Radiation sources providing increased UVA/UVB ratios attenuate the apoptotic effects of the UVB waveband UVA-dose-dependently in hairless mouse skin

J Invest Dermatol. 2007 Sep;127(9):2236-44. doi: 10.1038/sj.jid.5700856. Epub 2007 May 3.


UV radiation-induced epidermal apoptotic sunburn cells provide a mechanism for eliminating cells with irreparable DNA damage. The UVB (290-320 nm) waveband is mainly responsible, but the role of UVA (320-400 nm) is less clear, and possible waveband interactions have not been examined. Recent studies in mice reveal a protective role for UVA against UVB-induced inflammation and immunosuppression, mediated via cutaneous heme oxygenase (HO). As HO has antiapoptotic properties in other tissues, this study examines the effect of UVA/UVB waveband interaction on apoptosis in the Skh:hr-1 hairless mouse epidermis. Apoptosis was assessed by sunburn cell number, caspase-3-positive cell number, and degree of DNA fragmentation, in mice exposed to radiation sources providing a constant UVB dose with increasing proportions of UVA. The results indicated that as the UVA/UVB ratio was increased, both the sunburn cell and caspase-3-positive cell number decreased, and the degree of DNA fragmentation was reduced. Treatment of mice with the HO inhibitor, tin protoporphyrin-IX, markedly reduced the UVA antiapoptotic effect, confirming a major role for HO. The observations suggest that UVA reduces UVB-induced DNA damage, and may therefore have anti-photocarcinogenic properties that could be harnessed for better photoprotection in humans.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis*
  • Carcinogens / chemistry
  • Caspase 3 / metabolism
  • DNA Damage
  • DNA Fragmentation
  • Dose-Response Relationship, Drug
  • Enzyme Inhibitors / pharmacology
  • Epidermis / metabolism
  • Female
  • Heme Oxygenase (Decyclizing) / metabolism
  • Mice
  • Skin / metabolism*
  • Skin / radiation effects*
  • Sunburn
  • Ultraviolet Rays


  • Carcinogens
  • Enzyme Inhibitors
  • Heme Oxygenase (Decyclizing)
  • Caspase 3