Rbh. Idrus et al., DIFFERENTIAL EFFECT OF ADRENOCORTICOSTEROIDS ON 11-BETA-HYDROXYSTEROID DEHYDROGENASE BIOACTIVITY AT THE ANTERIOR-PITUITARY AND HYPOTHALAMUSIN RATS, Steroids, 61(8), 1996, pp. 448-452
11 beta-Hydroxysteroid dehydrogenase (11 beta-OHSD) is a microsomal en
zyme that catalyzes the dehydrogenation of cortisol (F) to cortisone (
E) in man and corticosterone (B) to 11-dehydrocorticosterone (A) in ra
ts. 11 beta-OHSD has been identified in a wide variety of tissues. The
differential distribution of 11 beta-OHSD suggests that this enzyme h
as locally defined functions that vary from region to legion. The aim
of this study was to investigate the effects of the glucocorticoids B
and dexamethasone (DM), the mineralocorticoid deoxycorticosterone (DOC
), and the inhibitors of 11 beta-OHSD glycyrrhizic acid (GI) and glycy
rrhetinic acid (GE) on 11 beta-OHSD bioactivity at the hypothalamus (H
T) and anterior pituitary (AP). Male Wistar rats were treated with GI
or were adrenalectomized (ADX) and treated with either B, DM, or DOC f
or 7 days. All treatments were in vivo except GE, which was used in vi
tro. Al the end of treatment, homogenates of HT and AP were assayed fo
r 11 beta-OHSD bioactivity, expressed as the percentage conversion of
B to A in the presence of NADP. 11 beta-OHSD bioactivity is significan
tly higher (P < 0.0001) in the AP compared with the HT Adrenalectomy s
ignificantly increased the enzyme activity in the AP (P < 0.05), an ef
fect reversed by B or DM. ADX rats treated with DOC showed decreased e
nzyme activity in the AP (P < 0.001) but increased the activity in the
HT (P < 0.0001). GI increased activity in both HT and AP, whereas GE
decreased activity significantly. We conclude that the modulation of 1
1 beta-OHSD is both steroid specific and tissue specific.