HYPERCORTICISM IN THE PATHOGENESIS OF ACUTE RADIATION SICKNESS AND CONDITIONS OF INCREASED RADIORESISTANCE.

Abstract

OBJECTIVE: To investigate the role of hypercorticism in the pathogenesis of acute radiation sickness (ARS) and under conditions of increased radioresistance, assessing the theoretical and clinical significance of impaired protein-steroid interactions. MATERIALS AND METHODS: An analysis was conducted of experimental data from irradiated animal models: chinchilla rabbits (n=20), dogs (n=15), WISTAR rats (n=63), guinea pigs (n=49), and BALB/c mice (n=32). Some animals underwent adrenal autotransplantation. Fluorometric and gel filtration methods were used to assess protein-steroid interactions; total-body γ-irradiation was administered at doses inducing grade IV ARS. Data were statistically processed using Student's t-test. RESULTS: A biphasic adrenocortical response to radiation was observed in most species, whereas rabbits exhibited a monophasic decline in corticosteroid levels. During the peak of ARS, impaired corticosteroid-binding globulin (CBG) function led to increased levels of free, biologically active corticoids, even with normal or reduced total 11-oxycorticosteroids. A consistent radiobiological pattern was established: an increase in the free hormone fraction due to diminished CBG binding capacity. Adrenal autotransplantation prior to irradiation reduced corticoid levels, enhanced CBG binding capacity during ARS, and decreased free corticoid concentrations, resulting in a protective effect and increased radioresistance. CONCLUSION: The findings underscore the critical role of corticosteroid regulation and CBG functional status in the body's response to radiation exposure. Modulation of adrenal activity and correction of protein-steroid interactions may be considered a promising strategy for enhancing radioresistance.