The present study was undertaken to explore the possible causes of ultraviolet radiation (UVR)-induced disappearance of ATPase-positive, epidermal Langerhans cells (LC). Monodelphis domestica was used because it has the capacity for photoreactivation of UVR-induced pyrimidine dimers in epidermal DNA. Single, 330 J/m2 (ears) or 500 J/m2 (back) UVR exposures (FS-40 sunlamps) reduced the numbers of ATPase-positive epidermal LC in M. domestica ears to approximately 15% of those in unirradiated ears and approximately 37% of those in unirradiated dorsal skin. Immediate 90-minute exposures to photoreactivating light (PRL, 320-400 nm) post-UVR reversed the effects of UVR, resulting in ATPase-positive LC numbers not being significantly different from controls. Exposure to PRL immediately preceeding UVR did not prevent ATPase-positive LC disappearance. The photoreactivation of UVR-induced ATPase-positive LC disappearance indicates that DNA damage (pyrimidine dimers) is involved in the loss of ATPase-positive LC.
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The present study was undertaken to explore the possible causes of ultraviolet radiation (UVR)-induced disappearance of ATPase-positive, epidermal Langerhans cells (LC). Monodelphis domestica was used because it has the capacity for photoreactivation of UVR-induced pyrimidine dimers in epidermal DNA. Single, 330 J/m2 (ears) or 500 J/m2 (back) UVR exposures (FS-40 sunlamps) reduced the numbers of ATPase-positive epidermal LC in M.
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