The perinatal encounter of the developing receptor and the appropriate hormone results in normal receptor development. In the perinatal critical period the receptors can also bind hormone-like molecules. This can cause false imprinting. Retinol and retinoic acid have receptors which belong to the steroid receptor superfamily. In the present study, receptor assays were used for demonstrating the maximum binding capacity (B(max)) and affinity (K(D)) of thymus glucocorticoid and uterus estrogen receptors of rats, neonatally treated or not treated with retinol or retinoic acid. Neonatal treatment of rats (imprinting) with vitamin A (retinol) increased the B(max) of thymus glucocorticoid receptors (P<0.001 in males and P<0.03 in females) and the affinity (K(D)) of uterine estrogen receptors (P<0.03) in adult animals. The affinity of thymus glucocorticoid receptors and maximum binding capacity of uterine estrogen receptors were not affected. Neonatal treatment with all-trans retinoic acid increased uterine estrogen receptor affinity (P<0.02) without changing the affinity or density of thymic glucocorticoid receptors and B(max) of uterine estrogen receptors. The effect of triple retinoic acid treatment was weaker than a single treatment with retinol. The experiments highlight the false imprinting-provoking effect of retinoids (acting on members of the nuclear receptor superfamily) on steroid receptors in the perinatal critical period and the possible impact in human cases.
|Number of pages||5|
|Journal||Endocrinology and Metabolism, Supplement|
|Publication status||Published - Jan 1 1997|
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism