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 physiolo...
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Published in | Journal of investigative dermatology Vol. 132; no. 7; pp. 1901 - 1907 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
New York, NY
Elsevier Inc
01.07.2012
Nature Publishing Group Elsevier Limited |
Subjects | |
Online Access | Get full text |
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Abstract | 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 (400–700nm). 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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AbstractList | 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. 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.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. 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 (400–700nm). 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. |
Author | Kaur, Simarna Ruvolo, Eduardo Liebel, Frank Kollias, Nikiforos Southall, Michael D. |
Author_xml | – sequence: 1 givenname: Frank surname: Liebel fullname: Liebel, Frank organization: Preclinical Pharmacology, Johnson & Johnson Skin Research Center, CPPW, a Unit of Johnson & Johnson Consumer Companies, Skillman, New Jersey, USA – sequence: 2 givenname: Simarna surname: Kaur fullname: Kaur, Simarna organization: Preclinical Pharmacology, Johnson & Johnson Skin Research Center, CPPW, a Unit of Johnson & Johnson Consumer Companies, Skillman, New Jersey, USA – sequence: 3 givenname: Eduardo surname: Ruvolo fullname: Ruvolo, Eduardo organization: Measurement Sciences, Johnson & Johnson Skin Research Center, CPPW, a Unit of Johnson & Johnson Consumer Companies, Skillman, New Jersey, USA – sequence: 4 givenname: Nikiforos surname: Kollias fullname: Kollias, Nikiforos organization: Measurement Sciences, Johnson & Johnson Skin Research Center, CPPW, a Unit of Johnson & Johnson Consumer Companies, Skillman, New Jersey, USA – sequence: 5 givenname: Michael D. surname: Southall fullname: Southall, Michael D. email: msoutha@its.jnj.com organization: Preclinical Pharmacology, Johnson & Johnson Skin Research Center, CPPW, a Unit of Johnson & Johnson Consumer Companies, Skillman, New Jersey, USA |
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ContentType | Journal Article |
Copyright | 2012 The Society for Investigative Dermatology, Inc 2015 INIST-CNRS Copyright Nature Publishing Group Jul 2012 |
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publication-title: J Invest Dermatol doi: 10.1038/jid.2010.95 – reference: 22695285 - J Invest Dermatol. 2012 Jul;132(7):1756-7 |
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Snippet | Daily skin exposure to solar radiation causes cells to produce reactive oxygen species (ROS), which are a primary factor in skin damage. Although the... |
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SubjectTerms | Antioxidants - pharmacology Biological and medical sciences Cells, Cultured Cytokines - biosynthesis Dermatology Extracellular Signal-Regulated MAP Kinases - physiology Humans Light Luminescent Measurements Matrix Metalloproteinases - biosynthesis Medical sciences Pyrimidine Dimers - biosynthesis Reactive Oxygen Species - metabolism Receptor, Epidermal Growth Factor - physiology Signal Transduction - radiation effects Skin - metabolism Skin - radiation effects Ultraviolet Rays |
Title | Irradiation of Skin with Visible Light Induces Reactive Oxygen Species and Matrix-Degrading Enzymes |
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