Radiation Injury and Antioxidant Mechanisms of Protection

Critical cellular biomolecules are damaged by ionizing radiation either directly, or indirectly by radicals generated from the radiolysis of cellular water (1,2). The free radicals thus produced can further interact among themselves or with cellular oxygen to perpetuate the radiation effects. Depending on the linear energy transfer (LET), dose rate, and duration of exposure these effects may vary. At the molecular level it is generally believed that damage to DNA is the critical event. Damage to DNA can be detected at the cellular level by chromosomal aberrations (3) and micronuclei formation (4). It should be possible to do this semi-invasively using lymphocytes from peripheral blood. Radiation damage may vary from transformation and mutagenesis in in vitro systems to carcinogenesis and cataractogenesis in the long term and lethality due to acute exposures. Lethality may be due to bone marrow depletion (hematopoietic syndrome), destruction of gastrointestinal mucosa (gastrointestinal syndrome), and neurovascular destruction (central nervous system syndrome) (5). Exposure to a nuclear accident may also cause injuries from shock, burns, or wounds that may accentuate lethal effects. Protection from these effects and mechanisms of protection are of importance in determining suitable regimens for different radiation exposure scenarios, such as radiation therapy, nuclear accidents, and manned space missions. The purpose of this paper is to review some of the new data obtained on radioprotection with agents which show a small margin of radioprotection and to show a possible correlation between antioxidant mechanisms and radioprotection based on these data.