Thyroid Hormone Regulates Rat lodothyronine Deiodinase Activi Changes Different from Those in in Rat Brain Placental Type III ty by Inducing Kinetic the Same Isozyme
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چکیده
The kinetics of type III iodothyronine deiodinase (5-D) in rat placenta and brain and the role of phospholipids in enzyme activity were determined. Pregnant Sprague-Dawley rats were given either vehicle (control group) or T4 (15 jug/100 g bw/day; hyperthyroid group) from the 14th to the 21st day of gestation. Mitochondrial-microsomal fractions of the placenta and brain were used as the source of T4 5D. Placental T4 5-D activity in the hyperthyroid group was increased when determined at 13 nM T4, but it was not significantly different from the control value when assayed at 1.3 ,uM T4. In contrast, T4 5-D in the brain was significantly increased in the hyperthyroid group regardless of the substrate concentration. Hyperthyroid rats showed decreased Km for placental 5-D and increased Vmax for brain 5-D. CM-Sephadex chromatography of solubilized placental microsomes was performed to determine whether phospholipids cause a reduction in the Km of placental 5-D in hyperthyroid rats. T3 5-D activity was undetectable unless protein-containing fractions were combined with phospholipidcontaining fractions in the reaction mixture. Kinetic studies revealed that phospholipids had no effects on either Km or Vmax of placental T3 5-D. These data indicate that 5-D activity in the rat placenta is increased in hyperthyroidism with different kinetic changes from those in the brain, and that phospholipids have no effects on the kinetic parameters of placental 5-D whereas they are essential for the enzyme activity.
منابع مشابه
Effects of pharmacological and nonpharmacological treatments on thyroid hormone metabolism and concentrations in rat brain.
The activities of the 5'I-deiodinase (5'D-I), 5'II deiodinase (5'D-II) and 5III-deiodinase (5D-III) isoenzymes and tissue concentrations of thyroxine (T4) and triiodothyronine (T3) were measured in up to 10 regions of the rat brain after acute and subchronic nonpharmacological (sleep deprivation, 12 h fasting, 14 days' calorie-reduced diet) and pharmacological (ethanol, haloperidol, clozapine, ...
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تاریخ انتشار 2006