期刊
MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS
卷 671, 期 1-2, 页码 20-25出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.mrfmmm.2009.08.006
关键词
Bystander effect; Adaptive response; Ionizing radiation mutagenesis
资金
- NIH [P01CA095227]
- National Science Foundation [DBI-0552425]
- Cancer Research UK JCUKJ [C1513/A7047]
- European Union NOTE project [FI6R 036465]
- NATIONAL CANCER INSTITUTE [P01CA095227] Funding Source: NIH RePORTER
This work explores several quantitative aspects of radiation-induced bystander mutagenesis in WTK1 human lymphoblast cells. Gamma-irradiation of cells was used to generate conditioned medium containing bystander signals, and that medium was transferred onto naive recipient cells. Kinetic studies revealed that it required up to 1 h to generate sufficient signal to induce the maximal level of mutations at the thymidine kinase locus in the bystander cells receiving the conditioned medium. Furthermore, it required at least I h of exposure to the signal in the bystander cells to induce mutations. Bystander signal was fairly stable in the medium, requiring 12-24 h to diminish. Medium that contained bystander signal was rendered ineffective by a 4-fold dilution; in contrast a greater than 20-fold decrease in the cell number irradiated to generate a bystander signal was needed to eliminate bystander-induced mutagenesis. This suggested some sort of feedback inhibition by bystander signal that prevented the signaling cells from releasing more signal. Finally, an ionizing radiation-induced adaptive response was shown to be effective in reducing bystander mutagenesis; in addition, low levels of exposure to bystander signal in the transferred medium induced adaptation that was effective in reducing mutations induced by subsequent gamma-ray exposures.(C) 2009 Elsevier B.V. All rights reserved.
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