Mechanisms of Radiation Toxicity in Transformed and Non-Transformed Cells

被引:90
作者
Panganiban, Ronald-Allan M. [1 ]
Snow, Andrew L. [1 ]
Day, Regina M. [1 ]
机构
[1] Uniformed Serv Univ Hlth Sci, Dept Pharmacol, Bethesda, MD 20814 USA
来源
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2013年 / 14卷 / 08期
关键词
ionizing radiation; apoptosis; necrosis; senescence; autophagy; cancer; primary cell; ENDOPLASMIC-RETICULUM STRESS; RAT LUNG IRRADIATION; DOUBLE-STRAND BREAKS; CASPASE RECRUITMENT DOMAIN; COLON-CANCER CELLS; FACTOR-KAPPA-B; WILD-TYPE P53; IONIZING-RADIATION; INDUCED APOPTOSIS; CELLULAR SENESCENCE;
D O I
10.3390/ijms140815931
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Radiation damage to biological systems is determined by the type of radiation, the total dosage of exposure, the dose rate, and the region of the body exposed. Three modes of cell deathnecrosis, apoptosis, and autophagyas well as accelerated senescence have been demonstrated to occur in vitro and in vivo in response to radiation in cancer cells as well as in normal cells. The basis for cellular selection for each mode depends on various factors including the specific cell type involved, the dose of radiation absorbed by the cell, and whether it is proliferating and/or transformed. Here we review the signaling mechanisms activated by radiation for the induction of toxicity in transformed and normal cells. Understanding the molecular mechanisms of radiation toxicity is critical for the development of radiation countermeasures as well as for the improvement of clinical radiation in cancer treatment.
引用
收藏
页码:15931 / 15958
页数:28
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