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DIRECT HEAT DEATH AND HEAT POTENTIATION OF RADIATION DAMAGE IN CANCER CELLS: MODIFICATION BY INTRACELLULAR AND ENVIRONMENTAL FACTORS

机译：癌细胞的直接热死亡和辐射损伤的热强化：细胞内和环境因素的修饰

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摘要

This investigation represents an attempt to evaluate the damaging effects of hyperthermia on mammalian cells, specifically Bp-8 murine sarcoma cells. Two types of heat damage were studied, thermal radiosensitization and direct thermal cell death. The experiments were designed to answer two fundamental questions: (1) Do thermal radiosensitization and direct thermal death share a common lesion? (2) What are the factors responsible for the enhanced thermal sensitivity of tumors as compared to normal body cells?;(I) Three types of experiments provided evidence against a common mode of action for thermal radiosensitization and direct thermal death. (1) Evaluation of kinetics of heat and radiation death. (2) Thermal radiosensitization and direct heat death as a function of heating time. (3) Independent modification of radiosensitization and thermal death.;(II) Although the two types of heat damage do not share the same mode of action, the two effects show certain common features and one is the fact that tumors are more sensitive to heat than normal body cells. This enhanced thermal sensitivity of tumors may be due to (a) poorly oxygenated regions (hypoxia) in tumors which unable them to deal with the adverse consequences of hyperthemia. (b) hypoxia may enhance tumor glycolysis, in turn cause tumor acidification and reduce the resistance of acidified cells.;To evaluate the influence of these factors on thermal response of cells, a method was developed to permit independent variation of cell pH and environmental oxygen. Experiments on the effects of cellular acidification indicated that reduced intracellular pH and not reduced environmental pH causes pronounced enhancement of thermal damage. Studies on the effect of acute hypoxia on thermal sensitization indicated that thermal radiosensitization and direct thermal death is the same for both euoxic and hypoxic cells.;In conclusion, it appears that hypoxia indued tumor acidification rather than hypoxia per se is responsible for the enhanced thermal sensitization of tumors. Moreover, the degree of thermal sensitization is proportional to the degree of intracellular and not environmental acidification.
机译：这项研究代表了评估高温对哺乳动物细胞，特别是Bp-8鼠肉瘤细胞的破坏作用的尝试。研究了两种类型的热损伤，热辐射敏化和直接热细胞死亡。实验旨在回答两个基本问题：（1）热辐射敏化和直接热死亡是否有共同的病变？ （2）与正常人体细胞相比，导致肿瘤对热敏感性增强的因素有哪些？（I）三种类型的实验提供了证据，证明对热放射致敏和直接热死亡的共同作用方式不明确。 （1）评估热和辐射死亡的动力学。 （2）热辐射敏化和直接热死亡与加热时间的关系。 （3）放射致敏作用和热死亡的独立改变；（II）尽管两种类型的热损伤不具有相同的作用方式，但这两种作用表现出某些共同特征，一种是肿瘤对热更敏感的事实比正常的人体细胞肿瘤的这种热敏感性增强可能是由于（a）肿瘤中的氧合不良区域（缺氧），使他们无法应对高血肿的不良后果。 （b）缺氧可能会增强肿瘤糖酵解，进而导致肿瘤酸化并降低酸化细胞的抵抗力;为了评估这些因素对细胞热反应的影响，开发了一种方法来允许细胞pH和环境氧的独立变化。细胞酸化作用的实验表明，降低细胞内pH值而不降低环境pH值会导致热损伤明显增强。关于急性缺氧对热敏化影响的研究表明，正常氧和缺氧细胞的热放射增敏和直接热死亡是相同的；总而言之，似乎低氧导致肿瘤酸化而不是低氧本身是热增强的原因。肿瘤致敏。而且，热敏化程度与细胞内而不是环境酸化程度成正比。

著录项

  • 作者

    MIVECHI, NAHID FATEME.;

  • 作者单位

    The Florida State University.;

  • 授予单位 The Florida State University.;
  • 学科 Medical imaging.
  • 学位 Ph.D.
  • 年度 1981
  • 页码 133 p.
  • 总页数 133
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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