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Dermal Damage Promoted by Repeated Low-Level UV-A1 Exposure Despite Tanning Response in Human Skin
Author(s) -
Frank Wang,
N. Smith,
Bao Anh Patrick Tran,
Sewon Kang,
John J. Voorhees,
Gary J. Fisher
Publication year - 2013
Publication title -
jama dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.128
H-Index - 166
eISSN - 2168-6084
pISSN - 2168-6068
DOI - 10.1001/jamadermatol.2013.8417
Subject(s) - irradiation , dermis , human skin , medicine , photoaging , matrix metalloproteinase , skin aging , melanin , epidermis (zoology) , skin cancer , dermatology , pathology , chemistry , anatomy , biochemistry , biology , cancer , physics , nuclear physics , genetics
Solar UV irradiation causes photoaging, characterized by fragmentation and reduced production of type I collagen fibrils that provide strength to skin. Exposure to UV-B irradiation (280-320 nm) causes these changes by inducing matrix metalloproteinase 1 and suppressing type I collagen synthesis. The role of UV-A irradiation (320-400 nm) in promoting similar molecular alterations is less clear yet important to consider because it is 10 to 100 times more abundant in natural sunlight than UV-B irradiation and penetrates deeper into the dermis than UV-B irradiation. Most (approximately 75%) of solar UV-A irradiation is composed of UV-A1 irradiation (340-400 nm), which is also the primary component of tanning beds.

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