Repeated ultraviolet exposure affords the same protection against DNA photodamage and erythema in human skin types II and IV but is associated with faster DNA repair in skin type IV
Open accessAbstract
We have investigated the photoprotective properties of induced pigmentation using erythema and epidermal DNA photodamage as endpoints. Previously unexposed buttock skin of 12 young, healthy adults (six skin type II and six skin type IV) was exposed daily (Monday to Friday) for 2 wk (days 1-12) with 0.65 minimal erythema dose of solar simulated radiation. Mean skin type IV minimal erythema dose was 1.8-fold greater than for skin type II. Compared to skin type II, solar simulated radiation treatments produced less erythema and more tanning in skin type IV. To assess DNA photodamage, biopsies were taken and prepared for paraffin sections that were stained with a monoclonal antibody for thymine dimers. Thymine dimers were quantified by image analysis. The single exposure data (0.65 and 2 minimal erythema dose) showed that DNA damage was related to physical dose (J per cm2) independent of skin type. Our data also showed that DNA photodamage accumulates in both skin types with repeated, suberythemal doses of solar simulated radiation. On day 12, there were more thymine dimers in skin type IV than skin type II, again indicating that physical rather than biologic dose determines the level of DNA damage. Comparisons on days 12 and 19, however, showed a much greater loss of thymine dimers in skin type IV, suggesting better thymine dimer repair. Protection factors for erythema and thymine dimers were calculated and shown to be about 2 in both skin types. This provides further indirect evidence that DNA is a chromophore for erythema, but also suggests that a tan may not be the major factor in natural photoprotection.
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Eumelanin in darker skin types plays a key role in reducing UV-induced DNA damage in keratinocytes.
“Consequently, eumelanin in darker skin types plays a key role in reducing UV-induced DNA damage in keratinocytes [24,26].”
From A Comprehensive Review of the Role of UV Radiation in Photoaging Processes Between Different Types of Skin (2025) · cites this paper as [24]
The study reports modest protection against UV-induced epidermal DNA damage after repeated exposure, but finds similar protection in skin types II and IV. Its Discussion (pp. 825–829) says that protection does not seem to be related to tanning per se and suggests faster DNA repair in type IV. It does not establish that eumelanin plays a key role in reducing keratinocyte DNA damage. (LLM, conf=0.84)
Experimental — accuracy not yet measuredDNA damage repair mechanisms are more effective in skin of color than in lighter skin types.
“Furthermore, studies have shown that DNA damage repair mechanisms are more effective in skin of color than in lighter skin types [24].”
From A Comprehensive Review of the Role of UV Radiation in Photoaging Processes Between Different Types of Skin (2025) · cites this paper as [24]
The Results and Discussion (pp. 825–829) report faster loss of UV-induced DNA lesions in skin type IV than type II during the week after repeated exposure, which the authors interpret as suggesting greater repair in type IV. The claim generalizes that finding to skin of color versus lighter skin types overall, without the study’s exposure condition or its qualification that greater repair is inferred. (LLM, conf=0.85)
Experimental — accuracy not yet measuredCumulative photodamage in dark skin is evidenced by fine lines, sagging skin, and irregular pigmentation.
“This is evidenced by fine lines, sagging skin, and irregular pigmentation.”
From A Comprehensive Review of the Role of UV Radiation in Photoaging Processes Between Different Types of Skin (2025) · cites this paper as [24]
The opening summary (p. 825) reports that DNA photodamage accumulated in skin type IV after repeated UV exposure. It does not identify fine lines, sagging skin, or irregular pigmentation as signs of that damage; the study measured thymine dimers, erythema, and tanning instead. (LLM, conf=0.85)
Experimental — accuracy not yet measuredTanning affords only moderate protection against cellular damage from UVR and appears to be triggered by signals from UVR-damaged DNA.
“Tanning affords only moderate protection against cellular damage from UVR (74,75) and, in fact, appears to be triggered by signals from UVR-damaged DNA.”
From Human skin pigmentation as an adaptation to UV radiation (2010) · cites this paper as [75]
Although dark skin gains certain advantages from the protective effects of melanin, it is not invulnerable to the costs of UV radiation; persistent sun exposure can cause cumulative photodamage.
“Although dark skin gains certain advantages from the protective effects of melanin, it is not invulnerable to the costs of UV radiation. Persistent sun exposure can nevertheless cause cumulative photodamage [24,29].”
From A Comprehensive Review of the Role of UV Radiation in Photoaging Processes Between Different Types of Skin (2025) · cites this paper as [24]
DNA strand breaks caused by UVA were observed more frequently in individuals with lighter skin.
“Additionally, DNA strand breaks caused by UVA were observed more frequently in individuals with lighter skin [19,24].”
From A Comprehensive Review of the Role of UV Radiation in Photoaging Processes Between Different Types of Skin (2025) · cites this paper as [24]
The Materials and Methods describe solar-simulated radiation exposure, and Figure 3 reports thymine-dimer damage by skin type; neither addresses UVA-induced DNA strand breaks. The claim’s specific lesion and exposure cannot be verified from this paper (page numbers unavailable in our copy). (LLM, conf=0.76)
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“Additionally, DNA strand breaks caused by UVA were observed more frequently in individuals with lighter skin [19,24].”
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- Authors
- Cragg, N., Chadwick, C. A., Potten, C. S., Sheehan, J. M., & Young, A. R.
- Affiliations
- Cancer Research UK Manchester Institute (GB)
- St Thomas' Hospital (GB)
- Corresponding author
- Sheehan, John M.
- Venue
- Journal of Investigative Dermatology
- Publisher
- Elsevier BV
- Published
- 2002-05
- Volume
- 118
- Issue
- 5
- Pages
- 825-829
- ISSN
- 0022-202X (ISSN-L)
- OpenAlex
- W2044750930
- Cited by
- 140
- References
- 36
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 3 · 2023: 3 · 2022: 5 · 2021: 1 · 2020: 6 · 2019: 2 · 2018: 9 · 2017: 6 · 2016: 11 · 2014: 8 · 2013: 4 · 2012: 6
- FWCI
- 8.03
- 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
- European Commission (ENV4-CT97, ENV4-CT97-0556)
- 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 › DNA Repair Mechanisms
- Keywords
- photoprotection, DNA photodamage, thymine dimers, DNA repair, erythema, skin type, tanning, simulated solar radiation, protection factor, UV-induced pigmentation
- MeSH terms
- DNA Damage, DNA Repair, Epidermis, Erythema, Humans, Melanins, Pyrimidine Dimers, Skin Pigmentation, Ultraviolet Rays
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