Ultraviolet exposure of thymocytes: selective inhibition of apoptosis

Purpose: To evaluate selective effects of ultraviolet (UV) irradiation on spontaneous and induced apoptosis in freshly extracted mice thymocytes. Materials and methods: Cells were exposed to UV radiation with emission peaks of 365 nm (UVA) exposures of 1620-10 200 J m^-2, of 312 nm (UVB) exposures of 34-1620 J m^-2 or of 254 nm (UVC) exposures of 1.5-1620 J m^-2, and incubated for 5.5 h with or without hydrocortisone, phorbol-12-myristate-13-acetate or anti-Fas antibody. Additionally, cells were irradiated with gamma-rays (5 Gy) before UVB exposure (408 J m^-2) at different times. Apoptosis was quantified by DNA fragmentation. Results: Up to an irradiation of 5000 J m^-2, UVA exposure did not show any effect on thymocyte apoptosis, while at 10 200 J m^-2 irradiation, considerable DNA fragmentation was observed. In contrast, UVB and UVC irradiation clearly inhibited natural and cortisoneinduced apoptosis. Moreover, UVB inhibited apoptosis triggered by phorbol-12-myristate-13acetate and gamma-irradiation, but not by anti-Fas antibody. Conclusions: The response of mouse thymocytes in culture to UV irradiation strongly depends on the wavelength used. It is suggested that either a survival or an apoptotic pathway occurs depending on the physiological state of the cell, spectral composition of the UV light and cell type. The possible involvement of extracellular signal-regulated kinase and stress-activated protein kinase/c-Jun N-terminal kinase in the apoptotic pathway is discussed.