MicroRNAs (miRNAs) represent small RNA molecules involved in the regulation of gene expression. They are implicated in the regulation of diverse cellular processes ranging from cellular homeostasis to stress responses. Unintended irradiation of the cells and tissues, e.g., during medical uses, induces various pathological conditions, including oxidative stress. miRNAs may regulate the expression of transcription factors (e.g., nuclear factor erythroid 2 related factor 2 (Nrf2), nuclear factor kappa B (NF-κB), tumor suppressor protein p53) and other redox-sensitive genes (e.g., mitogen-activated protein kinase (MAPKs), sirtuins (SIRTs)), which trigger and modulate cellular redox signaling. During irradiation, miRNAs mainly act with reactive oxygen species (ROS) to regulate the cell fate. Depending on the pathway involved and the extent of oxidative stress, this may lead to cell survival or cell death. In the context of radiation-induced oxidative stress, miRNA-21 and miRNA-34a are among the best-studied miRNAs. miRNA-21 has been shown to directly target superoxide dismutase (SOD), or NF-κB, whereas miRNA-34a is a direct regulator of NADPH oxidase (NOX), SIRT1, or p53. Understanding the mechanisms underlying radiation-induced injury including the involvement of redox-responsive miRNAs may help to develop novel approaches for modulating the cellular response to radiation exposure.

Ionizing radiation is a known risk factor for the occurrence and development of cardiovascular diseases, particularly in patients receiving thoracic radiotherapy. This exposure leads to oxidative stress and inflammation, which can damage cardiac tissue and vascular endothelium. Molecular hydrogen (H ₂ ) has been recognized for its therapeutic potential, including antioxidant effects. In this study, male Wistar rats were irradiated with a dose of 10 Gy (X-rays) in the chest area. Two and 9 days post-irradiation, significant increases in lactate dehydrogenase (LDH), catalase, glutathione peroxidase activity, malondialdehyde, superoxide, and tumor necrosis factor alpha levels were observed in the rat blood plasma or heart tissue. Administration of H ₂ either via drinking H ₂ -rich water (min. 4 mg/L) or inhaling H ₂ in air (4%), effectively decreased oxidative stress, LDH, and inflammatory proteins to normal levels. H ₂ also normalized the nuclear factor erythroid 2-related factor 2/Kelch-like ECH-associating protein 1 (Nrf2/Keap1) pathway, an important antioxidative response regulator activated by irradiation. Based on these results, we can conclude that H ₂ administration through both routes mitigated heart damage caused by irradiation after 2 and 9 days. The mitigating effect exerted more pronounced trend with H ₂ gas inhalation, but further research is needed for statistically relevant data and mechanistic insights.