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亚砷酸钠或热对正常细胞以及对热和亚砷酸钠具有诱导耐受性的细胞的X射线致敏作用。

Sensitization to x-rays by sodium arsenite or heat in normal cells and in cells with an induced tolerance for heat and arsenite.

作者信息

van Rijn J, van den Berg J, Wiegant F A, van Wijk R

机构信息

Department of Radiotherapy, Free University Hospital, Amsterdam, The Netherlands.

出版信息

Radiat Environ Biophys. 1995 Aug;34(3):169-75. doi: 10.1007/BF01211544.

DOI:10.1007/BF01211544
PMID:7480632
Abstract

In this study we compared sensitization to x-rays by heat or sodium arsenite and the effect of an induced heat or arsenite resistance on radiosensitization. Treatment of Reuber H35 hepatoma cells with either heat or arsenite causes a dose-dependent radiosensitization. Based on a comparison of isosurvival doses for arsenite and heat, arsenite causes a stronger enhancement of the radiosensitivity. Radiosensitization increases exponentially with increasing sensitizer dose. It is gradually lost when the time interval between irradiation and treatment with heat or arsenite increases, depending on the treatment sequence. For x-rays prior to heat, radiosensitization disappears approximately twice as fast as in the reverse case. Arsenite radiosensitization shows approximately the same kinetics for an isoeffective combination, but slightly longer times are needed for the complete clearance of the interaction. As with heat, an exposure to arsenite induces a stress response in cultured cells which results in the development of an increased tolerance towards a second exposure. Heat and arsenite induce self- as well as cross-tolerance. The reduction in arsenite or heat toxicity in tolerant cells is correlated with a reduction in radiosensitization. The mechanisms for heat and arsenite cytotoxicity appear to be different. A combination of non-toxic doses of heat and arsenite has a synergistic effect on the cytotoxicity. One hour incubation with 0.02 mM arsenite at 41 degrees C has the same cytotoxicity as 0.2 mM after 3 h incubation at 37 degrees C, and the amount of radiosensitization induced by these treatments is approximately the same.

摘要

在本研究中,我们比较了热或亚砷酸钠对X射线的致敏作用以及诱导产生的耐热性或抗砷性对放射致敏作用的影响。用热或亚砷酸钠处理鲁伯H35肝癌细胞会导致剂量依赖性放射致敏。基于对亚砷酸钠和热的等存活剂量的比较,亚砷酸钠对放射敏感性的增强作用更强。放射致敏作用随致敏剂剂量的增加呈指数增加。当照射与热或亚砷酸钠处理之间的时间间隔增加时,放射致敏作用会逐渐消失,这取决于处理顺序。对于先热后X射线照射的情况,放射致敏作用消失的速度大约是相反情况的两倍。对于等效组合,亚砷酸钠放射致敏作用表现出大致相同的动力学,但完全消除相互作用所需的时间略长。与热一样,暴露于亚砷酸钠会在培养细胞中诱导应激反应,从而导致对第二次暴露的耐受性增加。热和亚砷酸钠会诱导自身耐受性以及交叉耐受性。耐受性细胞中亚砷酸钠或热毒性的降低与放射致敏作用的降低相关。热和亚砷酸钠的细胞毒性机制似乎不同。无毒剂量的热和亚砷酸钠组合对细胞毒性具有协同作用。在41℃下用0.02 mM亚砷酸钠孵育1小时与在37℃下用0.2 mM亚砷酸钠孵育3小时具有相同的细胞毒性,并且这些处理诱导的放射致敏作用量大致相同。

相似文献

1
Sensitization to x-rays by sodium arsenite or heat in normal cells and in cells with an induced tolerance for heat and arsenite.亚砷酸钠或热对正常细胞以及对热和亚砷酸钠具有诱导耐受性的细胞的X射线致敏作用。
Radiat Environ Biophys. 1995 Aug;34(3):169-75. doi: 10.1007/BF01211544.
2
Arsenite induced sensitization and self-tolerance of Reuber H35 hepatoma cells.
Cell Biol Toxicol. 1993 Jan-Mar;9(1):49-59. doi: 10.1007/BF00755139.
3
Effect of thermotolerance on thermal radiosensitization in hepatoma cells.热耐受性对肝癌细胞热放射增敏作用的影响。
Radiat Res. 1984 Feb;97(2):318-28.
4
Stressor-specific enhancement of hsp induction by low doses of stressors in conditions of self- and cross-sensitization.在自身致敏和交叉致敏条件下,低剂量应激源对应激特异性热休克蛋白诱导的增强作用。
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5
Induction of arsenite tolerance and thermotolerance by arsenite occur by different mechanisms.亚砷酸盐诱导的对亚砷酸盐的耐受性和耐热性是通过不同机制发生的。
Environ Health Perspect. 1994 Sep;102 Suppl 3(Suppl 3):97-100. doi: 10.1289/ehp.94102s397.
6
Enhancement of the stress response by low concentrations of arsenite in arsenite-pretreated Reuber H35 hepatoma cells.低浓度亚砷酸盐对经亚砷酸盐预处理的鲁伯H35肝癌细胞应激反应的增强作用。
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Effect of hypothermia on cell kinetics and response to hyperthermia and X rays.低温对细胞动力学以及对热疗和X射线反应的影响。
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本文引用的文献

1
Arsenite induced sensitization and self-tolerance of Reuber H35 hepatoma cells.
Cell Biol Toxicol. 1993 Jan-Mar;9(1):49-59. doi: 10.1007/BF00755139.
2
Time-temperature relationships for step-down heating in normal and thermotolerant cells.正常细胞和耐热细胞中逐步降温的时间-温度关系。
Int J Hyperthermia. 1994 Sep-Oct;10(5):643-52. doi: 10.3109/02656739409022444.
3
Enhancement of the stress response by low concentrations of arsenite in arsenite-pretreated Reuber H35 hepatoma cells.低浓度亚砷酸盐对经亚砷酸盐预处理的鲁伯H35肝癌细胞应激反应的增强作用。
Toxicol Appl Pharmacol. 1995 May;132(1):146-55. doi: 10.1006/taap.1995.1095.
4
Induction of chromatid breaks and tetraploidy in Chinese hamster ovary cells by treatment with sodium arsenite during the G2 phase.在G2期用亚砷酸钠处理中国仓鼠卵巢细胞诱导染色单体断裂和四倍体形成。
Mutat Res. 1993 Oct;319(2):135-42. doi: 10.1016/0165-1218(93)90072-l.
5
Induction of thermotolerance and enhanced heat shock protein synthesis in Chinese hamster fibroblasts by sodium arsenite and by ethanol.亚砷酸钠和乙醇诱导中国仓鼠成纤维细胞产生耐热性并增强热休克蛋白合成
J Cell Physiol. 1983 May;115(2):116-22. doi: 10.1002/jcp.1041150203.
6
Effect of thermotolerance on thermal radiosensitization in hepatoma cells.热耐受性对肝癌细胞热放射增敏作用的影响。
Radiat Res. 1984 Feb;97(2):318-28.
7
Hyperthermic potentiation of unrejoined DNA strand breaks following irradiation.照射后未连接的DNA链断裂的热增强作用。
Radiat Res. 1983 Aug;95(2):327-38.
8
The occurrence of DNA strand breaks after hyperthermic treatments of mammalian cells with and without radiation.对哺乳动物细胞进行有辐射和无辐射的热疗后DNA链断裂的发生情况。
Radiat Res. 1984 Apr;98(1):198-208.
9
DNA polymerase alpha and beta activities during the cell cycle and their role in heat radiosensitization in Chinese hamster ovary cells.中国仓鼠卵巢细胞在细胞周期中的DNA聚合酶α和β活性及其在热放射增敏中的作用。
Radiat Res. 1985 Sep;103(3):337-50.
10
Inhibition of human excision DNA repair by inorganic arsenic and the co-mutagenic effect in V79 Chinese hamster cells.无机砷对人类切除修复DNA的抑制作用及在V79中国仓鼠细胞中的共诱变效应。
Mutat Res. 1986 Oct;172(1):69-76. doi: 10.1016/0165-1218(86)90108-4.