LeVee G J, Applegate L A, Ley R D
Biomedical Research Division, Lovelace Medical Foundation, Albuquerque, New Mexico.
J Leukoc Biol. 1988 Dec;44(6):508-13. doi: 10.1002/jlb.44.6.508.
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.
本研究旨在探究紫外线辐射（UVR）导致三磷酸腺苷酶（ATPase）阳性的表皮朗格汉斯细胞（LC）消失的可能原因。选用家短尾负鼠（Monodelphis domestica）是因为其具有对UVR诱导的表皮DNA嘧啶二聚体进行光复活的能力。单次UVR照射（FS - 40型太阳灯），耳部为330 J/m²，背部为500 J/m²，可使家短尾负鼠耳部ATPase阳性的表皮LC数量降至未照射耳部的约15%，以及未照射背部皮肤的约37%。UVR照射后立即进行90分钟的光复活光（PRL，320 - 400 nm）照射可逆转UVR的影响，使得ATPase阳性LC数量与对照组无显著差异。在UVR照射之前立即进行PRL照射并不能防止ATPase阳性LC消失。UVR诱导的ATPase阳性LC消失的光复活表明DNA损伤（嘧啶二聚体）与ATPase阳性LC的丢失有关。
