Molecular Insights into Radiation Effects and Protective Mechanisms: A Focus on Cellular Damage and Radioprotectors

Abstract

Ionizing radiation has been a critical tool in various fields, such as medicine, agriculture, and energy production, since its discovery in 1895. While its applications-particularly in cancer treatment and diagnostics-offer significant benefits, ionizing radiation also poses risks due to its potential to cause molecular and cellular damage. This damage can occur through the direct ionization of biological macromolecules, such as deoxyribonucleic acid (DNA), or indirectly through the radiolysis of water, which generates reactive oxygen species (ROS) that further damage cellular components. Radioprotectors, compounds that protect against radiation-induced damage, have been extensively researched since World War II. These agents work by enhancing DNA repair, scavenging free radicals, and boosting antioxidant defenses, thereby protecting healthy tissues. Furthermore, some radioprotective agents also stimulate DNA repair mechanisms even after radiation exposure, aiding in recovery from radiation-induced damage. This article explores the molecular mechanisms of radiation-induced damage, focusing on both direct and indirect effects on DNA, and discusses the role of radioprotectors, their mechanisms of action, and recent advancements in the field. The findings underscore the importance of developing effective radioprotective strategies, particularly in medical and industrial settings, where radiation exposure is prevalent.

Keywords: DNA damage; antioxidants; free radicals; ionizing radiation; molecular mechanisms; radiation protection; radiation-induced damage; radioprotectors; radiotherapy; reactive oxygen species (ROS).

Figure 1

Direct (radical-induced primary damage) and indirect (reactive free radicals, that is, ^•OH, produced following radiolysis of water) route action of ionizing radiation. Radiation protection of radioprotector is carried out in the indirect route. The X symbol indicates the pathway inhibited by this radioprotector. Figure created using Render (Render Inc., San Francisco, CA, USA).