The DNA concentration effect on DNA radiation damage induced by 7Li ions and γ rays

To evaluate the influence of the DNA concentration in the aqueous solution on DNA radiation damage, the plasmid DNA in the presence or absence of Mannitol (scavenger of free radical OH·) was irradiated by 7Li ions and γ rays at various DNA concentrations. Gel electrophoresis analysis revealed that the DNA damage of single and double strand breaks induced by irradiation became more severe at lower DNA concentration. In the condition of γ-ray irradiation, most of double strand breaks (DSB) damage was neutralized and less associated with DNA concentration in the presence of mannitol. However, under 7Li irradiation, DSB damage could not be cleared by mannitol but was gradually aggravated with decreasing DNA concentrations. These findings imply that under low-LET irradiation, most of the DSB damage is generated by free radical OH? diffusion, and thus may be counteracted by scavengers, while at higher-LET irradiation, quite a fraction of DSB induction is caused by direct ionizing energy deposi- tion of heavy ions, which cannot be eliminated. This work also indicates that the proportion between free radical damage and direct ionizing damage is a constant which is independent of DNA concentra- tion when the DNA concentration is under a certain value (50 ng/μL). Our study sheds light on the un- derlying mechanisms in the DNA radiation damage process.

To evaluate the influence of the DNA concentration in the aqueous solution on DNA radiation damage, the plasmid DNA in the presence or absence of Mannitol （scavenger of free radical OH.） was irradiated by ^7Li ions and γ rays at various DNA concentrations. Gel electrophoresis analysis revealed that the DNA damage of single and double strand breaks induced by irradiation became more severe at lower DNA concentration. In the condition of γ-ray irradiation, most of double strand breaks （DSB） damage was neutralized and less associated with DNA concentration in the presence of mannitol. However, under ^7Li irradiation, DSB damage could not be cleared by mannitol but was gradually aggravated with decreasing DNA concentrations. These findings imply that under low-LET irradiation, most of the DSB damage is generated by free radical OH·diffusion, and thus may be counteracted by scavengers, while at higher-LET irradiation, quite a fraction of DSB induction is caused by direct ionizing energy deposition of heavy ions, which cannot be eliminated. This work also indicates that the proportion between free radical damage and direct ionizing damage is s constant which is independent of DNA concentration when the DNA concentration is under a certain value （50ng/μL）. Our study sheds light on the un- derlying mechanisms in the DNA radiation damage process.