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CHRONIC ULTRAVIOLET RADIATION‐INDUCED INCREASE IN SKIN IRON and THE PHOTOPROTECTIVE EFFECT OF TOPICALLY APPLIED IRON CHELATORS 1,*
Author(s) -
Bissett Donald L.,
Chatterjee Ranjit,
Han Daniel P.
Publication year - 1991
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.1991.tb02009.x
Subject(s) - hairless , chemistry , heme , reactive oxygen species , photochemistry , photosensitivity , in vivo , human skin , biophysics , oxygen , biochemistry , biology , enzyme , organic chemistry , physics , quantum mechanics , genetics , microbiology and biotechnology
Abstract In the skin of albino hairless mice (Skh:HR‐l) there is a basal level of non‐heme iron. Chronic exposure of mice to sub‐erythemal doses of ultraviolet (UV) B radiation results in an increased skin level of non‐heme iron. The iron increase may be the result of a UVB radiation‐induced increase in vascular permeability, which we measured in vivo with the dye marker Evans Blue. We also observed greater non‐heme iron in sun‐exposed vs non‐exposed body sites of human skin, suggesting that similar events occur in man. Iron may have a role in skin photodamage by participating in formation of reactive oxygen species. These species have been implicated in skin photodamage. It is known that iron can contribute to oxygen radical production by acting catalytically in the formation of species such as hydroxyl radical. While the basal level of skin iron may be available for catalysis, the elevated iron content of UV‐exposed skin increases the potential for iron‐catalyzed radical production. Topical application of certain iron chelators to Skh albino hairless mice dramatically delayed the onset of UVB radiation‐induced skin photodamage. Non‐chelating analogs provided no significant protection.