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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. Vitamin C transport proteins are increased in keratinocytes in response to UV light, suggesting an increased need for vitamin C uptake for adequate protection.
UV light decreases vitamin C content of skin, an effect that is dependent on the intensity and duration of UV exposure. 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. Vitamin C also modulates redox-sensitive cell signaling in cultured skin cells and consequently increases cell survival following UV exposure.
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. 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. 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. 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. 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. 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 , increased MED, and decreased cell damage.
Limited human studies are available on photoprotection by topical application of vitamin C. Although topical ascorbic acid reduces radicals in UV-exposed human skin. only one study examined its effect on UV-induced erythemal response; this study reported no significant benefit of topical vitamin C . Like animal research, human studies using combinations of vitamin C and vitamin E have documented UV protective effects,
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. Hydroxylation of collagen is necessary for its extracellular stability and support of the epidermis.
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