Sousa C, Mazière C, Melo T S, Vincent-Fiquet O, Rogez J C, Santus R, Mazière J C
Centro de Quimica Fisica Molecular, Instituto Superior Técnico, Lisboa, Portugal.
Cancer Lett. 1998 Jun 19;128(2):177-82. doi: 10.1016/s0304-3835(98)00069-x.
Pretreatment of EMT-6 murine tumor cells for 24 h with 10(-4) M 8-methoxypsoralen (8-MOP) increased the photocytotoxicity of Photofrin II (P2) after cell exposure to low doses (1-1.5 J/cm2) of UVA by two- to three-fold. 8-MOP alone had no cytotoxic action under these experimental conditions and did not significantly change the amount of P2 recovered in cells. 8-MOP enhanced the lipid peroxidation end product formation measured as thiobarbituric acid reactive substances (TBARS) during cell photosensitization by P2. The psoralen alone also slightly increased the TBARS level after UVA exposure. These results suggest that 8-MOP, albeit non-photocytotoxic by itself under our experimental conditions, could enhance the efficiency of P2 by increasing cellular lipid peroxidation following light exposure.
用10(-4)M 8-甲氧基补骨脂素(8-MOP)对EMT-6小鼠肿瘤细胞进行24小时预处理,可使细胞在暴露于低剂量(1-1.5 J/cm2)紫外线A(UVA)后,光卟啉II(P2)的光细胞毒性提高两到三倍。在这些实验条件下,单独使用8-MOP没有细胞毒性作用,也没有显著改变细胞中回收的P2量。8-MOP增强了在P2细胞光敏化过程中以硫代巴比妥酸反应性物质(TBARS)衡量的脂质过氧化终产物的形成。单独使用补骨脂素在紫外线A照射后也会使TBARS水平略有升高。这些结果表明,尽管在我们的实验条件下8-MOP本身没有光细胞毒性,但它可以通过增加光照后细胞的脂质过氧化来提高P2的效率。