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The mechanism by which radiation exposure leads to death in mammalian organisms remains unknown, although numerous hypotheses have been discussed. At the lowest total body radiation doses leading to mammalian mortality, death occurs from the hematopoietic syndrome (HS). HS is thought to result from the cell killing effects of radiation in the bone marrow that lead to low numbers of circulating blood cells and the resultant HS symptoms, such as infection [from the loss of white blood cells (WBC)] and bleeding (presumably from the loss of platelets). Over approximately the last half century, the dose of ionizing radiation that kills half of an experimental group/exposed population, known as the LD50, has been used as a parameter to compare the radiation sensitivity of various mammalian species. It is well known that the LD50 is highly variable for different mammalian species; however, the bone marrow cells of different species, strains and individuals are known to have remarkably similar sensitivities to the cell killing effects of ionizing radiation (1, 2). These results suggest that the lethal effects of radiation in blood cells may not be the primary mechanism by which the HS causes death. Our results have suggested that radiation induced activation of the coagulation cascade, resulting in a condition known as disseminated intravascular coagulation (DIC), could be the major mechanism by which relatively low doses of radiation could lead to animal, including human, mortality.

Is Disseminated Intravascular Coagulation the Major Cause of Mortality from Radiation at Relatively Low Whole Body Doses?