International journal of radiation biology, 80(6), 445-450.
Ojeda, F., Guarda, M. I., Lovengreen, C., Hidalgo, M. A., Folch, H., Härtel, S., & Maldonado, C. (2004).
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 cortisone‐induced apoptosis. Moreover, UVB inhibited apoptosis triggered by phorbol‐12‐myristate‐13‐acetate 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.