The deceptive nature of UVA tanning versus the modest protective effects of UVB tanning on human skin
Open accessAbstract
Summary: The relationship between human skin pigmentation and protection from ultraviolet (UV) radiation is an important element underlying differences in skin carcinogenesis rates. The association between UV damage and the risk of skin cancer is clear, yet a strategic balance in exposure to UV needs to be met. Dark skin is protected from UV‐induced DNA damage significantly more than light skin owing to the constitutively higher pigmentation, but an as yet unresolved and important question is what photoprotective benefit, if any, is afforded by facultative pigmentation (i.e. a tan induced by UV exposure). To address that and to compare the effects of various wavelengths of UV, we repetitively exposed human skin to suberythemal doses of UVA and/or UVB over 2 weeks after which a challenge dose of UVA and UVB was given. Although visual skin pigmentation (tanning) elicited by different UV exposure protocols was similar, the melanin content and UV‐protective effects against DNA damage in UVB‐tanned skin (but not in UVA‐tanned skin) were significantly higher. UVA‐induced tans seem to result from the photooxidation of existing melanin and its precursors with some redistribution of pigment granules, while UVB stimulates melanocytes to up‐regulate melanin synthesis and increases pigmentation coverage, effects that are synergistically stimulated in UVA and UVB‐exposed skin. Thus, UVA tanning contributes essentially no photoprotection, although all types of UV‐induced tanning result in DNA and cellular damage, which can eventually lead to photocarcinogenesis.
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UVB is more cytotoxic than UVA, causing direct DNA damage through CPDs or 6,4-photoproducts that induce mutagenesis and skin cancers.
“Although UVB accounts for approximately 6% of all UVR that reaches the earth's surface, it is more cytotoxic than UVA, causing direct DNA damage through photon absorption in the form of cyclobutane pyrimidine dimers (CPDs) or 6,4-photoproducts that eventually induce mutagenesis and skin cancers [7, 8].”
From Sunscreens and Photoaging: A Review of Current Literature (2021) · cites this paper as [7]
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- Authors
- Miyamura, Y., Coelho, S. G., Schlenz, K., Batzer, J., Smuda, C., Choi, W., Brenner, M., Passeron, T., Zhang, G., Kolbe, L., Wolber, R., & Hearing, V. J.
- Affiliations
- National Cancer Institute (US)
- Beiersdorf (Germany) (DE)
- National Institute of Biomedical Imaging and Bioengineering (US)
- Corresponding author
- Hearing, Vincent J.
- Venue
- Pigment Cell & Melanoma Research
- Publisher
- Wiley
- Published
- 2010-10-06
- Volume
- 24
- Issue
- 1
- Pages
- 136-147
- ISSN
- 1755-1471 (ISSN-L)
- 1755-148X
- PMC
- PMC3021652
- OpenAlex
- W2171991822
- Cited by
- 140
- References
- 66
- Citations by year
- 2026: 7 · 2025: 8 · 2024: 13 · 2023: 7 · 2022: 9 · 2021: 10 · 2020: 8 · 2019: 8 · 2018: 6 · 2017: 11 · 2016: 8 · 2015: 9 · 2014: 9 · 2013: 11 · 2012: 9
- FWCI
- 10.06
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Pigment Cell & Melanoma Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (ZIABC010784)
- Topics
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › melanin and skin pigmentation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
- Keywords
- photoprotection, melanin, melanocyte stimulation, DNA damage, skin pigmentation, photocarcinogenesis, skin cancer risk, melanogenesis
- MeSH terms
- DNA Damage, Humans, Melanins, Pyrimidine Dimers, Skin, Skin Pigmentation, Ultraviolet Rays, Skin, Artificial, Protective Agents, Sunbathing
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