ONCOGENESIS FROM LOW-DOES-RATE X-IRRADIATION

我们的目标是获得关于致癌频率的信息 作为曝光时间的显式函数的变换 延长后潜伏相变损伤残留的剂量率 X射线照射。这种潜在的损伤及其启动子的表达 12-0-十四酰-佛波醇-13-乙酸酯将被慢性 TPA-用高剂量率或高剂量率X射线照射的细胞的治疗 持续时间长达8小时。 我们将继续使用从小鼠细胞来源的C3H/10T1/2细胞系 在这种情况下，转换是通过在 融合的单层。实验将在37摄氏度的条件下进行 积极发展的文化。我们将继续使用持续的曝光 降低剂量率的细胞照射时间技术。在… 累积或急性剂量为0.25至4Gy时，我们将分析 0.1微克/毫升的TPA立即开始X射线照射细胞 在被激怒之后。对照组(不含TPA，但使用自来水) 都会遵循同样的程序。相关因素将从以下方面估计 长时间曝光的转化频率比 从急性照射(4Gymin)到相同剂量的频率的时间T， 使用或不使用TPA与(A)获取信息的剂量 配对过程的有效性，或(B)获得 关于修复过程动力学的信息。

Our aim is to obtain information on the frequency of oncogenic transformation as an explicit function of exposure time for a variety of dose rates on latent transformation damage remaining after protracted X-irradiation. This latent damage and its expression by the promoter 12-0-tetradecanoyl-phorbol-13-acetate will be investigated by chronic TPA-treatment of cells initiated with X-rays delivered at high dose rate or protracted over times up to 8 h. We will continue to use the C3H/10T1/2 cell line derived from mouse cells in which transformation is quantitated by scoring piled-up foci on top of a confluent monolayer. Experiments will be performed at 37 degrees C with actively growing cultures. We will continue to use a constant exposure time technique for cellular irradiation at reduced dose rates. At cumulative or acute doses of .25 to 4 Gy, we will assay the population of X-ray initiated cells by TPA-treatments at 0.1 Mug/ml beginning immediately after irratiation. The control groups (without TPA but with TAP-solvent) will follow the same procedure. Relative factors will be estimated from the ratio of the transformation frequencies from protracted exposures over time T to frequency from an acute exposure (4 Gy/min) to the same dose, with or without TPA versus (a) the dose to obtain information on the efficacy of rapair processes, or (b) the total exposure time to obtain information on the kinetics of repair processes.