Archives of Dermatological Research

, Volume 300, Supplement 1, pp 43–50

Melanin mediated apoptosis of epidermal cells damaged by ultraviolet radiation: factors influencing the incidence of skin cancer

  • Yuji Yamaguchi
  • Janusz Z. Beer
  • Vincent J. Hearing
Original Paper

DOI: 10.1007/s00403-007-0807-0

Cite this article as:
Yamaguchi, Y., Beer, J.Z. & Hearing, V.J. Arch Dermatol Res (2008) 300(Suppl 1): 43. doi:10.1007/s00403-007-0807-0


Ultraviolet (UV)-induced skin cancers, including melanomas and basal/squamous cell carcinomas, occur more frequently in individuals with fair skin than in those with dark skin. Melanin plays an important role in protecting the skin against UV radiation and levels of melanin correlate inversely with amounts of DNA damage induced by UV in human skin of different racial/ethnic groups. The objectives of this study are to review recent progress in our understanding of mechanisms underlying differences in cancer incidence in skins of different colors, particularly between Black and White skin. More specifically, we review DNA damage and apoptosis in various types of skin before and after exposure to UV in our human study protocols using a single UV dose, either one minimal erythema dose (MED) or a similar low dose of 180–200 J/m2. Our data and other published reports indicate that several major mechanisms underlie the increased rates of photocarcinogenesis in fair/light skin. First, UV-induced DNA damage in the lower epidermis (including keratinocyte stem cells and melanocytes) is more effectively prevented in darker skin. Second, rates of repair of DNA damage can differ significantly in individuals. Third, UV-induced apoptosis to remove potentially precancerous cells is significantly greater in darker skin. These results suggest that pigmented epidermis is an efficient UV filter and that UV damaged cells are removed more efficiently in darker skin. The combination of decreased DNA damage and more efficient removal of UV-damaged cells may play a critical role in the decreased photocarcinogenesis seen in individuals with darker skin.


Apoptosis UV Photocarcinogenesis Melanin DNA repair 



(6-4) Photoproducts


Cyclobutane pyrimidine dimers


Melanocortin 1 receptor


Minimal erythema dose


Microphthalmia transcription factor


Protease activated receptor-2


Propidium iodide


TdT-mediated dUTP nick end labeling



Copyright information

© Springer-Verlag 2007

Authors and Affiliations

  • Yuji Yamaguchi
    • 1
    • 2
    • 3
  • Janusz Z. Beer
    • 4
  • Vincent J. Hearing
    • 1
  1. 1.Pigment Cell Research Section, Laboratory of Cell BiologyNational Cancer Institute, National Institutes of HealthBethesdaUSA
  2. 2.Department of DermatologyOsaka University Graduate School of MedicineOsakaJapan
  3. 3.Department of Geriatric and Environmental DermatologyNagoya City University Graduate School of Medical SciencesAichiJapan
  4. 4.Center for Devices and Radiological HealthFood and Drug AdministrationRockvilleUSA

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