Document Detail

The role of radiation quality in the stimulation of intercellular induction of apoptosis in transformed cells at very low doses.
MedLine Citation:
PMID:  21663396     Owner:  NLM     Status:  MEDLINE    
An important stage in tumorigenesis is the ability of precancerous cells to escape natural anticancer signals. Apoptosis can be selectively induced in transformed cells by neighboring normal cells through cytokine and ROS/RNS signaling. The intercellular induction of apoptosis in transformed cells has previously been found to be enhanced after exposure of the normal cells to very low doses of both low- and high-LET ionizing radiation. Low-LET ultrasoft X rays with a range of irradiation masks were used to vary both the dose to the cells and the percentage of normal cells irradiated. The results obtained were compared with those after α-particle irradiation. The intercellular induction of apoptosis in nonirradiated src-transformed 208Fsrc3 cells observed after exposure of normal 208F cells to ultrasoft X rays was similar to that observed for γ rays. Intercellular induction of apoptosis was stimulated by irradiation of greater than 1% of the nontransformed 208F cells and increased with the fraction of cells irradiated. A maximal response was observed when ∼10-12% of the cells were irradiated, which gave a similar response to 100% irradiated cells. Between 1% and 10%, high-LET α particles were more effective than low-LET ultrasoft X rays in stimulating intercellular induction of apoptosis for a given fraction of cells irradiated. Scavenger experiments show that the increase in intercellular induction of apoptosis results from NO(•) and peroxidase signaling mediated by TGF-β. In the absence of radiation, intercellular induction of apoptosis was also stimulated by TGF-β treatment of the nontransformed 208F cells prior to coculture; however, no additional increase in intercellular induction of apoptosis was observed if these cells were also irradiated. These data suggest that the TGF-β-mediated ROS/RNS production reaches a maximum at low doses or fluences of particles, leading to a plateau in radiation-stimulated intercellular induction of apoptosis at higher doses.
Abdelrazek B Abdelrazzak; David L Stevens; Georg Bauer; Peter O'Neill; Mark A Hill
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-06-10
Journal Detail:
Title:  Radiation research     Volume:  176     ISSN:  1938-5404     ISO Abbreviation:  Radiat. Res.     Publication Date:  2011 Sep 
Date Detail:
Created Date:  2011-08-26     Completed Date:  2011-10-13     Revised Date:  2014-03-19    
Medline Journal Info:
Nlm Unique ID:  0401245     Medline TA:  Radiat Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  346-55     Citation Subset:  IM; S    
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MeSH Terms
Apoptosis / radiation effects*
Cell Line, Transformed
Dose-Response Relationship, Drug*
Grant Support
G0700730//Medical Research Council; MC_PC_12001//Medical Research Council; //Cancer Research UK; //Medical Research Council

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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