin JC, Darr D, Kaufman R, Murad S, Pinnell SR. Ascorbic acid specifically increases type I and type III procollagen messenger RNA levels in human skin fibroblast. J Invest Dermatol 1988;90:420-424.  (PubMed)

48.  Davidson JM, LuValle PA, Zoia O, Quaglino D, Jr., Giro M. Ascorbate differentially regulates elastin and collagen biosynthesis in vascular smooth muscle cells and skin fibroblasts by pretranslational mechanisms. J Biol Chem 1997;272:345-352.  (PubMed)

49.  Phillips CL, Combs SB, Pinnell SR. Effects of ascorbic acid on proliferation and collagen synthesis in relation to the donor age of human dermal fibroblasts. J Invest Dermatol 1994;103:228-232.  (PubMed)

50.  Duarte TL, Cooke MS, Jones GD. Gene expression profiling reveals new protective roles for vitamin C in human skin cells. Free Radic Biol Med 2009;46:78-87.  (PubMed)

51.  Cosgrove MC, Franco OH, Granger SP, Murray PG, Mayes AE. Dietary nutrient intakes and skin-aging appearance among middle-aged American women. Am J Clin Nutr 2007;86:1225-1231.  (PubMed)

52.  Purba MB, Kouris-Blazos A, Wattanapenpaiboon N, et al. Skin wrinkling: can food make a difference? J Am Coll Nutr 2001;20:71-80.  (PubMed)

53.  Kim M, Otsuka M, Yu R, Kurata T, Arakawa N. The distribution of ascorbic acid and dehydroascorbic acid during tissue regeneration in wounded dorsal skin of guinea pigs. Int J Vitam Nutr Res 1994;64:56-59.  (PubMed)

54.  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;26:93-101.  (PubMed)

55.  Sorensen LT, Toft BG, Rygaard J, et al. Effect of smoking, smoking cessation, and nicotine patch on wound dimension, vitamin C, and systemic markers of collagen metabolism. Surgery 2010;148:982-990.  (PubMed)

56.  Savini I, Catani MV, Rossi A, Duranti G, Melino G, Avigliano L. Characterization of keratinocyte differentiation induced by ascorbic acid: protein kinase C involvement and vitamin C homeostasis. J Invest Dermatol 2002;118:372-379.  (PubMed)

57.  Boyce ST, Supp AP, Swope VB, Warden GD. Vitamin C regulates keratinocyte viability, epidermal barrier, and basement membrane in vitro, and reduces wound contraction after grafting of cultured skin substitutes. J Invest Dermatol 2002;118:565-572.  (PubMed)

58.  Ponec M, Weerheim A, Kempenaar J, et al. The formation of competent barrier lipids in reconstructed human epidermis requires the presence of vitamin C. J Invest Dermatol 1997;109:348-355.  (PubMed)

59.  Kramer GM, Fillios LC, Bowler EC. Ascorbic acid treatment on early collagen production and wound healing in the guinea pig. J Periodontol 1979;50:189-192.  (PubMed)

60.  Young ME. Malnutrition and wound healing. Heart Lung 1988;17:60-67.  (PubMed)

61.  Dunphy JE, Edwards LC, Udupa KN. Wound healing; a new perspective with particular reference to ascorbic acid deficiency. Ann Surg 1956;144:304-317.  (PubMed)

62.  Silverstein RJ, Landsman AS. The effects of a moderate and high dose of vitamin C on wound healing in a controlled guinea pig model. J Foot Ankle Surg 1999;38:333-338.  (PubMed)

63.  Thompson C, Fuhrman MP. Nutrients and wound healing: still searching for the magic bullet. Nutr Clin Pract 2005;20:331-347.  (PubMed)

64.  Vaxman F, Olender S, Lambert A, et al. Effect of pantothenic acid and ascorbic acid supplementation on human skin wound healing process. A double-blind, prospective and randomized trial. Eur Surg Res 1995;27:158-166.  (PubMed)

65.  Desneves KJ, Todorovic BE, Cassar A, Crowe TC. Treatment with supplementary arginine, vitamin C and zinc in patients with pressure ulcers: a randomised controlled trial. Clin Nutr 2005;24:979-987.  (PubMed)

66.  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;12:588-595.  (PubMed)

67.  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;30:859-866.  (PubMed)

68.  Pasonen-Seppanen S, Suhonen TM, Kirjavainen M, et al. Vitamin C enhances differentiation of a continuous keratinocyte cell line (REK) into epidermis with normal stratum corneum ultrastructure and functional permeability barrier. Histochem Cell Biol 2001;116:287-297.  (PubMed)

69.  Klock J, Ikeno H, Ohmori K, Nishikawa T, Vollhardt J, Schehlmann V. Sodium ascorbyl phosphate shows in vitro and in vivo efficacy in the prevention and treatment of acne vulgaris. Int J Cosmet Sci 2005;27:171-176.  (PubMed)

70.  Kameyama K, Sakai C, Kondoh S, et al. Inhibitory effect of magnesium L-ascorbyl-2-phosphate (VC-PMG) on melanogenesis in vitro and in vivo. J Am Acad Dermatol 1996;34:29-33.  (PubMed)