1. ¹Faculty of Veterinary Science, University of Sydney, Sydney, New South Wales, Australia
2. ²Laboratory of Radiation Biology, Graduate School of Nutritional and Environmental Sciences, University of Shizuoka, Shizuoka, Japan
3. ³Department of Physiology, University of Sydney, Sydney, New South Wales, Australia

Correspondence: Dr Vivienne E. Reeve, Faculty of Veterinary Science, McMaster Building B14, University of Sydney, Sydney, New South Wales 2006, Australia. E-mail: v.reeve@vetp.usyd.edu.au

Received 17 July 2006; Revised 11 January 2007; Accepted 31 January 2007; Published online 3 May 2007.

Abstract

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.