Effects of Hyperthermia (45°) on Macromolecular Synthesis in Chinese Hamster Ovary Cells
Effects of Hyperthermia (45°) on Macromolecular Synthesis in Chinese Hamster Ovary Cells
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热疗（45°）对中国仓鼠卵巢细胞大分子合成的影响
DOI：
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发表时间：
1979
期刊：
影响因子：
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通讯作者：
D. Leeper
中科院分区：
文献类型：
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作者：
K. Henle;D. Leeper
记录了 45° 高温后异步中国仓鼠卵巢细胞生物合成活性的抑制和恢复，试图将大分子合成的变化与亚致死热损伤的恢复或耐热性的发展联系起来。
45°热激10或17.5分钟后的生长曲线表明细胞分裂分别被抑制10或17小时；恢复后，倍增时间分别从 13 小时增加到 37 小时或 46 小时。在45°加热10分钟的细胞中，高温后45小时，倍增时间缩短至16.5小时；而在加热 17.5 分钟的细胞中，倍增时间保持在 46 小时。
核酸合成（脉冲[3H]胸苷或[3H]尿苷掺入）立即减少90%，并在4至6小时后恢复，与热疗暴露时间无关。热疗后 10 小时，DNA 合成率恢复至对照的 20% 至 40%，而标记指数保持接近对照水平，直到热疗后约 12 小时，此时标记指数下降至约 20%（25 至 30 小时）。在45°加热10分钟的细胞中，随着倍增时间从37小时缩短至16.5小时，标记指数恢复至45%；而在 45° 17.5 分钟后，标记指数仍然下降约 22%，对应于 46 小时的倍增时间。
恢复开始后，RNA 合成率增加，在热疗后 50 小时超过对照的 150%。高温抑制蛋白质合成（脉冲掺入 14C 标记的氨基酸），但在 45° 10 分钟后 4 至 8 小时或 45° 17.5 分钟后 4 至 26 小时内恢复，在这两种情况下恢复到对照的约 90%。前体掺入在脉冲标记期间呈线性，并且细胞对前体的渗透性并未因高温而显着改变。
45° 10 分钟后 4 至 8 小时内蛋白质合成的恢复与耐热性的开始时间相关，耐热性也在加热后 4 小时开始并在加热后 8 小时完成。然而，一般来说，高热引起的生物合成活性扰动并不表现出对高热暴露的强烈依赖性，并且与亚致死损伤的恢复不相关。
The inhibition and resumption of biosynthetic activity in asynchronous Chinese hamster ovary cells following 45° hyperthermia were documented in an attempt to correlate changes in macromolecular synthesis either with the recovery of sublethal heat damage or with the development of thermotolerance.
Growth curves after a heat shock of either 10 or 17.5 min at 45° indicated that cell division was inhibited for 10 or 17 hr, respectively; following recovery, the doubling time was increased from 13 to 37 or 46 hr, respectively. In the cells heated 10 min at 45°, the doubling time shortened to 16.5 hr by 45 hr posthyperthermia; whereas in the cells heated 17.5 min, the doubling time remained at 46 hr.
Nucleic acid synthesis (pulsed [3H]thymidine or [3H]uridine incorporation) was immediately reduced by 90% and resumed after 4 to 6 hr, independently of the hyperthermia exposure time. The rate of DNA synthesis recovered to 20 to 40% of control by 10 hr posthyperthermia, whereas the labeling index remained near control levels until about 12 hr posthyperthermia when it decreased to approximately 20% (25 to 30 hr). In the cells heated 10 min at 45°, the labeling index returned to 45% as the doubling time shortened from 37 to 16.5 hr; whereas after 17.5 min at 45°, the labeling index remained depressed at approximately 22% corresponding to the doubling time of 46 hr.
After the onset of recovery, the rate of RNA synthesis increased so that it exceeded 150% of control by 50 hr posthyperthermia. Hyperthermia inhibited protein synthesis (pulsed incorporation of 14C-labeled amino acids), but recovery occurred over the period 4 to 8 hr after 10 min at 45° or 4 to 26 hr after 17.5 min at 45° to approximately 90% of control in both cases. Precursor incorporation was linear over the period of the pulse label, and cellular permeability to the precursors was not significantly altered by hyperthermia.
The recovery of protein synthesis over the period of 4 to 8 hr after 10 min at 45° correlated in time with the onset of thermotolerance which also began at 4 hr and was completed by 8 hr after heating. In general, however, hyperthermia-induced perturbation of biosynthetic activity did not exhibit a strong dependence on hyperthermia exposure and did not correlate with recovery from sublethal damage.