A new glucocorticoid receptor detected in host rat liver but not in various hepatomas.

ABSTRACT

Previously a new glucocorticoid receptor (Peak C), which eluted with 0.12 to 0.14 M NaCl from DEAE-cellulose column, was identified in addition to another receptor (Peak B), a classic type of glucocorticoid receptor, which eluted with 0.05 to 0.08 M NaCl. Peak C appeared after stress or injection of a high dose (20 micrograms/100 g body weight) of dexamethasone into rats. Peak C was also detected in the liver of rats bearing various tumors, but it was not found in malignant tumors (Yoshida sarcoma and Yoshida ascites hepatoma AH 130), a less malignant Yoshida ascites hepatoma (LY-5), or in minimal deviation-type hepatomas (Morris hepatomas 7316A and 7794A). The absence of Peak C in these tumors coincided with the inability of the glucocorticoid to induce tryptophan oxygenase in these tumors and in the liver of rats during early postnatal development. Peak B was consistently observed in various hepatomas and immature rat liver with capability to induce tyrosine aminotransferase. Thus Peak C appeared to be a highly differentiated type of glucocorticoid receptor mediating specific hormone actions and to be present in mature liver cells, but not in immature liver or tumor cells, even of the minimal deviation type.