In vivo radioadaptive response

Abstract

<jats:p> Radioadaptive response (RAR) describes phenomena where small conditioning doses of ionizing radiation (IR) reduce detrimental effects of subsequent higher IR doses. Current radiation protection regulations do not include RAR because of the large variability in expression among individuals and uncertainties of the mechanism. However, RAR should be regarded as an indispensable factor for estimation and control of individual IR sensitivity. In this article, RAR studies relevant to individual cancer risk are reviewed. Using various stains of mice, carcinogenic RAR has been demonstrated. Consistently much in vivo evidence for RAR with end points of DNA and chromosome damage is reported. Most in vivo RAR studies revealed efficient induction of RAR by chronic or repeated low-dose priming irradiation. Chronic IR-induced RAR was observed also in human individuals after environmental, occupational, and nuclear accident radiation exposure. These observations may be associated with an intrinsically distinct feature of in vivo experimental systems that mainly consist of nonproliferating mature cells. Alternatively, induction of RAR by gap junction-mediated bystander effects suggests that multicellular systems comprising densely communicating cells may be capable of responding to long-lasting low-dose-rate priming irradiation. Regulation by endocrine factors is also a plausible mechanism for RAR at an individual level. Emerging evidence suggests that glucocorticoids, known as stress hormones, participate in in vivo RAR induction following long-term low-dose-rate exposure to IR. </jats:p>

Global transcriptome profile reveals abundance of DNA damage response and repair genes in individuals from high level natural radiation areas of Kerala coast

“…Immune response, cell to cell communication and gap junction genes and proteins are known to play important role in radio-adaptive response [ 63 , 64 , 65 ]. However, such information on PBMC at G 0 /G 1 exposed to chronic low dose exposure is limited.…”

Assessment of Individual Radiosensitivity in Inhabitants of Takandeang Village － A High Background Radiation Area in Indonesia

“…The high level of DNA damage in people living in HBRAs could come from the high level of reactive oxygen species (ROS). As already known, ionizing radiation can generate ROS, cause DNA damage, and induce delays in different phases of the cell cycle [40,41]. Thus, it can be assumed that the antioxidant level in HBRA inhabitants should be lower than in the control samples due to the utilization of antioxidants that could scavenge the higher free radical concentrations.…”

Donor-Specific Cell-Based Assays in Studying Sensitivity to Low-Dose Radiation: A Population-Based Perspective

“…In this setting, individual variability can arise both from genetic predisposition that determines intrinsic radiosensitivity and individual exposures to different factors. For example, differences in diet ( 41 – 43 ), tobacco use ( 44 , 45 ), or prescribed medications ( 46 ) can affect individual response ( 47 ). Such confounding background factors cannot be easily controlled, compromising comparisons of radiation responses between individuals in vivo .…”