Abstract
Even today, 70 years after Hiroshima and accidents like in Chernobyl and Fukushima, we still have limited knowledge about the health effects of low dose rate (LDR) radiation. Despite their human relevance after occupational and accidental exposure, only few animal studies on the genotoxic effects of chronic LDR radiation have been performed. Selenium (Se) is involved in oxidative stress defence, protecting DNA and other biomolecules from reactive oxygen species (ROS). It is hypothesised that Se deficiency, as it occurs in several parts of the world, may aggravate harmful effects of ROS-inducing stressors such as ionising radiation. We performed a study in the newly established LDR-facility Figaro on the combined effects of Se deprivation and LDR γ exposure in DNA repair knockout mice (Ogg1−/−) and control animals (Ogg1+/−). Genotoxic effects were seen after continuous radiation (1.4 mGy/h) for 45 days. Chromosomal damage (micronucleus), phenotypic mutations (Pig-a gene mutation of RBCCD24−) and DNA lesions (single strand breaks/alkali labile sites) were significantly increased in blood cells of irradiated animals, covering three types of genotoxic activity. This study demonstrates that chronic LDR γ radiation is genotoxic in an exposure scenario realistic for humans, supporting the hypothesis that even LDR γ radiation may induce cancer.
Highlights
In order to investigate the potential influence of a low Se intake on the effects of chronic low dose rates (LDR) γirradiation, mice were Se depleted through two generations
Only few studies have addressed the effects of LDR radiation within a range which is of human relevance as it can be found after accidents like in Chernobyl and Fukushima
Even fewer have investigated the biological effects of continuous chronic LDR radiation despite their relevance in occupational and environmental contamination settings
Summary
Radiation damages DNA either directly (electrons attack DNA) or indirectly (radiolysis of water forming ROS such as H2O2, O2−, lipid hydroperoxides). Radiolysis of water is the predominant mechanism at low doses When this event occurs in close proximity to DNA it will contribute to oxidative stress in form of ROS. An impaired repair of oxidised DNA lesions may aggravate the effects of chronic exposure to radiation. Mice that lack the repair enzyme OGG1 (Ogg1−/−), which removes 8–oxoguanine[12], would be expected to accumulate radiation induced lesions and thereby serve as a sensitive model for oxidative stress. The aim of the present study was to investigate the genotoxic effects of chronic LDR γradiation (1.4 mGy/h for 45 days) in blood from mice. Two factors that could potentially influence the manifestation of the genotoxic radiation effects were studied: diet (Se deficiency) and genotype (OGG1 deficiency), as well as combinations thereof
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
