HYPERTHERMIC STRESS MODULATES THE FUNCTIONS OF RAT-LIVER GLUCOCORTICOID RECEPTOR

A mild whole body hyperthermic stress causes a rapid and reversible re duction of rat liver glucocorticoid receptor (GR) binding capacity and affects the stability of the GR-DNA complexes formed after thermal tr ansformation of the receptor. These changes appear to be physiological ly relevant, since they are accompanied by a decrease in dexamethasone induction of hepatic tyrosine aminotransferase (TAT). In spite of the decreased rate of the GR degradation in Liver cytosol of hyperthermic as compared to control rats, the total amount of the GR and its prote olytic products recognized by BuGR2 monoclonal antibody was found to b e lower in the former cytosol, bur higher in the respective nuclei.