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1 August 2007 Adaptive Response to Gamma Radiation in Mammalian Cells Proficient and Deficient in Components of Nucleotide Excision Repair
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Abstract

Hafer, K., Iwamoto, K., Scuric, Z. and Schiestl, R. H. Adaptive Response to Gamma Radiation in Mammalian Cells Proficient and Deficient in Components of Nucleotide Excision Repair. Radiat. Res. 168, 168–174 (2007).

Cells preconditioned with low doses of low-linear energy transfer (LET) ionizing radiation become more resistant to later challenges of radiation. The mechanism(s) by which cells adaptively respond to radiation remains unclear, although it has been suggested that DNA repair induced by low doses of radiation increases cellular radioresistance. Recent gene expression profiles have consistently indicated that proteins involved in the nucleotide excision repair pathway are up-regulated after exposure to ionizing radiation. Here we test the role of the nucleotide excision repair pathway for adaptive response to γ radiation in vitro. Wild-type CHO cells exhibited both greater survival and fewer HPRT mutations when preconditioned with a low dose of γ rays before exposure to a later challenging dose. Cells mutated for ERCC1, ERCC3, ERCC4 or ERCC5 did not express either adaptive response to radiation; cells mutated for ERCC2 expressed a survival adaptive response but no mutation adaptive response. These results suggest that some components of the nucleotide excision repair pathway are required for phenotypic low-dose induction of resistance to γ radiation in mammalian cells.

Kurt Hafer, Keisuke K. Iwamoto, Zorica Scuric, and Robert H. Schiestl "Adaptive Response to Gamma Radiation in Mammalian Cells Proficient and Deficient in Components of Nucleotide Excision Repair," Radiation Research 168(2), 168-174, (1 August 2007). https://doi.org/10.1667/RR0717.1
Received: 13 June 2006; Accepted: 1 March 2007; Published: 1 August 2007
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