Interaction of hyperthermia and rhodamine 123 in HeLa S-3 cells in culture.
Interaction of hyperthermia and rhodamine 123 in HeLa S-3 cells in culture.
复制标题
DOI：
10.3109/02656738509029289
复制
发表时间：
1985
期刊：
影响因子：
--
通讯作者：
J. Kim;S. Kim;A. Alfieri
中科院分区：
文献类型：
--
作者：
J. Kim;S. Kim;A. Alfieri
先前已经表明，通过氧化或糖酵解代谢继续产生能量的能力是细胞在高温下存活的先决条件。由于罗丹明123是抑制氧化磷酸化的特异性线粒体结合剂，因此进行本实验以检查细胞暴露于在升高的温度下降低能量产生的药物的影响。HeLa细胞暴露于罗丹明123（10微克/毫升）长达4小时，在37 ℃的培养基中存在或不存在葡萄糖的情况下没有细胞毒性。当从培养基中除去葡萄糖时，细胞长期暴露于药物长达24小时具有相当的细胞毒性。当细胞暴露于罗丹明123在升高的温度（高达42摄氏度）4小时，有一个显着的增强细胞杀死葡萄糖剥夺的细胞。在葡萄糖喂养的细胞中未观察到热的增强效应。在酸性pH下的过热处理没有进一步增强葡萄糖剥夺细胞中的热的细胞毒性作用;相反，在降低的pH的影响下的细胞杀伤远小于在pH 7.4下观察到的细胞毒性。罗丹明123选择性增强葡萄糖剥夺细胞中的热细胞毒性似乎与热杀死细胞取决于细胞能量平衡的临界水平的概念一致。
It has previously been shown that the capacity to continue energy production by either oxidative or glycolytic metabolism is a pre-requisite for cellular survival at elevated temperatures. Since rhodamine 123 is a specific mitochondrial binding agent that inhibits oxidative phosphorylation, the present experiments were carried out to examine the influence of cell exposure to the drug which reduces the energy production at elevated temperatures. Exposure of HeLa cells to rhodamine 123 (10 micrograms/ml) up to 4 h was not cytotoxic in the presence or absence of glucose in the medium at 37 degrees C. Prolonged exposure of cells to the drug up to 24 h was quite cytotoxic when glucose was removed from the medium. When cells were exposed to rhodamine 123 at elevated temperatures (up to 42 degrees C) for 4 h, there was a pronounced enhancement of cell kill in the glucose-deprived cells. No enhanced effects of heat were seen in the glucose-fed cells. Hyperthermic treatment under the acidic pH did not further enhance the cytotoxic effects of heat in the glucose-deprived cells; instead, the cell kill under the influence of reduced pH was far less than the cytotoxicity observed at pH 7.4. Selective enhancement of hyperthermic cytotoxicity in glucose-deprived cells by rhodamine 123 appears to be in agreement with the concept that cell kill by heat is dependent on the critical level of cellular energy equilibrium.