Ramauge M, Pallud S, Esfandiari A, Gavaret J, Lennon A, Pierre M, Courtin F
U. 96 INSERM - Unité de Recherche sur la Glande Thyroïde et la Régulation Hormonale, Le Kremlin-Bicêtre Cedex, France.
Endocrinology. 1996 Jul;137(7):3021-5. doi: 10.1210/endo.137.7.8770927.
A type III iodothyronine deiodinase (D-III) that inactivates thyroid hormones has been recently cloned and identified as a selenoprotein in neonatal rat skin. However, selenium (Se) deficiency does not affect the D-III activity in the rat placenta and decreases the D-III in the rat brain only slightly. This study examines the effect of Se on the D-III activity in cultures of rat brain astrocytes. Astrocytes were depleted in Se by maintaining them in Se-free chemically defined medium for 7 days. These conditions decreased the activity of a recognized selenoprotein, glutathione peroxidase, 3-10-fold. D-III activity induced by 12-0-tetradecanoylphorbol-13-acetate (TPA) was also decreased 2-6-fold. Addition of 30 nM Se to the culture medium caused a rapid increase in TPA-induced D-III activity visible within 1 h. This Se effect was maximal at 3 h (4-fold increase) and dose-dependent. Se also increased the induction of D-III by acidic Fibroblast Growth Factor, 8-bromo-cAMP, T4, or retinoic acid. Cycloheximide blocked the effect of Se on TPA-induced D-III activity, whereas actinomycin D did not. Thus the rapid effect of Se does not require messenger RNA synthesis but requires protein synthesis. We conclude that the D-III in astrocytes is probably a selenoprotein.
