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首页> 美国政府科技报告 >Biological Toxicity of Intracellular Radionuclide Decay. Part of a Coordinated Programme on Radiation Biology of Auger Emitters and Their Therapeutic Applications. Final Report for the Period 15 November 1976 - 31 March 1980
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Biological Toxicity of Intracellular Radionuclide Decay. Part of a Coordinated Programme on Radiation Biology of Auger Emitters and Their Therapeutic Applications. Final Report for the Period 15 November 1976 - 31 March 1980

机译：细胞内放射性核素衰变的生物毒性。俄歇发射器及其治疗应用的辐射生物学协调计划的一部分。 1976年11月15日至1980年3月31日期间的最终报告

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Internal radiotherapy should be performed with short-lived radionuclides which emit high LET radiation and short ranged radiation, and accumulated within cancers. Based on these considerations, several radionuclides (tritium, copper-64, gallium-67, iodine-123, iodine 125, iodine-131 and astatine-211) were chosen and their toxicity was assessed using cell division in mammalian cultured cells as a criterion. It was apparent that the toxic effects obtained with exp 125 I greatly exceeded those observed in cells treated with any other radionuclides. The possible hypotheses to explain the excessive radiosensitivity of exp 125 I were discussed in relation to microdosimetry calculation. It was also found that the division delay induced by radionuclide decay is primarily due to damage to the cell nucleus but not to the plasma membrane. The key problem remains the development of agents which can serve as carriers for radionuclide accumulation within tumors. Although several promising approaches (Synkavit, tamoxifen, iododeoxyuridine, antibodies, liposomes) were investigated, only /sup 125/I-labelled Synkavit would be desirable for clinical application. (Atomindex citation 12:588035)

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