With the advancement of nuclear technology, the application of radiation in scientific and technological fields such as medicine, industry, agriculture, energy, and so on has brought tremendous benefits to humans. On the other hand, under certain scenarios, people may suffer from harmful effects from exposure to radiation unavoidably due to nuclear disasters, or inevitably when receiving radiotherapy, in workplaces for occupational workers, or during manned space missions. It is well-known that biological effects are predominantly dependent on the doses of radiation, but the final impact of ionizing radiation on the human body is very complex depending on many conditions. There is a clear conclusion that exposure to ionizing radiation at higher than 0.1 Gy (or 100 mGy) induces cancer in a linear manner. Although the linear no-threshold model is currently used in radiation protection to estimate the cancer risk, there is overwhelming evidence that, under certain circumstances, radiation at low doses, particularly less than 0.1 Gy, could be beneficial, and thus the concept of 'hormesis', derived from toxicology, has gradually gained more attention from radiobiologists. Exposure of cells to ionizing radiation results in redox reactions that alter molecular structure through direct interaction of radiation with target macromolecules or through radiolysis products of water.

Furthermore, oxidative damage may spread from targeted cells to adjacent non-targeted bystander cells through redox-regulated intercellular communication mechanisms. The effects on these bystander cells could be harmful and beneficial depending on the dose of radiation received by the target cells, therefore, the molecular biological events may lead to mitochondrial dysfunction and DNA damage and may also activate beneficial intracellular signaling pathways to increase DNA repair and/or anti-oxidative capacity as well as autophagy, resulting in cellular resistance to subsequent radiation- or chemicals-induced toxicity. Intracellular redox reactions play important roles in radiation-induced normal tissue senescence, cellular fibrosis, neurodegeneration, cell fate selection, abscopal effects, long-term effects, and adaptive responses. At the same time, how the above-mentioned effects are achieved through the intracellular signal transduction pathway is still largely unknown. Of great interest, the mechanism of intracellular redox reaction-induced biological effects can fundamentally explain the relationship between radiation dose and biological effects. The essence of redox is the gain and loss of electrons, which may be also the true essence of life. Many biological events whose mechanisms are unclear may be answered by redox.

This Special Issue welcomes original research and review articles related to explaining the mechanism of the bio-effects caused by ionizing radiation-induced intracellular redox reactions, to achieve the purpose of extensive communication among researchers. The aim and scope are to summarize the past and present works on the biological effects caused by radiation-induced redox reactions.

Potential topics include but are not limited to the following:

• New progress in studies on the role of ionizing radiation-induced redox reactions in the mechanism of normal tissue senescence, cellular fibrosis, neurodegeneration, cell fate selection, abscopal effects, long-term effects, and adaptive responses
• Research that shows any harmful or beneficial bystander effect of low dose radiation (less 100 mGy) during cancer therapy
• New insights into the biological effects of low-dose long-term radiation in animal models
• New insights to understand the mechanisms responsible for the potentially beneficial biological effects of low-dose radiation
• Systemic evaluation of the value for CT-scan cancer screening to diagnostic cancer at early, curable stages and the potential risk of the diagnostic radiation dose-induced cancer