Ultraviolet B-induced cell death in four cutaneous cell lines exhibiting different enzymatic antioxidant defences: involvement of apoptosis

Reactive oxygen species (ROS) play a role in the modulation of apoptosis. Antioxidant defence mechanisms against cell death involving apoptosis due to WE irradiation were studied on three established cell lines (SCC derived from human skin squamous cell carcinoma, F-SV and F-ST derived from human skin fibroblasts) which were susceptible to cell death by UVB irradiation (12.5-250 mJ/cm(2)), and one cell line (N-F) derived from primary cultured human skin fibroblasts which was resistant to cell death. We compared antioxidant defences between the three established cell lines and N-F, measuring four antioxidant enzymes (superoxide dismutase (SOD), catalase, glutathione peroxidase (GSH-Px) and glutathione reductase (GR)) and a non-enzymatic antioxidant glutathione. The greatest difference was that Cu, Zn-SOD activity in N-F was 3-4-times the three other cell lines. Though SCC had much larger amounts of glutathione and higher antioxidant enzyme activities except for Cu, Zn-SOD than N-F, SCC was very susceptible to cell death. After UVB irradiation (at 16 h after 12.5 mJ/cm(2)), in all cell lines, SOD activity increased 1.1-1.3-times that of non-irradiated cells, while other enzyme activities remained constant. This presumably represents a protective response against ROS generated during WE irradiation. N-F which was resistant to UVB-induced cell death had higher Cu, Zn-SOD activity before UVB irradiation, and a larger increase of SOD (mainly Mn-SOD) after UVB exposure than the other cell lines which were susceptible to cell death. Therefore, we conclude that the most important enzymatic antioxidant to protect cells from WE damage is SOD. (C) 1998 Elsevier Science Ireland Ltd. All rights reserved.