Kraemer K H, Waters H L
Natl Cancer Inst Monogr. 1984 Dec;66:221-3.
Photochemotherapy with oral 8-methoxypsoralen (8-MOP) plus long wavelength UV radiation (UVA) has been shown to affect lymphoid cells circulating through the skin. An in vitro assay was developed to mimic some of the therapeutic parameters of 8-MOP concentration and UVA exposure estimated to impinge upon lymphoid cells. In vitro treatment with these presumed therapeutic levels of 8-MOP plus UVA induced a level of inhibition of lymphoid cell DNA synthesis similar to that observed in vivo. Furthermore, the DNA synthesis inhibition was associated with DNA interstrand cross-link induction, reduced cell survival, and impaired immune reactivity. This assay predicts that such effects would be induced in vivo. A lymphoblastoid cell line from a patient with Cockayne's syndrome was shown to be hypersensitive to killing by radiation (280-320 nm) from a fluorescent sunlamp (UVB) but to have normal survival after treatment with 8-MOP plus UVA. Thus there is at least one major UVB recovery pathway in human cells that is different from the recovery pathway for 8-MOP plus UVA damage and leads us to believe that combined treatment with UVB and 8-MOP plus UVA may have a greater effect than either treatment alone.
口服8-甲氧基补骨脂素（8-MOP）加用长波紫外线辐射（UVA）进行光化学疗法已被证明会影响通过皮肤循环的淋巴细胞。开发了一种体外测定法，以模拟估计会作用于淋巴细胞的8-MOP浓度和UVA照射的一些治疗参数。用这些假定的8-MOP治疗水平加UVA进行体外处理，可诱导出与体内观察到的类似水平的淋巴细胞DNA合成抑制。此外，DNA合成抑制与DNA链间交联诱导、细胞存活率降低和免疫反应性受损有关。该测定法预测这些效应会在体内被诱导。来自科凯恩综合征患者的淋巴母细胞系对荧光太阳灯（UVB）发出的辐射（280 - 320纳米）杀伤高度敏感，但在用8-MOP加UVA处理后具有正常存活率。因此，人类细胞中至少存在一条主要的UVB修复途径，它与8-MOP加UVA损伤的修复途径不同，这使我们相信UVB与8-MOP加UVA联合治疗可能比单独任何一种治疗都有更大的效果。
