The glucocorticoid receptor (GCR) of the cytosol of liver and brain was studied by radioligand binding assay, using [~3H] dexamethasone (Dex) as the ligand in lethally and nonlethally scalded rats. As compared with controls, the binding capacity (R_0) was decreased and the apparent K_d of [~3H] Dex specific binding was increased in both scalded groups. In the lethal group, the R_u is much lower than that in the nonlethal group. In order to determine whether the decrease of R_0 was due to the translocation of [~3H] Dex-GCR complex into the cell nuclei, the [~3H] corticosterone (B) specific binding of the hepatic nuclei was measured by the exchange assay. There was no significant difference between the control and scalded groups. The possible mechanisms and the clinical significance of these changes were discussed. The glucocorticoid receptor (GCR) of the cytosol of liver and brain was studied by radioligand binding assay, using [~ 3H] dexamethasone (Dex) as the ligand in lethally and nonlethally scalded rats. As compared with controls, the binding capacity (R_0) was decreased and the apparent K_d of [~ 3H] Dex specific binding was increased in both scalded groups. In the lethal group, the R_u is much lower than that in the nonlethal group. In order to determine whether the decrease of R_0 was due to The translocation of [~ 3H] Dex-GCR complex into the cell nuclei, the [~ 3H] corticosterone (B) specific binding of the hepatic nuclei was measured by the exchange assay. There was no significant difference between the control and scalded groups. The possible mechanisms and the clinical significance of these changes were discussed.