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*DEXAMETHASONE
*HYDROCORTISONE
*RU-486
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Journal of Clinical Endocrinology & Metabolism, Vol 73, 192-196, Copyright © 1991 by Endocrine Society

ARTICLES

Quantitative comparison of aromatase induction by dexamethasone in fibroblasts from a patient with familial cortisol resistance and a patient with cortisol hyperreactive syndrome

S Iida, K Moriwaki, H Fujii, M Gomi, M Tsugawa, Y Nakamura, T Kitani and S Tarui
Second Department of Internal Medicine, Osaka University Medical School, Japan.

The ability of dexamethasone to induce aromatase activity was tested in fibroblasts from a patient with familial cortisol resistance, a patient with cortisol hyperreactive syndrome, and five normal subjects. Dexamethasone increased enzyme activity in all cases in a concentration- dependent manner (over a range of 1-1000 nmol/L). In fibroblasts from a patient with familial cortisol resistance, the response curve of dexamethasone-induced aromatase activity was shifted to the right compared to that of normal cells. However, the maximal induction of the enzyme at 1 mumol/L dexamethasone was unchanged in cortisol-resistant fibroblasts. On the other hand, in fibroblasts from the patient with the cortisol hyperreactive syndrome, the half-maximal effect of dexamethasone was similar to that in normal cells, but maximum induction of aromatase activity was 2 times greater than that in normal cells. The glucocorticoid antagonist RU 486 inhibited dexamethasone- induced aromatase activity in these patients' cells and in normal cells in a concentration-dependent manner, indicating that the altered effects of dexamethasone on aromatase induction observed in each cell type were mediated through glucocorticoid receptors.


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