Abstract：
PURPOSE:To investigate the mechanisms inducing and maintaining the permanent elimination of low dose hyper-radiosensitivity (HRS) in cells given a dose of 0.3 Gy at low dose-rate (LDR) (0.3 Gy/h). MATERIALS AND METHODS:Two human HRS-positive cell lines (T-47D, T98G) were used. The effects of pretreatments with transforming growth factor beta (TGF-β) neutralizers, TGF-β3 or peroxynitrite scavenger on HRS were investigated using the colony assay. Cytoplasmic levels of TGF-β3 were measured using post-embedding immunogold electron microscopic analysis. RESULTS:TGF-β3 neutralizer inhibited the removal of HRS by LDR irradiation. Adding 0.001 ng/ml TGF-β3 to cells removed HRS in T98G cells while 0.01 ng/ml additionally induced resistance to higher doses. Cytoplasmic levels of TGF-β3 were higher in LDR-primed cells than in unirradiated cells. The presence of the peroxynitrite scavenger uric acid inhibited the effect of LDR irradiation. Furthermore, the permanent elimination of HRS in LDR-primed cells was reversed by treatment with uric acid. The removal of HRS by medium from hypoxic cells was inhibited by adding TGF-β3 neutralizer to the medium before transfer or by adding hypoxia inducible factor 1 (HIF-1) inhibitor chetomin to the cell medium during hypoxia. CONCLUSIONS:TGF-β3 is involved in the regulation of cellular responses to small doses of acute irradiation. TGF-β3 activation seems to be induced by low dose-rate irradiation by a mechanism involving inducible nitric oxide (iNOS) and peroxynitrite, or during cycling hypoxia by a mechanism most likely involving HIF-1. The study suggests methods to turn resistance to doses in the HRS-range on (by TGF-β3) or off (by TGF-β3 neutralizer or by peroxynitrite inhibition).
journal_name
Int J Radiat Bioljournal_title
International journal of radiation biologyauthors
Edin NJ,Sandvik JA,Cheng C,Bergersen L,Pettersen EOdoi
10.3109/09553002.2014.906767subject
Has Abstractpub_date
2014-07-01 00:00:00pages
527-37issue
7eissn
0955-3002issn
1362-3095journal_volume
90pub_type
杂志文章abstract：PURPOSE:To determine the involvement of c-Jun NH(2)-terminal kinase-1 (JNK1) and possibly of HSP27 in heat-induced apoptosis of human monoblastic leukaemia U937 cells. MATERIALS AND METHODS:Dominant negative JNK1 (APF), in which the phosphorylation sites Thr-Pro-Tyr were changed to Ala-Pro-Phe, was overexpressed in U9...
journal_title：International journal of radiation biology
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journal_title：International journal of radiation biology
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journal_title：International journal of radiation biology
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journal_title：International journal of radiation biology
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journal_title：International journal of radiation biology
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journal_title：International journal of radiation biology
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journal_title：International journal of radiation biology
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更新日期：2007-06-01 00:00:00
