Lanks K W, Gao J P, Sharma T
Department of Pathology and Laboratory Medicine, Staten Island University Hospital, NY 10305.
Cancer Chemother Pharmacol. 1994;35(1):17-20. doi: 10.1007/BF00686279.
Argon ion laser irradiation at 514.1 nm and 488 nm dramatically increased doxorubicin cytotoxicity in an L929 cell clonogenic survival assay. The cytotoxicity was dependent on both the drug concentration and the total light energy delivered such that at 5 micrograms doxorubicin/ml and 800 J/cm2, cytotoxicity was enhanced by a factor of > 10(4) relative to that achieved with drug alone. Irradiation times in excess of 2 min and power densities in excess of 100 J/cm2 were required to produce the effect. Beyond this 2-min limit, cytotoxicity was not related to the duration of exposure if the total energy delivered was held constant. The ability of catalase and superoxide dismutase to abolish completely the increase in cytotoxicity produced by laser irradiation suggests that the cytotoxic mechanism may depend on the generation of active oxygen species by the photodynamically excited drug.
在L929细胞克隆形成存活试验中,514.1纳米和488纳米的氩离子激光照射显著增强了阿霉素的细胞毒性。细胞毒性取决于药物浓度和传递的总光能,因此在5微克阿霉素/毫升和800焦/平方厘米的条件下,相对于单独使用药物时,细胞毒性增强了10⁴倍以上。产生这种效应需要照射时间超过2分钟且功率密度超过100焦/平方厘米。超过这个2分钟的限制,如果传递的总能量保持恒定,细胞毒性与暴露持续时间无关。过氧化氢酶和超氧化物歧化酶完全消除激光照射产生的细胞毒性增加的能力表明,细胞毒性机制可能取决于光动力学激发药物产生活性氧。