Mitigation of Iron Irradiation-Induced Genotoxicity and Genomic Instability by Postexposure Dietary Restriction in Mice

Background and Purpose. Postexposure onset of dietary restriction (DR) is expected to provide therapeutic nutritional approachesto reduce health risk from exposure to ionizing radiation (IR) due to such as manned space exploration, radiotherapy, or nuclearaccidents as IR could alleviate radiocarcinogenesis in animal models. However, the underlying mechanisms remain largelyunknown. This study is aimed at investigating the effect from postexposure onset of DR on genotoxicity and genomicinstability (GI) induced by total body irradiation (TBI) in mice.Materials and Methods. Mice were exposed to 2.0 Gy ofaccelerated iron particles with an initial energy of 500 MeV/nucleon and a linear energy transfer (LET) value of about 200 keV/μm. After TBI, mice were either allowed to free access to a standard laboratory chow or treated under DR (25% cut in diet).Using micronucleus frequency (MNF) in bone marrow erythrocytes, induction of acute genotoxicity and GI in thehematopoietic system was, respectively, determined 1 and 2 months after TBI.Results and Conclusions. TBI alone caused asignificant increase in MNF while DR alone did not markedly influence the MNF. DR induced a significant decrease in MNFcompared to the treatment by TBI alone. Results demonstrated that postexposure onset of DR could relieve the elevated MNFinduced by TBI with high-LET iron particles. Thesefindings indicated that reduction in acute genotoxicity and late GI may beat least a part of the mechanisms underlying decreased radiocarcinogenesis by DR