ABSTRACT
At the onset of radiation exposure, free radicals are formed through ionizing reactions, such as the photoelectric, Compton and Auger effects. These free radicals react with DNA and RNA, causing molecular alterations, improper segregation of chromosomes during mitosis, and radiation-induced mitotic death (mitotic catastrophe) (Cohen-Jonathan et al. 1999; Nair et al. 2001). Furthermore, radiation-induced cellular oxidative damage is initiated by the generation of reactive oxygen species (ROS), which are known to change the oxidative status of cells, resulting in changes in mitochondrial function and activation/inactivation of various proteins involved in the apoptosis (cell death) process (Pradhan et al. 1973). When healthy (normal) cells are exposed to radiation, they ameliorate the damaging effect of free radicals by the release of innate protective molecules such as superoxide dismutase (SOD), glutathione, and metallothionine, which increase and intensify DNA repair mechanisms (Pradhan et al. 1973). Nonetheless, while these protective and repair mechanisms for cells are effi cient, they are not capable of blocking all of the damage, which ultimately leads to normal tissue death.
