Binding capacity of plasma corticosteroid-binding globulin as a mechanism for increasing the free fraction of the hormone in the pathogenesis of acute radiation sickness

The research of the hormonal level of the body in the pathogenesis of acute radiation sickness does not lose its relevance due to the expansion of the list of radiation hazard sources. The study results are necessary for clarification of a number of radiobiology concepts on the role of the binding capacity of plasma corticosteroid-binding globulin to blood plasma proteins for increasing the free fraction of the hormone in the dynamics of acute radiation sickness. Determination of the role of free corticoids in the hormonal effect in acute radiation sickness in animals with mono- and biphasic curves of adrenocortical response to radiation was the aim of the work. The experiments were carried out on male rabbits and outbred rats. Animals received a dose of gamma-irradiation, that caused acute radiation sickness of the stage IV. The total content of 11-OX, mcg% was determined by the fluorimetric method Guillemin et al. in the author's modification. To determine the free 11-OX and the binding capacity of CSG, the gel filtration method was used by De Moor et al. in the author's modification. Rabbits were tested 2 hours after irradiation, on days 4 and 8 of radiation sickness. Rats were tested one hour after irradiation, on days 1, 3, 8, and 10 of radiation sickness. The results of the study showed that acute radiation syndrome occurs against the background of an increase in free corticosteroids, which is essential in the pathogenesis of acute radiation sickness. The increase in free corticosteroids in the midst of radiation sickness is primarily due to a decrease in the binding capacity of corticosteroid-binding globulin (CSG or transcortin) and does not depend on the total concentration of the hormone in the blood plasma, which is a general radiobiological pattern. The magnitude of the binding capacity of transcortin is an indicator of protein-steroid interaction.