Abstract

When energetic particles irradiate matter, it becomes activated by nuclear reactions. Radioactivation induced cellular effects are not clearly understood, but it could be a part of bystander effects. This investigation is aimed at understanding the biological effects from radioactivation in solution induced by hadron radiation. Water or phosphate buffered saline was activated by being exposed to hadron radiation including protons, carbon- and iron-ions. 1 mL of radioactivated solution was transferred to flasks with Chinese hamster ovary (CHO) cells cultured in 5 mL of complete media. The induction of sister chromatid exchanges (SCE) was used to observe any increase in DNA damage responses. The energy spectrum and the half-lives of the radioactivation were analyzed by NaI scintillation detector in order to identify generated radionuclides. In the radioactivated solution, 511 keV gamma-rays were observed, and their half-lives were approximately 2 min, 10 min, and 20 min. They respectively correspond to the beta+ decay of 15O, 13N, and 11C. The SCE frequencies in CHO cells increased depending on the amount of radioactivation in the solution. These were suppressed with a 2-hour delayed solution transfer or pretreatment with dimethyl sulfoxide (DMSO). Our results suggest that the SCE induction by radioactivated solution was mediated by free radicals produced by the annihilated gamma-rays. Since the SCE induction and DMSO modulation are also reported in radiation-induced bystander effects, our results imply that radioactivation of the solution may have some contribution to the bystander effects from hadron radiation. Further investigations are required to assess if radioactivation effects would attribute an additional level of cancer risk of the hadron radiation therapy itself.

Highlights

  • Non-radioactive atoms can become radioactive through nuclear reactions when the atoms are hit by other high-energy particles

  • Positron emitters and the subsequent annihilation gamma-rays generated from the atomic nuclei of the tissue during hadron radiation therapy have been investigated for the potential application of monitoring dose distribution inside the patient using positron emission tomography (PET) techniques [5,6,7,8]

  • The radioactivities based on every 15–40 minute time measurements using GM counter were fit with one-phase exponential decay models with similar slopes for all different doses and types of hadron radiation exposures, with the exception of 0.1 Gy of carbon-ions (Fig 1C and 1D)

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Summary

Introduction

Non-radioactive atoms can become radioactive through nuclear reactions when the atoms are hit by other high-energy particles These radioactivations are observed in neutron exposure, and in hadron radiation therapy, such as proton and carbon-ion radiotherapy [1,2,3,4]. Radiation oncologists were familiar with radiation induced whole-body and tissue-based abscopal effects in vivo, which are explained with the post-irradiation induced soluble factors [11]. Such non-targeted radiation effects have been recognized as a bystander effect, which was originally reported from in vitro research by Nagasawa and Little in 1992 [12]. The involvement of oxidative and inflammatory response is considered crucial, mechanisms of bystander effects are still under investigation [14, 15]

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