UVA1 induces cyclobutane pyrimidine dimers but not 6-4 photoproducts in human skin in vivo
Open accessAbstract
UVB readily induces cyclobutane pyrimidine dimers, mainly thymine dimers (TTs), and pyrimidine (6-4) pyrimidone photoproducts (6-4PPs) in DNA. These lesions result in "UVB signature mutations" found in skin cancers. We have investigated the induction of TTs and 6-4PPs in human skin in vivo by broadband UVA1, and have compared this with comparable erythemal doses of monochromatic UVB (300 nm). In vitro and ex vivo studies have shown the production of TTs, without 6-4PPs, by UVA1. We show that UVA1 induces TTs, without 6-4PPs, in the epidermis of healthy volunteers in vivo, whereas UVB induced both photoproducts. UVB induced more TTs than UVA1 for the same level of erythema. The level of UVA1-induced TTs increased with epidermal depth in contrast to a decrease that was seen with UVB. UVA1- and UVB-induced TTs were repaired in epidermal cells at a similar rate. The mechanism by which UVA1 induces TTs is unknown, but a lack of intra-individual correlation between our subjects' UVB and UVA1 minimal erythema doses implies that UVA1 and UVB erythema occur by different mechanisms. Our data suggest that UVA1 may be more carcinogenic than has previously been thought.
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Psoralen photosensitization causes an alteration in the expression of cytokines and cytokine receptors.
“Psoralen photosensitization also causes an alteration in the expression of cytokines and cytokine receptors [111].”
From Molecular Mechanisms of UV-Induced Apoptosis and Its Effects on Skin Residential Cells: The Implication in UV-Based Phototherapy (2013) · cites this paper as [111]
The Discussion addresses UVA1-induced DNA lesions, not cytokine or cytokine-receptor expression. Searches for psoralen photosensitization, cytokines, and PUVA found no passage in our copy supporting the attributed claim; PUVA appears only in a reference about erythema and pigmentation. (LLM, conf=0.76)
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- Authors
- Tewari, A., Sarkany, R. P., & Young, A. R.
- Affiliations
- King's College London (GB)
- Corresponding author
- Tewari, Angela
- Venue
- Journal of Investigative Dermatology
- Publisher
- Elsevier BV
- Published
- 2012-02
- Volume
- 132
- Issue
- 2
- Pages
- 394-400
- ISSN
- 0022-202X (ISSN-L)
- OpenAlex
- W2155554906
- Cited by
- 141
- References
- 8
- Citations by year
- 2026: 6 · 2025: 2 · 2024: 6 · 2023: 8 · 2022: 6 · 2021: 8 · 2020: 9 · 2019: 11 · 2018: 12 · 2017: 11 · 2016: 11 · 2015: 13 · 2014: 9 · 2013: 16 · 2012: 10
- FWCI
- 16.25
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of Investigative Dermatology (publishedVersion)
- PubMed (publishedVersion)
- Research Portal (King's College London) (submittedVersion)
- Funders
- King's College Hospital NHS Foundation Trust
- National Institute for Health and Care Research
- British Skin Foundation
- King's College London
- Medical Research Council
- Topics
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
- Keywords
- UVA1, UV-B radiation, cyclobutane pyrimidine dimers, thymine dimers, 6-4 photoproducts, DNA photoproducts, human skin, epidermis, minimal erythema dose, DNA repair
- MeSH terms
- DNA Repair, Dose-Response Relationship, Radiation, Erythema, Humans, Neoplasms, Radiation-Induced, Pyrimidine Dimers, Skin, Skin Neoplasms, Ultraviolet Rays
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