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      High‐energy visible light at ambient doses and intensities induces oxidative stress of skin—Protective effects of the antioxidant and Nrf2 inducer Licochalcone A in vitro and in vivo

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          Abstract

          Background

          Solar radiation causes skin damage through the generation of reactive oxygen species (ROS). While UV filters effectively reduce UV‐induced ROS, they cannot prevent VIS‐induced (400‐760 nm) oxidative stress. Therefore, potent antioxidants are needed as additives to sunscreen products.

          Methods

          We investigated VIS‐induced ROS formation and the photoprotective effects of the Nrf2 inducer Licochalcone A (LicA).

          Results

          Visible spectrum of 400‐500 nm dose‐dependently induced ROS in cultured human fibroblasts at doses equivalent to 1 hour of sunshine on a sunny summer day (150 J/cm 2). A pretreatment for 24 hours with 1 µmol/L LicA reduced ROS formation to the level of unirradiated cells while UV filters alone were ineffective, even at SPF50+. In vivo, topical treatment with a LicA‐containing SPF50 + formulation significantly prevented the depletion of intradermal carotenoids by VIS irradiation while SPF50 + control did not protect.

          Conclusion

          LicA may be a useful additive antioxidant for sunscreens.

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          Most cited references84

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          Wavelength dependence of oxidative DNA damage induced by UV and visible light.

          DNA damage induced by UV radiation and visible light (290-500 nm) in AS52 Chinese hamster cells was analysed by an alkaline elution assay with specific repair endonucleases. Cells were exposed to extensively filtered monochrome or broad-band radiation. Between 290 and 315 nm, the ratio of base modifications sensitive to Fpg protein (i.e. 8-hydroxyguanine and formamidopyrimidines) and T4 endonuclease V (i.e. cyclobutane pyrimidine dimers) was constant (approximately 1:200), indicating that the direct excitation of DNA is responsible for both types of damage in this range of the spectrum. While the yield of pyrimidine dimers per unit dose continued to decrease exponentially beyond 315 nm, the yield of Fpg-sensitive modifications increased to a second maximum between 400 and 450 nm. The damage spectrum in this wavelength range consisted of only a few other modifications (strand breaks, abasic sites and pyrimidine modifications sensitive to endonuclease III) and is attributed to endogenous photosensitizers that give rise to oxidative DNA damage via singlet oxygen and/or type I reactions. The generation of Fpg-sensitive modifications by visible light was not linear with dose but followed a saturation curve. It is calculated that the exposure of the cells to low doses of solar radiation results in the formation of cyclobutane pyrimidine dimers and Fpg-sensitive modifications in a ratio of 10:1.
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            Irradiation of skin with visible light induces reactive oxygen species and matrix-degrading enzymes.

            Daily skin exposure to solar radiation causes cells to produce reactive oxygen species (ROS), which are a primary factor in skin damage. Although the contribution of the UV component to skin damage has been established, few studies have examined the effects of non-UV solar radiation on skin physiology. Solar radiation comprises <10% of UV, and thus the purpose of this study was to examine the physiological response of skin to visible light (400-700 nm). Irradiation of human skin equivalents with visible light induced production of ROS, proinflammatory cytokines, and matrix metalloproteinase (MMP)-1 expression. Commercially available sunscreens were found to have minimal effects on reducing visible light-induced ROS, suggesting that UVA/UVB sunscreens do not protect the skin from visible light-induced responses. Using clinical models to assess the generation of free radicals from oxidative stress, higher levels of free radical activity were found after visible light exposure. Pretreatment with a photostable UVA/UVB sunscreen containing an antioxidant combination significantly reduced the production of ROS, cytokines, and MMP expression in vitro, and decreased oxidative stress in human subjects after visible light irradiation. Taken together, these findings suggest that other portions of the solar spectrum aside from UV, particularly visible light, may also contribute to signs of premature photoaging in skin.
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              Impact of long-wavelength UVA and visible light on melanocompetent skin.

              The purpose of this study was to determine the effect of visible light on the immediate pigmentation and delayed tanning of melanocompetent skin; the results were compared with those induced by long-wavelength UVA (UVA1). Two electromagnetic radiation sources were used to irradiate the lower back of 20 volunteers with skin types IV-VI: UVA1 (340-400 nm) and visible light (400-700 nm). Pigmentation was assessed by visual examination, digital photography with a cross-polarized filter, and diffused reflectance spectroscopy at 7 time points over a 2-week period. Confocal microscopy and skin biopsies for histopathological examination using different stains were carried out. Irradiation was also carried out on skin type II. Results showed that although both UVA1 and visible light can induce pigmentation in skin types IV-VI, pigmentation induced by visible light was darker and more sustained. No pigmentation was observed in skin type II. The quality and quantity of pigment induced by visible light and UVA1 were different. These findings have potential implications on the management of photoaggravated pigmentary disorders, the proper use of sunscreens, and the treatment of depigmented lesions.
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                Author and article information

                Contributors
                Ludger.Kolbe@Beiersdorf.com
                Journal
                Photodermatol Photoimmunol Photomed
                Photodermatol Photoimmunol Photomed
                10.1111/(ISSN)1600-0781
                PHPP
                Photodermatology, Photoimmunology & Photomedicine
                John Wiley and Sons Inc. (Hoboken )
                0905-4383
                1600-0781
                17 November 2019
                March 2020
                : 36
                : 2 ( doiID: 10.1111/phpp.v36.2 )
                : 135-144
                Affiliations
                [ 1 ] Beiersdorf AG, Research and Development Hamburg Germany
                [ 2 ] Center of Experimental and Applied Cutaneous Physiology Department of Dermatology, Venerology and Allergology Charité – Universitätsmedizin Berlin Berlin Germany
                Author notes
                [*] [* ] Correspondence

                Ludger Kolbe, Front End Innovation, Beiersdorf AG, Hamburg, Germany.

                Email: Ludger.Kolbe@ 123456Beiersdorf.com

                Author information
                https://orcid.org/0000-0001-8608-8901
                Article
                PHPP12523
                10.1111/phpp.12523
                7078816
                31661571
                35be0ec5-9e1f-4b1b-9fb4-44a05dcb1d62
                © 2019 The Authors. Photodermatology, Photoimmunology & Photomedicine published by John Wiley & Sons Ltd

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 16 January 2019
                : 24 September 2019
                : 23 October 2019
                Page count
                Figures: 5, Tables: 1, Pages: 10, Words: 7345
                Categories
                Original Article
                Original Articles
                Custom metadata
                2.0
                March 2020
                Converter:WILEY_ML3GV2_TO_JATSPMC version:5.7.8 mode:remove_FC converted:18.03.2020

                antioxidant,licochalcone a,reactive oxygen species,sunscreen,visible light

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