Bredberg A, Forsgren A
Br J Dermatol. 1984 Aug;111(2):159-68. doi: 10.1111/j.1365-2133.1984.tb04039.x.
Human polymorphonuclear and monomorphonuclear leukocytes (PMNL and MMNL) were exposed in vitro to 8-methoxypsoralen (8-MOP, 0.1-80 micrograms/ml) and/or UV-A radiation (0.03-2 J/cm2) and then analysed for the following functions: chemotaxis, bactericidal activity and proliferation in response to mitogen stimulation. The functions of PMNL became depressed only at a high PUVA dose level (about 20 micrograms/ml of 8-MOP plus 2 J/cm2 of UV-A), whereas with MMNL chemotaxis was inhibited at 1 microgram/ml of 8-MOP plus 2 J/cm2 of UV-A and lymphocyte proliferation was diminished at 0.1 microgram/ml plus 0.1 J/cm2. Since with the MMNL, as compared with the PMNL, a longer time period was present between PUVA exposure and analysis, and since no difference between these cell types in trypan blue exclusion could be seen, the relative sensitivity of the MMNL functions was taken as evidence of DNA damage being a mechanism for the observed PUVA-induced effects.
将人多形核白细胞和单核白细胞（PMNL和MMNL）在体外暴露于8-甲氧基补骨脂素（8-MOP，0.1 - 80微克/毫升）和/或UV-A辐射（0.03 - 2焦/平方厘米），然后分析以下功能：趋化性、杀菌活性以及对丝裂原刺激的增殖反应。仅在高PUVA剂量水平（约20微克/毫升的8-MOP加2焦/平方厘米的UV-A）时，PMNL的功能才会受到抑制，而对于MMNL，在1微克/毫升的8-MOP加2焦/平方厘米的UV-A时趋化性受到抑制，在0.1微克/毫升加0.1焦/平方厘米时淋巴细胞增殖减少。由于与PMNL相比，MMNL在PUVA暴露和分析之间存在更长的时间段，并且由于在台盼蓝排斥试验中未观察到这些细胞类型之间的差异，因此MMNL功能的相对敏感性被视为DNA损伤是所观察到的PUVA诱导效应的一种机制的证据。
