PLD REPAIR IN RAT RHABDOMYOSARCOMA TUMOR-CELLS IRRADIATED INVIVO AND INVITRO WITH HIGH-LET AND LOW-LET RADIATION
PLD REPAIR IN RAT RHABDOMYOSARCOMA TUMOR-CELLS IRRADIATED INVIVO AND INVITRO WITH HIGH-LET AND LOW-LET RADIATION
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DOI：
10.2307/3576839
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发表时间：
1986-09-01
影响因子：
3.4
通讯作者：
CURTIS, SB
中科院分区：
文献类型：
--
作者：
AFZAL, SMJ;TENFORDE, TS;CURTIS, SB
在体内和体外高let或低let辐射照射后，测量大鼠横纹肌肉瘤肿瘤细胞潜在致死损伤（PLD）恢复程度的研究报告了结果。研究发现，在低let X射线或高let氖离子的延伸峰电离区照射下，静止期培养物表现出PLD的修复。在9 gy剂量的225 kvp X射线或3.5 gy剂量的峰值氖离子照射后，初始细胞存活率均降低至6-8%，最大PLD恢复因子分别为3.4和1.6。相比之下，用X射线或峰值氖离子原位照射肿瘤时，标准肿瘤切除测定程序未能显示任何PLD的恢复。然而，当加入一种已知的PLD修复抑制剂改变切除实验程序时，可以观察到体内肿瘤细胞对PLD的修复。-arabinofuranosyladenine (.beta.-ara-A)。当一个无细胞毒性的50。M的浓度。在14.5 gy原位X射线照射后立即将-ara-A添加到切除的肿瘤细胞中，抑制剂处理的细胞的细胞存活率低于未处理的细胞（0.018比0.056），导致PLD修复抑制因子为3.1。延迟添加。beta。肿瘤切除后1、2、3小时，-ara-A可将PLD修复抑制因子分别降低至1.6、1.5和0.9。肿瘤在展峰电离区用氖离子原位照射后（中位LET = 145 keV/.mu）。m)，与X照射后相比，PLD修复较少。对于5.8 Gy的峰值氖离子，在0、1、2和3 h时PLD修复抑制因子分别为2.1、1.5、1.3和1.3，以及1.1。我们解释说，使用标准的肿瘤切除测定程序，PLD修复的缺失是由于在细胞解离和电镀过程所需的长时间间隔（约2小时）内无法检测到修复。我们的结论是，至少在我们的肿瘤系统中，原位肿瘤照射后确实发生了PLD修复，尽管使用标准肿瘤切除测定程序无法检测到。因此，在一个给定的肿瘤系统中，不能通过这种试验来测量这种修复并不一定意味着细胞不能修复PLD。
Results are reported of studies to measure the extent of recovery of potentially lethal damage (PLD) in rat rhabdomyosarcoma tumor cells after irradiation both in vivo and in vitro with either high-LET or low-LET radiation. Stationary-phase cultures were found to exhibit repair of PLD following irradiation in vitro either with low-LET X rays or with high-LET neon ions in the extended-peak ionization region. Following a 9-Gy dose of 225-kVp X rays or a 3.5-Gy dose of peak neon ions, both of which reduced the initial cell survival to 6-8%, the maximum PLD recovery factors were 3.4 and 1.6, respectively. In contrast, the standard tumor excision assay procedure failed to reveal any recovery form PLD in tumors irradiated in situ with either X rays or peak neon ions. PLD repair by the in vivo tumor cells could be observed, however, when the excision assay procedure was altered by the addition of a known PLD repair inhibitor .beta.-arabinofuranosyladenine (.beta.-ara-A). When a nonocytotoxic 50 .mu.M concentration of .beta.-ara-A was added to the excised tumor cells immediately following a 14.5-Gy in situ dose of X rays, cell survival in the inhibitor-treated cells was lower than in the untreated cells (0.018 compared to 0.056), resulting in a PLD repair inhibition factor of 3.1. Delaying the addition of .beta.-ara-A for 1,2, or 3 h following tumor excision reduced the PLD repair inhibition factor to 1.6, 1.5, and 0.9, respectively. Following tumor irradiation in situ with neon ions in the extended-peak ionization region (median LET = 145 keV/.mu.m), less PLD repair was observed than after X irradiation. For 5.8 Gy of peak neon ions, the PLD repair inhibition factors were 2.1, 1.5, 1.3, and 1.3, and 1.1 at 0, 1, 2, and 3 h, respectively. We interpret the absence of measurable PLD repair using the standard tumor excision assay procedure as resulting from undetectable repair occurring during the long interval (about 2 h) required for the cell dissociation and plating procedures. We conclude that at least for our tumor system, PLD repair does occur after irradiation of tumors in situ, even though it is not detectable using the standard tumor excision assay procedure. Thus a failure to measure such repair by this assay in a given tumor system does not necessarily mean the cells are incapable of PLD repair.