DNA methylation is a common endogenous chemical modification in eukaryotic DNA, primarily involving the covalent attachment of a methyl group to the fifth carbon of cytosine residues, leading to the formation of 5-methylcytosine (5mC). This epigenetic modification plays a crucial role in gene expression regulation and genomic stability maintenance in eukaryotic systems. Ionizing radiation (IR) has been shown to induce changes in global DNA methylation patterns, which exhibit significant temporal stability. This stability makes DNA methylation profiles promising candidates for radiation-specific biomarkers. This review systematically examines the impact of IR on genome-wide DNA methylation landscapes and evaluates their potential as molecular indicators of radiation exposure. Advancing the knowledge of radiation-induced epigenetic modifications in radiobiology contributes to a deeper understanding of IR-driven epigenetic reprogramming and facilitates the development of novel molecular tools for the early detection and quantitative risk assessment of radiation exposure.

With growing public concern about the health effects of low-dose radiation, numerous studies have demonstrated that low-dose radiation can cause damage to the immune system, making intervention measures essential. This study investigated the protective effects of silybin against low-dose radiation-induced immune system damage and its underlying mechanisms at both the cellular and animal levels. At the cellular level, CCK-8 assays, ROS measurements, and RT-qPCR analysis revealed that silybin alleviated the reduction in RAW264.7 cell proliferation, intracellular ROS levels, and inflammatory cytokine expression following low-dose radiation exposure. At the animal level, comparative analyses of post-irradiation body weight, peripheral blood cell counts, immune organ coefficients, spleen HE/IHC staining, and spleen immune cell numbers demonstrated that silybin mitigated the radiation-induced decrease in body weight, reduction in peripheral blood leukocyte counts, inflammatory cell infiltration in the spleen, decline in spleen immune cell numbers, and increase in cGAS protein-positive cells. These findings indicate that silybin exerts protective effects against low-dose radiation-induced immune system damage, potentially by regulating the cGAS signaling pathway to reduce radiation-induced cellular injury, thereby enhancing its radioprotective properties.