Radiation Toxins – Effects of Radiation Toxicity, Molecular Mechanisms of Action, Radiomimetic Properties and Possible Countermeasures for Radiation Injury

Acute Radiation Disease (ARD) or Acute Radiation Syndromes (ARS) are defined as the collective toxic clinical states observed from the acute pathological processes in various doses of irradiated mammals; to include: systemic inflammatory response syndrome (SIRS), toxic multiple organ injury (TMOI), toxic multiple organ dysfunction syndromes (TMODS), and finally, toxic multiple organ failure (TMOF). [2, 10, 18, 21 ] Moderate and high doses of radiation induces necrosis of radiosensitive cells with the subsequent formation of radiation toxins and their induced acute inflammatory processes. Radiation necrosis is the most substantial and most severe form of radiation induced injury, and when widespread, has grave therapeutic implications [1, 3, 53]. Low doses of radiation exposure induces apoptosis (controlled, programmed death of radiosensitive cells) without significant levels of specific radiation-induced toxin formation and with only low levels of inflammatory response [17, 50, 62]. Studying the trigger mechanism for radiation-induced lymphocyte death, N.I. Sorokina used the results of numerous experiments to show that ionizing radiation induces changes in the antigen phenotype of immature thymocytes in mice. This has the same type of effect as chemical differentiation inductors and thymotropin, which indirectly attests to the specific modifying effect of ionizing radiation [97, 98]. B.D. Zhivotovskiy described radiation-induced apoptosis and demonstrated a quantitative association between the pyknotic changes in the cell nuclei of thymocytes and production of postradiation chromatin decay products. The enzyme responsible for the decomposition of chromatin in irradiated cells is Ca/Mg-dependent endonuclease. Areas of endonuclease