Dark cyclobutane pyrimidine dimers are formed in the epidermis of Fitzpatrick skin types I/II and VI in vivo after exposure to solar‐simulated radiation

Abstract

Introduction Unlike “light” cylobutane pyrimidine dimers (CPD) formed during ultraviolet radiation (UVR) exposure, dark CPD (dCPD) are formed afterwards. Studies have attributed this to delayed melanin sensitization. There are no data on the role of melanin in dCPD formation in human skin. Methods and Results Volunteers of Fitzpatrick skin types (FST I/II vs. VI) were exposed to erythemally equivalent doses of solar simulated radiation. CPD were assessed by semi‐quantitative immunostaining in whole epidermis and in three epidermal zones, and quantitative HPLC‐MS/MS (whole epidermis) at different times post‐exposure up to 24 hr. A CPD peak that appeared at 1–2 hr post‐exposure in whole epidermis measurements, in all skin types, demonstrated dCPD. However, both dCPD and light CPD were absent in the basal layer of FST VI with the greatest melanin concentration. Modelling the whole epidermis data showed no differences between the repair kinetics of FST I/II and VI. Discussion Melanin may be a sensitizer or “sunscreen” for dCPD depending on its location and concentration. Previous CPD repair studies in human skin have assumed peak CPD immediately after UVR exposure and so have overestimated total repair.

The photoprotective properties of α-tocopherol phosphate against long-wave UVA1 (385 nm) radiation in keratinocytes in vitro

“…Such CPD are formed after UVR exposure by a delayed reaction between DNA and reactive compounds, currently believed to be excited carbonyls 25,26 . Dark CPD have been reported in human skin in vivo after 385 nm 4 and SSR 27 , but their biological significance is unknown. Numerous limitations of α-T hinder its effectiveness in cosmeceutical products.…”

The Photoprotective Properties of α-Tocopherol Phosphate Against Long-Wave UVA1 (385 nm) Radiation in Keratinocytes in Vitro

“…Such CPD are formed after UVR exposure by a delayed reaction between DNA and reactive compounds, currently believed to be excited carbonyls 26,27 . Dark CPD have been reported in human skin in vivo after 385nm 4 and SSR 28 , but their biological signi cance is unknown.…”

CHAPTER 7. Ultraviolet-induced Formation of DNA Damage in Cells and their Mutational Consequences

“…On the average, protection factors of 20 and 70 against melanoma and carcinomas, respectively, were observed when skin of phototypes VI were compared to phototype II 153,154 . This was only partially explained by the decrease in the mean level of CPD in keratinocytes that was found to be only 10-times lower in skin of phototype VI compared to II following exposure to simulated sunlight or UVB 62,155 . The same values were observed for both immediate and dark CPDs 62 .…”

“…This pathway remains yet to be completely established in order to explain why C-containing dark CPDs are produced in significant amounts while photosensitized triplet-triplet energy transfer leads to the overwhelming formation of TT-CPD [59][60][61] . The biological relevance of this process was assessed by the observation of dark CPDs in human skin in vivo 62 . Their formation was observed even at the highest UVA wavelengths but not in the visible range 63 .…”

“…Their formation was observed even at the highest UVA wavelengths but not in the visible range 63 . An interesting phenomenon is the fast decrease in the peak of CPDs following exposure 56,57,62 64 . This strategy has been used for many years, with a first germicidal action spectra published as early as 1946 65 and confirmed since then by countless works.…”