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Melanogenesis: a photoprotective response to DNA damage?
1St. John's Institute of Dermatology, Guy's, Kings and St. Thomas' School of Medicine, Kings College London, London, UK.
Mutation Research
|March 8, 2005
Summary
Tanning may indicate DNA repair capacity, not just melanin pigment, offering protection against skin cancer. This suggests pigmentation acts as a cellular response to UV damage.
Area of Science:
- Dermatology
- Genetics
- Photobiology
Background:
- Ultra violet radiation (UVR) exposure causes skin cancer and pigmentation.
- Skin pigmentation is traditionally considered photoprotective, with darker skin having lower photocarcinogenesis risk.
- The relationship between pigmentation and photoprotection is complex and requires further investigation.
Purpose of the Study:
- To investigate the complex relationship between skin pigmentation and photoprotection.
- To explore the role of DNA repair in UVR-induced melanogenesis.
- To re-evaluate the function of melanin in the context of skin cancer risk.
Main Methods:
- Review of existing research on UVR, skin pigmentation, DNA damage, and repair.
- Analysis of studies comparing DNA repair rates in different human skin types (e.g., type II vs. IV) after UVR exposure.
- Exploration of the hypothesis that tanning reflects inducible DNA repair capacity.
Main Results:
- Photoprotection against erythema and DNA damage can be independent of induced pigmentation levels in fair skin.
- UVR-induced DNA photodamage and its repair stimulate melanogenesis (tanning).
- Individuals with darker skin (type IV) exhibit faster DNA repair after repeated UVR exposure compared to fairer skin types (type II).
Conclusions:
- Tanning may serve as an indicator of inducible DNA repair capacity rather than solely pigment.
- Faster DNA repair in darker skin types could explain their lower skin cancer incidence.
- Epidermal pigmentation might function as a mammalian equivalent of a bacterial SOS response to DNA damage.