Bech-Thomsen N, Wulf H C, Poulsen T, Lundgren K
Laboratory of Photobiology, Rigshospital, Copenhagen, Denmark.
Arch Dermatol. 1988 Aug;124(8):1215-8.
The carcinogenic effects of long-wave ultraviolet radiation (UV-A) (320 to 400 nm) irradiation followed by exposure to broad-spectrum ultraviolet (UV) irradiation were studied in 200 lightly pigmented, hairless, hr/hr C3H/Tif mice. No skin tumors were observed in the group irradiated with UV-A for four weeks (total dose, 4050 kJ/m2, observed for 57 weeks). Ultraviolet exposure induced skin tumors in a dose-dependent manner. In a group exposed to UV irradiation for 13 weeks, 35% of the mice had developed tumors after 57 weeks. Twenty-six weeks of exposure resulted in 88% of the animals being affected. In contrast it was found that treatment with UV-A irradiation (four weeks, total dose up to 4200 kJ/m2) preceding exposure to UV irradiation (13 or 26 weeks) resulted in a significantly delayed tumor development. Exposure with UV-A induced no visible changes of the skin, and subsequent microscopic examination revealed no measurable changes in epidermal thickness or melanin content. Our results suggest that, depending on the exposure schedule, UV-A in addition to previously reported carcinogenic properties also may act as an antitumor agent.
在200只浅色、无毛、hr/hr C3H/Tif小鼠中研究了长波紫外线辐射(UV-A)(320至400纳米)照射后再暴露于广谱紫外线(UV)照射的致癌作用。接受UV-A照射四周(总剂量4050 kJ/m²,观察57周)的组未观察到皮肤肿瘤。紫外线暴露以剂量依赖方式诱发皮肤肿瘤。在接受UV照射13周的组中,57周后35%的小鼠发生了肿瘤。暴露26周导致88%的动物受到影响。相比之下,发现先接受UV-A照射(四周,总剂量高达4200 kJ/m²)再接受UV照射(13周或26周)会显著延迟肿瘤发生。UV-A照射未引起皮肤可见变化,随后的显微镜检查显示表皮厚度或黑色素含量无明显变化。我们的结果表明,根据暴露方案,UV-A除了具有先前报道的致癌特性外,还可能作为一种抗肿瘤剂。