Winther J
Danish Cancer Society, Department of Experimental Clinical Oncology, Radiumstationen, Aarhus, Denmark.
Br J Cancer. 1989 Jun;59(6):869-72. doi: 10.1038/bjc.1989.184.
Cell survival was investigated in an intraocular retinoblastoma-like tumour 30 min to 48 h after photodynamic therapy. The survival of the cells was assessed by an in vivo to in vitro colony forming assay, estimated by either the plating efficiency of the treated tumour cells compared to non-treated cells or the number of clonogenic cells per mg excised tumour. Curves showing cell survival as a function of the time between light irradiation and excision of the intraocular tumours were biphasic. This suggests more than one PDT tissue destruction mechanism in vivo (i.e. an early direct cell damage plus a subsequent late damage occurring in the tumour tissue left in situ after treatment). The delayed mechanism may be due to changes in the environment of the tumours probably caused by vascular damage. Tumour cells sensitised by Photofrin II in vivo and excised from the eyes were damaged by light when irradiated in vitro and this was dependent on the light energy dose. This showed that cellular Photofrin II uptake in the eye tumours was sufficient for direct cell damage and thus supports the suggestion that direct and indirect tumour destruction occurs in this eye tumour after photodynamic therapy.
在光动力治疗后30分钟至48小时,对眼内视网膜母细胞瘤样肿瘤中的细胞存活情况进行了研究。通过体内到体外集落形成试验评估细胞的存活情况,通过将处理过的肿瘤细胞与未处理的细胞的接种效率进行比较,或者通过每毫克切除肿瘤中的克隆形成细胞数量来估计。显示细胞存活情况作为眼内肿瘤光照与切除之间时间函数的曲线是双相的。这表明体内存在不止一种光动力疗法组织破坏机制(即早期直接细胞损伤加上治疗后留在原位的肿瘤组织中随后发生的晚期损伤)。延迟机制可能是由于肿瘤环境的变化,可能是由血管损伤引起的。体内用二血卟啉醚敏化并从眼中切除的肿瘤细胞在体外照射时会被光损伤,这取决于光能剂量。这表明眼肿瘤中细胞对二血卟啉醚的摄取足以造成直接细胞损伤,因此支持了光动力治疗后该眼肿瘤中发生直接和间接肿瘤破坏的观点。