Abstract
We determined the frequencies of dicentric chromosomes per cell in non-dividing confluent normal human fibroblasts (MRC-5) irradiated with a single 1 Gy dose or a fractionated 1 Gy dose (10X0.1 Gy, 5X0.2 Gy, and 2X0.5 Gy). The interval between fractions was between 1 min to 1440 min. After the completion of X-irradiation, the cells were incubated for 24 hours before re-plating at a low density. Then, demecolcine was administrated at 6 hours, and the first mitotic cells were collected for 42 hours. Our study demonstrated that frequencies of dicentric chromosomes in cells irradiated with a 1 Gy dose at different fractions were significantly reduced if the fraction interval was increased from 1 min to 5 min (p<0.05, χ2-test). Further increasing the fraction interval from 5 up to 1440 min did not significantly affect the frequency of dicentric chromosomes. Since misrejoining of two independent chromosome breaks introduced in close proximity gives rise to dicentric chromosome, our results indicated that such circumstances might be quite infrequent in cells exposed to fractionated X-irradiation with prolonged fraction intervals. Our findings should contribute to improve current estimation of cancer risk from chronic low-dose-rate exposure, or intermittent exposure of low-dose radiation by medical exposure.
Highlights
Exposure to ionizing radiation (IR) induces multiple types of DNA damage—including base and sugar damage, single-strand breaks, double-strand breaks (DSBs), and cross-links involving DNA and proteins
We examined the frequencies of dicentric chromosomes in MRC-5 cells following different courses of fractionated X-irradiation
We found that fractionated X-irradiation of 10×0.1 Gy, 5×0.2 Gy, and 2×0.5 Gy with a 1 min fraction interval resulted in a dicentric chromosome frequency similar to that obtained by a single 1 Gy dose of X-irradiation (p>0.05), the frequencies of dicentric chromosomes were slightly lower for the fractionated X-irradiations (10×0.1 Gy and 5×0.2 Gy), than for the acute 1 Gy
Summary
Exposure to ionizing radiation (IR) induces multiple types of DNA damage—including base and sugar damage, single-strand breaks, double-strand breaks (DSBs), and cross-links involving DNA and proteins. Among various types of damage, DSBs are the most deleterious, which result in cell death and chromosome aberrations [1,2,3,4]. DSBs trigger structural alterations in higher-order chromatin structure, which activates ATM protein encoded by the ataxia telangiectasia mutated (ATM) gene. Activated ATM by auto-phosphorylation stimulates phosphorylation of an array of downstream targets, including the tumor suppressor protein p53, which regulates DNA damage response (DDR). DDR stimulates DNA repair, and simultaneously, it arrests cell cycle while repair is ongoing. DSBs can be repaired by two major repair processes: PLOS ONE | DOI:10.1371/journal.pone.0116645. DSBs can be repaired by two major repair processes: PLOS ONE | DOI:10.1371/journal.pone.0116645 February 27, 2015
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