Ben-Hur E, Clay M E, Vicioso E F, Antunez A R, Rihter B D, Kenney M E, Oleinick N L
Nuclear Research Center-Negev, Beer-Sheva, Israel.
Photochem Photobiol. 1992 Feb;55(2):231-7. doi: 10.1111/j.1751-1097.1992.tb04232.x.
When a dilute F- solution was added to a culture of Chinese hamster cells that had been preincubated with an aluminium phthalocyanine sensitizer derived from AlPcCl, the photosensitivity of the cells was markedly reduced compared to control cells not treated with F-. Under the same treatment conditions, the reduction in [3H]thymidine incorporation into cellular DNA caused by light and this sensitizer and the production of DNA-protein crosslinks caused by light and this sensitizer were also inhibited by F-. In contrast, the killing of Chinese hamster cells, the reduction of thymidine incorporation by the cells, and the production of DNA-protein crosslinks in the cells caused by the combination of light and either Photofrin II or the silicon phthalocyanine HOSiPcOSi(CH3)2(CH2)3-N(CH3)2 were not inhibited by F-. We conclude that the aluminium phthalocyanine sensitizer used is largely or completely AlPc(OH)(H2O), that it is converted to a fluoro complex by F-, and that this compound probably is a less efficient generator of photochemical damage at a critical cellular target(s) than is AlPc(OH)(H2O). The inhibition of thymidine incorporation and DNA-protein crosslink formation indicates that the effects of F- can be expressed at intracellular sites. It is further concluded that the silicon phthalocyanine sensitizer and Photofrin II do not interact significantly with F-.
当向预先用由AlPcCl衍生的铝酞菁敏化剂孵育过的中国仓鼠细胞培养物中加入稀氟溶液时,与未用氟处理的对照细胞相比,细胞的光敏性显著降低。在相同处理条件下,氟也抑制了由光和该敏化剂引起的[³H]胸腺嘧啶核苷掺入细胞DNA的减少以及由光和该敏化剂引起的DNA-蛋白质交联的产生。相反,由光与二血卟啉醚或硅酞菁HOSiPcOSi(CH₃)₂(CH₂)₃-N(CH₃)₂组合引起的中国仓鼠细胞杀伤、细胞中胸腺嘧啶核苷掺入的减少以及细胞中DNA-蛋白质交联的产生不受氟的抑制。我们得出结论,所使用的铝酞菁敏化剂大部分或完全是AlPc(OH)(H₂O),它被氟转化为氟配合物,并且该化合物在关键细胞靶点处可能比AlPc(OH)(H₂O)产生光化学损伤的效率更低。胸腺嘧啶核苷掺入和DNA-蛋白质交联形成的抑制表明氟的作用可以在细胞内位点表现出来。进一步得出结论,硅酞菁敏化剂和二血卟啉醚与氟没有显著相互作用。