PEER-REVIEW | DERMATOLOGY | manifestations of photoaging such as pigmentation,


telangiectasias, coarse texture, deep wrinkles and solar elastosis. UV-reactive oxygen species triggers the signal transduction cascade, which leads to upregulation of activation protein-1 (AP-1) and nuclear factor-B (NF-kB), and downregulation of transforming growth factor-. These proteases collectively upregulate matrix metalloproteinases (MMPs), which degrade collagen, reduce collagen production, and increase elastin accumulation24


. Sunscreens are only partially effective in


blocking free radicals produced by UV exposure. Vitamin C exerts a photoprotective effect against photoaging by preventing UV-induced erythema and pigmentation, sunburn cell formation, and induces collagen repair. Vitamin C has been shown to inhibit the activation of AP-1, which leads to a reduction in MMP production and collagen damage24


. In laboratory studies, vitamin C


deficient mice have been shown to have significant UVB-induced pigmentation25


.


Fibroblasts stimulated with ascorbic acid in cell culture have also been shown to increase gene expression of collagen and produce more collagen26


.


Beneficial effects of vitamin C on elastin have also been observed. Elastin is an enzyme that degrades elastic fibres leading to the characteristic appearance of photoaging known as solar elastosis. In vitro studies have shown that vitamin C inhibits the biosynthesis of elastin27 Although UV irradiation depletes


.


vitamin C transporters in the epidermis, transporters found in the dermis where collagen production takes place are unaffected28


. Therefore, increasing the level of


vitamin C in the skin may hypothetically reduce the damaging effects caused by UV radiation. In animal studies, it was found that application of 5% ascorbic acid two hours prior to UV exposure reduced skin wrinkling29


. Fibroblasts


stimulated with ascorbic acid in cell culture have also been shown to increase gene expression of collagen and produce more collagen.


The photoprotective effects of vitamin C are also seen in


human clinical studies. One double-blind placebo- controlled study on 10 subjects using 10% topical vitamin C over a 12-week period showed a statistically significant reduction in photoaged scores and improvement in wrinkling in vitamin C treated patients, compared to placebo30


histology and clinical appearance was seen in another double-blind, placebo-controlled study using 5% topical vitamin C on 20 subjects over a 6-month period31


. However,


the effect of oral supplementation of vitamin C remains controversial32


vitamin at sufficiently high concentrations in the skin.


Protection against UV-induced immunosuppression CD1a-expressing Langerhans cells are antigen-presenting cells present in the epidermis, which act by initiating a


28  January/February 2016 | prime-journal.com , owing to the reduced bioavailability of the


protective immune response. Their numbers


are decreased upon acute and chronic UV exposure33


. Vitamin C


containing topical solutions have been shown to prevent the reduction of CD1a-expressing Langerhans cells upon UV radiation34


.


Protection against photocarcinogenesis UV-induced erythema and thymine dimer mutations contribute to photocarcinogenesis. In addition, UV- induced reactive oxygen species induce mutations on the p53 gene, which affects the repair of damaged DNA and induces a process of programmed cell death (apoptosis)35


. In laboratory studies, application of 10%


topical vitamin C has been shown to reduce UVB- induced erythema by 52% and apoptotic sunburn cell formation by 40–60%36


. In clinical studies, vitamin C . A significant improvement in furrows on skin


containing solutions have been shown to be particularly effective at reducing UV-induced thymine dimers, thereby potentially reducing the risk of photocarcinogenesis37


.


Anti-ageing effect Although the exact mechanisms of intrinsic ageing are not clear, both intrinsic and photo-aged skin are associated with MMP-mediated collagen breakdown leading to thinning of dermal papillae and flattening of the epidermal- dermal junction. In intrinsically aged skin, there is an increase in AP-1, MMP-1, and MMP-9 levels. Consistent


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