Changes of Circulating Thyroxine, Triiodothyronine and Reverse Triiodothyronine After Radiographic Contrast Agents

Bürgi, H; Wimpfheimer, C; Burger, Albert; Zaunbauer, Wolfgang; Rösler, H; Lemarchand-Béraud, T

doi:10.1210/jcem-43-6-1203

Cited by 190 publications

(58 citation statements)

References 16 publications

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“…T4 was also administered to dams in order to increase the rT3 concentration in AF and to emphasize its fall. In this study, the administration of IOP in vivo caused a rise in serum concentrations of T4 and rT3 and a fall in serum concentration of T3 in rats, as previously described in humans and rats [23][24][25][26]. It is known that, in such peripheral tissues as the liver and kidney, T4 is deiodinated to T3, and rT3 is deiodinated to 3,3'-T2 by type I 5'-deiodinase [27].…”

Section: Discussionsupporting

confidence: 69%

Inhibition of Placental Thyroxine 5-Deiodinase Activity Decreases Amniotic Fluid Concentration of 3,3',5'-Triiodothyronine in Rat.

et al. 1993

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Abstract. We investigated whether the inhibition of placental T4 5-deiodinase (5-D) activity would decrease the amniotic fluid (AF) concentration of rT3. Iopanoic acid (TOP) was used to inhibit placental T4 5-D activity. From gestation days 14 to 17, a group of rats received IOP (10 mg/100 g bwlday, sc) once daily in experiment (exp) 1, and received it (40 mg/100 g bw/day) four times daily in exp 2. In exp 2, control dams received propylthiouracil (PTU; 2 mg/100 g bw/day) instead of IOP. Methimazole and T4 were also given to all dams in exp 1 and 2. On day 17 of gestation, we collected the liver, placenta, blood, and AF of each animal. In the IOP-treated group in both experiments, the serum T4 concentration was significantly increased. Hepatic T4 5'-deiodinase activity was significantly decreased by either PTU or IOP administration. In both experiments placental T4 5-D activity was significantly decreased in the IOP-treated group. The concentration of rT3 in AF was significantly decreased in the TOP-treated group in exp 2 (1.71 vs. 0.75 nmol/l, P<0.01) despite a higher serum T4 concentration. There was a significant positive correlation between placental T4 5-D activity and the concentration of rT3 in AF in exp 2 (r=0.62, P<0.05). These observations indicate that the inhibition of placental T4 5-D activity decreases the concentration of rT3 in rat AF, and that placental 14 5-D and the T4 concentration in maternal serum plays important roles in maintaining the concentration of rT3 in rat AF.

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Section: Discussionsupporting

confidence: 69%

Inhibition of Placental Thyroxine 5-Deiodinase Activity Decreases Amniotic Fluid Concentration of 3,3',5'-Triiodothyronine in Rat.

et al. 1993

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“…The conversion is enzymatic, because it is temperature, pH, and substrate concentration dependent (29)(30)(31)(32)(33). Compounds such as iopanoic acid, propylthiouracil, and rT3 have been demonstrated to be potent inhibitors of T4 to T3 conversion in vitro (29,33,34) and in vivo (35)(36)(37). Visser et al (38) first reported the importance of sulfhydryl groups in the conversion of T4 to T3 because thiol protective agents such as glutathione or dithiothreitol (DTT) added in vitro enhanced 5'-deiodinating enzyme activity, whereas thiol oxidizing agents abolished it.…”

Section: Introductionmentioning

confidence: 99%

The Role of Sulfhydryl Groups on the Impaired Hepatic 3′,3,5-Triiodothyronine Generation from Thyroxine in the Hypothyroid, Starved, Fetal, and Neonatal Rodent

Harris¹,

Fang²,

Hinerfeld³

et al. 1979

J. Clin. Invest.

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A B S T R A C T The role of nonprotein sulflhydryl groups (NPSH) in the decreased in vitro hepatic 3',3,5-triiodothyronine (T3) generation from thyroxine (T4) in the starved, hypothyroid, fetal and 1-to 4-d-old neonatal rat and dwarf mouse was assessed. NPSH were measured in fresh 25% liver homogenates prepared in 0.1 M P04/10 mM EDTA buffer. As 516 4-d-old neonates, but had little or no effect in the fetal and hypothyroid rat and dwarf mouse. Liver homogenates stored for 6 mo at -20°C lost their capacity to generate T3 from T4. NPSH concentrations in the frozen homogenates decreased progressively with increasing storage and were absent by 6 mo. 5'-Deiodinase activity correlated with NPSH concentration in the stored homogenates (r = 0.95, P < 0.005). Addition of DTT partially restored hepatic T3 generation in the frozen homogenate. It is concluded that NPSH are important for the action of the liver 5'-deiodinase. The decreased hepatic T3 generation in the starved rat is associated with decreased NPSH but not with a decrease in the absolute quantity of 5'-deiodinase because provision of sulfhydryl groups restored hepatic T3 generation to normal. In contrast, the decreased hepatic T3 generation in the adult hypothyroid rodent and in the fetal rat is probably due to a decrease in the enzyme concentration per se. In the 1-and 4-d neonatal rat, the decrease in hepatic T3 generation is secondary to a decrease in NPSH and the deiodinating enzyme.

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“…propylthiouracil (23,24), glucocorticoids in high doses (25)(26)(27), certain radiographic contrast media (28,29), and the beta adrenergic blocking agents, propranolol (30) and amiodarone (31). It has generally been assumed that all of these factors act primarily to decrease production of T3 from T4, rather than to increase peripheral degradation ofT3, and direct studies have shown this to be true in the case of cirrhosis (5,22), fasting (12,32), and diabetes (15).…”

mentioning

confidence: 99%

Observations on the factors that control the generation of triiodothyronine from thyroxine in rat liver and the nature of the defect induced by fasting.

Balsam¹,

Ingbar²

1979

J. Clin. Invest.

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A B S T R A C T Studies were performed to explore the mechanism underlying the impaired generation of 125-I-3,5,3'-triiodothyronine (T3) from 1251-thyroxine (T4) (T3-neogenesis) in preparations of liver from rats fasted for 48 h and the prevention of this effect by the feeding of glucose. T3-neogenesis in livers from fasted animals and those fed chow or glucose was assessed in various mixtures of crude microsomal fractions with either buffer or cytosols. T3-neogenesis was mediated by an enzyme present in the microsomal fraction whose activity was enhanced by cytosolic cofactor(s). In livers from animals fasted for 48 h, the supporting activity of cytosol was decreased, whereas the activity of the enzyme was unaffected. Administration of glucose as the sole nutritional source prevented the decrease in the supporting activity of hepatic cytosol that was regularly observed in the case of animals totally deprived of food.The diminished supporting activity for T3-neogenesis provided by liver cytosol from fasted animals was restored to normal by enrichment with either NADPH or GSH, but the two cofactors appeared to act at different loci. GSH stimulated T3-neogenesis in microsomes incubated in the absence of cytosol, i.e., in buffer, whereas NADPH did not. The stimulatory effect of both agents was blocked by the sulfhydryl oxidant, diamide, which also inhibited T3-neogenesis in mixtures of microsomes with cytosols. Taken together, these observations suggest that GSH acts directly on the enzyme in the crude microsomal fraction, whereas NADPH acts within the cytosol, possibly by increasing the concentration of GSH through the action of the enzyme glutathione reductase, for which NADPH is a cofactor. In this light, the decreased supporting activity of hepatic cytosol

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Changes of Circulating Thyroxine, Triiodothyronine and Reverse Triiodothyronine After Radiographic Contrast Agents

Cited by 190 publications

References 16 publications

Inhibition of Placental Thyroxine 5-Deiodinase Activity Decreases Amniotic Fluid Concentration of 3,3',5'-Triiodothyronine in Rat.

Inhibition of Placental Thyroxine 5-Deiodinase Activity Decreases Amniotic Fluid Concentration of 3,3',5'-Triiodothyronine in Rat.

The Role of Sulfhydryl Groups on the Impaired Hepatic 3′,3,5-Triiodothyronine Generation from Thyroxine in the Hypothyroid, Starved, Fetal, and Neonatal Rodent

Observations on the factors that control the generation of triiodothyronine from thyroxine in rat liver and the nature of the defect induced by fasting.

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