Enhancement of DNA double-strand break induction and cell killing by K-shell absorption of phosphorus in human cell lines

Abstract

Purpose: To investigate an enhancement of DNA double-strand break (DSB) induction and cell killing effect by K-shell ionization of phosphorus atoms and Auger electrons on human cell lines.

Materials and methods: Induction of DSB, DNA damage responses, cell cycle distributions, and cell killing effects were investigated after exposures of the cells with monochromatic synchrotron radiation soft X-rays of 2153 and 2147 eV, which were the resonance peak and off peak, respectively, of the K-shell photoabsorption of phosphorus.

Results: Higher biological effects in the cells irradiated with soft X-rays at 2153 eV than at 2147 eV were observed in (i) the efficiency of 53BP1/γ-H2AX co-localized foci formation per dose and residual number of foci, (ii) prolonged phosphorylation levels of DSB repair and/or cell cycle checkpoint related proteins and G2 arrest, (iii) the cell killing effects at the 10% survival level of normal human fibroblasts, HeLa cells, and human glioblastoma M059K cells (1.2–1.5 times higher) and that of human ataxia telangiectasia mutated (ATM)-defective cells and glioblastoma DNA-dependent protein kinase catalytic subunit (DNA-PKcs)-defective cells (1.2 times).

Conclusion: The yield of DSB and partly less-reparable complex DNA damage induction in human cells was enhanced by K-shell photoabsorption of phosphorus and low-energy Auger electrons.

Keywords:

• Soft X-rays
• Auger effect
• double-strand break
• DNA repair
• cell death

Acknowledgements

The authors thank Ms Rie Sano and Ms Masako Mizuno for excellent technical assistance, and are grateful to Drs Hiroshi Maezawa, Atsushi Ito, and Kotaro Hieda for helpful comments and discussions. This work was performed under the approval of the Photon Factory Program Advisory Committee (Proposal No. 2008G096, 2010G040 and 2012G129).

Disclosure statement

The authors report no conflicts of interest. The authors alone are response for the content and writing of the paper.