Bech-Thomsen N, Poulsen T, Christensen F G, Lundgren K, Wulf H C
Department of Dermatology, Copenhagen University Hospital, Denmark.
J Photochem Photobiol B. 1994 Feb;22(2):119-23. doi: 10.1016/1011-1344(93)06956-4.
The effect of UVA radiation (321-400 nm) on UVB photocarcinogenesis was examined in lightly pigmented hairless hr/hr C3H/Tif mice. Five groups of 22 mice were exposed to UVB radiation (281-320 nm) from one Philips 12 tube for 10 min per day and 4 days per week. Four of the groups were simultaneously exposed to UVA from two to six filtered Philips 09 tubes. The daily dose of UVB was 2.0 kJ m-2 in all five groups; the UVA2 (321-340 nm) dose varied from 0.7 to 4.5 kJ m-2 and the UVA1 (341-400 nm) dose from 0.3 to 45.6 kJ m-2. A sixth group was exclusively irradiated with the filtered UVA tubes and served as a control. Skin tumor development was not significantly different for the groups exposed to the UVB source alone or the UVB source in combination with the largest daily UVA dose (0.2 > p > 0.1). Skin tumor development was significantly delayed in the other groups irradiated with the UVB source and the lower doses of UVA (p < 0.001). No tumors were observed in the control group. This study suggests that UVA1 radiation delays UVB-induced skin tumor development. However, the delay cannot be expected to persist when UVA is administered in higher daily doses.
在浅色无毛hr/hr C3H/Tif小鼠中研究了UVA辐射(321 - 400纳米)对UVB光致癌作用的影响。将五组每组22只小鼠暴露于来自一根飞利浦12管的UVB辐射(281 - 320纳米)下,每天照射10分钟,每周照射4天。其中四组同时暴露于来自两到六根经过滤的飞利浦09管的UVA下。所有五组的UVB日剂量均为2.0 kJ m-2;UVA2(321 - 340纳米)剂量从0.7到4.5 kJ m-2不等,UVA1(341 - 400纳米)剂量从0.3到45.6 kJ m-2不等。第六组仅用经过滤的UVA管照射,作为对照组。单独暴露于UVB源或暴露于UVB源并结合最大日UVA剂量的组之间,皮肤肿瘤的发生没有显著差异(0.2 > p > 0.1)。在用UVB源和较低剂量UVA照射的其他组中,皮肤肿瘤的发生明显延迟(p < 0.001)。对照组未观察到肿瘤。这项研究表明,UVA1辐射会延迟UVB诱导的皮肤肿瘤发生。然而,当每天给予更高剂量的UVA时,这种延迟预计不会持续。