Ley R D, Applegate L A, Fry R J, Sanchez A B
Center for Photomedicine, Lovelace Medical Foundation, Albuquerque, New Mexico 87108.
Cancer Res. 1991 Dec 15;51(24):6539-42.
Chronic exposure of the opossum Monodelphis domestica to UV radiation (UVR) leads to the formation of cutaneous and corneal tumors. Groups of shaved opossums were exposed 3 times/week to: (a) UVR alone; (b) UVR followed immediately by 1 h of photoreactivating light (PRL) (320-700 nm); (c) 1 h of PRL followed by UVR; and (d) 1 h of PRL alone. Exposures were terminated after 70 weeks of treatment. Analysis of data plotted as probability of tumor formation versus weeks from first exposure shows that post-UVR exposure to PRL significantly (P less than 0.005) delayed the time to appearance of cutaneous tumors from a 50% probability of tumor formation at 73 weeks for those animals exposed to UVR alone to 128 weeks for those animals exposed to PRL after UVR. Pre-UVR exposure to PRL delayed the appearance of tumors by 6 weeks when compared to the UVR alone group, but the difference between the two groups was not statistically significant. The yield (number of tumors/surviving animal) of cutaneous tumors at 70 and 110 weeks following initiation of treatments also was significantly less in those animals exposed to PRL after, but not before, UVR. Based on the specificity of the PR repair pathway to act only on pyrimidine dimers, these results suggest that dimers are involved in the induction of cutaneous tumors. The results obtained with the induction of corneal tumors are more difficult to interpret. While exposure to PRL significantly delayed the appearance of corneal tumors, the magnitude of the effect was the same regardless of whether the PRL was given before or after each UVR exposure.
将负鼠(Monodelphis domestica)长期暴露于紫外线辐射(UVR)会导致皮肤和角膜肿瘤的形成。将几组剃毛的负鼠每周暴露3次,分别接受以下处理:(a)仅紫外线辐射;(b)紫外线辐射后立即照射1小时光复活光(PRL)(320 - 700纳米);(c)先照射1小时PRL,然后再进行紫外线辐射;(d)仅照射1小时PRL。处理70周后终止暴露。将肿瘤形成概率与首次暴露后的周数绘制数据进行分析表明,紫外线辐射后暴露于PRL显著(P小于0.005)延迟了皮肤肿瘤出现的时间,对于仅接受紫外线辐射的动物,在73周时肿瘤形成概率达到50%,而对于紫外线辐射后接受PRL的动物,这一概率出现的时间延迟至128周。与仅接受紫外线辐射的组相比,紫外线辐射前暴露于PRL使肿瘤出现时间延迟了6周,但两组之间的差异无统计学意义。在开始处理后70周和110周时,紫外线辐射后(而非之前)接受PRL的动物皮肤肿瘤的发生率(肿瘤数量/存活动物数)也显著较低。基于PR修复途径仅作用于嘧啶二聚体的特异性,这些结果表明二聚体参与了皮肤肿瘤的诱导过程。关于角膜肿瘤诱导所获得的结果更难解释。虽然暴露于PRL显著延迟了角膜肿瘤的出现,但无论在每次紫外线辐射之前还是之后给予PRL,其效果大小相同。