INTERACTION OF HYPERTHERMIA AND RADIATION IN CHO CELLS - RECOVERY KINETICS
INTERACTION OF HYPERTHERMIA AND RADIATION IN CHO CELLS - RECOVERY KINETICS
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DOI：
10.2307/3574455
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发表时间：
1976-01-01
影响因子：
3.4
通讯作者：
LEEPER, DB
中科院分区：
文献类型：
--
作者：
HENLE, KJ;LEEPER, DB
对高温损伤（45 ℃）的敏感性。C .+-。0.05 °）并在单层培养的中国仓鼠卵巢（CHO）成纤维细胞中测定了热损伤与辐射损伤的相互作用。在45 ℃加热的异步细胞的存活曲线。C是指数的，有一个肩（D 0 [细胞灵敏度] = 3.6 min，Dq [准阈值剂量] = 7.5 min，n [外推数] = 7.3）。2个相等的热处理，每个17.5分钟的分馏表明，细胞存活率最大限度地提高在分馏间隔为12小时的存活率约为400。其中，60倍是由于耐热性的诱导，即D 0增加。积累亚致死性损伤的能力（n恢复至7.3）完全恢复，并在前4小时内发生。到72小时，D 0恢复到正常，尽管Dq在45 ℃下持续20分钟。C.加热（45度下17.5分钟）C）随后立即辐射（450 rad）或辐射随后立即加热没有产生显著不同的存活值。热疗降低了D 0的辐射生存曲线的一个因素的1.9和增加了一个因素的3的n。Dq保持不变。在长达48小时的时间间隔内，先前的高温将辐射生存曲线的n和Dq分别增加至约1000和650 rad。然而，在0-72 h的整个时间间隔内，D 0保持不变，约为83 rad。对于辐射后热疗的顺序，在45 ℃时，热疗-存活曲线的Dq降低到2.9分钟。C，但恢复到接近正常值后，分馏间隔2小时。高血压生存曲线的D 0不受先前照射的影响。热疗降低了放射-生存曲线的斜率并加宽了肩部，而先前的放射仅影响随后的热疗-生存曲线的肩部。恢复动力学和加热细胞对第二次加热剂量的广泛抵抗很难单独用蛋白质变性的速率过程理论来解释。然而，与细胞内恢复机制相关的膜或染色质蛋白的变性可以解释单独热疗对细胞存活及其对辐射反应的修饰的影响。
The sensitivity to hyperthermic damage (45.degree. C .+-. 0.05.degree.) and the interaction of hyperthermic damage with radiation damage was determined in Chinese hamster ovary (CHO) fibroblasts in monolayer culture. The survival curve for asynchronous cells heated at 45.degree. C was exponential with a shoulder (D0 [cell sensitivity] = 3.6 min, Dq [quasi-threshold dose] = 7.5 min, n [extrapolation number] = 7.3). Fractionation of 2 equal heat treatments each of 17.5 min indicated that cell survival was maximally enhanced at a fractionation interval of 12 h to a survival ratio of approximately 400. Of this, a factor of 60 was due to induction of thermotolerance in terms of an increased D0. Recovery of the capacity to accumulate sublethal damage (return of n to 7.3) was complete and occurred within the first 4 h. By 72 h the D0 returned to normal although the Dq persisted at 20 min at 45.degree. C. Heating (17.5 min at 45.degree. C) followed immediately by radiation (450 rad) or radiation followed immediately by heating did not produce significantly different survival values. Hyperthermia reduced the D0 of the radiation-survival curve by a factor of 1.9 and increased the n by a factor of 3. The Dq remained unchanged. For intervals up to 48 h, prior hyperthermia increased the n and Dq of the radiation-survival curve to approximately 1000 and 650 rad, respectively. However, the D0 remained unchanged at approximately 83 rad over the entire interval of 0-72 h. For the sequence of radiation followed by hyperthermia, the Dq of the hyperthermia-survival curve was reduced to 2.9 min at 45.degree. C by simultaneous irradiation but returned to near-normal values after a fractionation interval of 2 h. The D0 of the hyperthermia-survival curve was unaffected by prior irradiation. Hyperthermia decreased the slope and widened the shoulder of the radiation-survival curve while prior irradiation only affected the shoulder of the subsequent hyperthermia-survival curve. The recovery kinetics and extensive resistance of heated cells to a 2nd heat dose are difficult to explain solely by the rate process theory of protein denaturation. However, denaturation of membrane or chromatin proteins associated with intracellular recovery mechanisms may account for the effects of hyperthermia alone on cell survival and its modification of the radiation response.