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 inJournal of investigative dermatology Vol. 132; no. 7; pp. 1901 - 1907
Main Authors Liebel, Frank, Kaur, Simarna, Ruvolo, Eduardo, Kollias, Nikiforos, Southall, Michael D.
Format Journal Article
LanguageEnglish
Published New York, NY Elsevier Inc 01.07.2012
Nature Publishing Group
Elsevier Limited
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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.
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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Dermatology
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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
URI https://dx.doi.org/10.1038/jid.2011.476
https://www.ncbi.nlm.nih.gov/pubmed/22318388
https://www.proquest.com/docview/1020298956
https://www.proquest.com/docview/1020834531
Volume 132
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