Skin cancer is the most commonly occurring cancer in Ireland with non-melanoma skin cancer (basal and squamous cell carcinomas) accounting for 28% of all cancers recorded by the National Cancer Registry. Epidemiological evidence suggests that exposure to ultraviolet (UV) radiation is the main environmental carcinogen responsible for the formation of basal and squamous cell carcinomas. Most of the current literature on skin cancer research involves the use of broad band UVA, UVB or UVC radiation from non-solar type UV lamp sources and there are questions in the literature regarding the biological relevance of some of these lamps as they do not simulate the solar spectrum. In addition, much of the available data in the literature are somewhat conflicting because of the different UV wavelengths and doses used as well as the different cell models used. This research aims to reconcile these inconsistent results using environmentally relevant doses of solar simulated radiation. An immortalised human keratinocyte cell line, HaCaT was used for these studies. The HaCaT cells were exposed to radiation from a Q-Sun solar spectrum simulator at a range of biologically relevant doses. Following exposure, cell damage was measured using clonogenic assays and alamar blue assays which determine the colony forming ability and cell viability of the exposed cells respectively. Caspase activity, mitochondrial membrane potential and levels of reactive oxygen species (ROS) were also determined. Prior to exposure cross-calibration measurements were carried out between the Q-Sun and natural sunlight to ensure the Q-Sun’s output spectrum was biologically relevant and uniform throughout the test chamber. Transmission spectra of all glassware and plastics used during exposure were obtained to ensure that there was minimum loss of radiation to test cells during enclosed exposure. Q-Sun calibration and uniformity data is shown together with initial full spectrum dose response curves of the test cell line. HaCaT cells showed a significant reduction in survival following solar radiation. Significant caspase activity was also observed in addition to induction of ROS and a decrease in mitochondrial membrane potential. The effect on the dose response curve of exposure to selected UV wavebands is also shown. These results will aid in future work on the mechanisms of solar radiation induced apoptosis.
[Proc Amer Assoc Cancer Res, Volume 47, 2006]