l-Triiodothyronine and l-Reverse-Triiodothyronine Generation in the Human Polymorphonuclear Leukocyte

Woeber, Kenneth A.; Maddux, Betty A.

doi:10.1172/jci109163

Cited by 31 publications

(13 citation statements)

References 29 publications

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“…This would suggest that the fetus possesses the enzyme system necessary for 0-deiodination but that it is normally inactive. A similar result has been obtained by Woebber (1978) using human polymorphonuclear leukocytes from adult and cord blood. It would seem that around the time o f birth there is a change in the nature o f intracellular sulphydryl groups or in the mechanisms responsible for the generation of cellular reducing activity with a resulting in crease in the rate of j3-deiodination.…”

Section: Discussionsupporting

confidence: 86%

Thyroid Hormone Relationships in the Fetal and Newborn Lamb

et al. 1980

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Plasma thyroxine (T4) and reverse triiodothyronine (rT3) concentrations have been measured in chronically catheterised sheep fetuses during the last third of gestation. In some animals T4 and rT3 concentrations fell before delivery but there was no change in the T4/rT3 ratio. In several serially sampled fetuses a small rise in plasma triiodothyronine concentration has been demonstrated in the days preceding delivery. Infusion of cortisol to fetuses commencing at 130 days of gestation (term 147 days) with the simultaneous administration of progesterone to delay labour resulted in changes, in T4 and rT3 concentrations which were similar to those normally seen at term. The nature of the changes in the peripheral metabolism of T4 around the time or birth are discussed.

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Section: Discussionsupporting

confidence: 86%

Thyroid Hormone Relationships in the Fetal and Newborn Lamb

et al. 1980

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“…The erythrocytes were washed twice with 2-3 vol of both 0.9% NaCl and KHBB before use. Because leukocytes are reported to concentrate amino acids (26) and to convert T4 to T3 and rT3 (27), the leukocyte layer was carefully aspirated with each washing. Unless otherwise stated, the T4 and glucose concentrations were 10 ,ug/dl and 100 mg/dl, respectively.…”

Section: Methodsmentioning

confidence: 99%

“…The homogenate was twice extracted with 4 ml 100% ethanol and the extracts pooled. The pooled extract was stored at -20°C for [24][25][26][27][28][29][30][31][32][33][34][35][36] h to allow further precipitation of liver tissue, recentrifuged, the final volume recorded, and an aliquot stored at -20°C for assay. Using this method, [125I]T3 was extracted with an efficiency that was inversely proportional to the liver weight according to the following equation: extraction efficiency (%) = -21.6 x liver weight (g) + 91.9 (r = 0.96, P < 0.001).…”

Section: Methodsmentioning

confidence: 99%

Regulation of the Conversion of Thyroxine to Triiodothyronine in the Perfused Rat Liver

Jennings¹,

Ferguson²,

Utiger³

1979

J. Clin. Invest.

100

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A B S T R A C T This study was undertaken to de-termine what factors control the conversion of thyroxine (T4) to triiodothyronine (T3) in rat liver under conditions approximating those found in vivo. Conversion of T4 to T3 was studied in the isolated perfused rat liver, a preparation in which the cellular and structural integrity is maintained and that can perform most of the physiologic functions of the liver. The perfused liver readily extracted T4 from perfusion medium and converted it to T3. Production of T3 by the perfused liver was a function of the size of the liver, the uptake of T4 by the liver, and the presence of T4-5'-deiodinase activity. Production of T3 was increased by increasing the uptake of T4 by liver, which could be accomplished by increasing the liver size, by increasing the perfusate T4 concentration, or by decreasing the perfusate albumin concentration. These changes occurred without altering the conversion of T4 to T3. The liver had a large capacity for extracting T4 and for T4-5'-deiodination to T3, which was not saturated at a T4 concentration of 60 ,ug/dl. Production of T3 was decreased by inhibiting hepatic T4-5'-deiodinase with propylthiouracil, which decreased T3 production by decreasing the conversion of T4 to T3. Propylthiouracil did not alter hepatic T4 uptake.Fasting resulted in a progressive decrease in hepatic T4 uptake to 42% of control levels by the 3rd d of fasting; this was accompanied by a proportionate decrease in T3 production. The rate of conversion of T4 to T3 did not change during fasting. When T4 uptake in 2-d-fasted rat livers was raised to levels found in fed rats by increasing the perfusate T4 concentration from 10 to 30 ,g/dl, T3 production retumed to normal. Again, no change in the rate of conversion of T4 to T3 was observed.Presented in part at the Annual Meeting of The American Society for Clinical Investigation, Washington, D. C., 6 May 1979(1979 1614These results indicate that the decreased hepatic T3 production during fasting primarily results from decreased hepatic uptake of T4, rather than from changes in T4-5'-deiodinase activity. Thus, these studies have delineated a new mechanism that functions independently of enzyme quantity or activity whereby production of T3 from T4 is regulated.

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“…It has long been known that activated neutrophils are capable of deiodinating both T 3 and T 4 (Woeber 1971, Woeber et al 1972, Klebanoff & Green 1973, Woeber & Ingbar 1973. Research from the seventies already found that phagocytosing human neutrophils can generate both T 3 and rT 3 from T 4 and that this deiodinating activity was mainly present in the granule fraction of the cells (Woeber 1976(Woeber , 1978. Neutrophils were also shown to contain saturable nuclear-binding sites for T 3 (Woeber 1977).…”

Section: Intracellular Thyroid Hormone Metabolism In Neutrophilsmentioning

confidence: 99%

Thyroid hormone metabolism in innate immune cells

Spek

Fliers

Boelen

2017

Journal of Endocrinology

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Thyroid hormone (TH) metabolism and thyroid status have been linked to various aspects of the immune response. There is extensive literature available on the effects of thyroid hormone on innate immune cells. However, only recently have authors begun to study the mechanisms behind these effects and the role of intracellular TH metabolism in innate immune cell function during inflammation. This review provides an overview of the molecular machinery of intracellular TH metabolism present in neutrophils, macrophages and dendritic cells and the role and effects of intracellular TH metabolism in these cells. Circulating TH levels have a profound effect on neutrophil, macrophage and dendritic cell function. In general, increased TH levels result in an amplification of the pro-inflammatory response of these cells. The mechanisms behind these effects include both genomic and non-genomic effects of TH. Besides a pro-inflammatory effect induced by extracellular TH, the cellular response to pro-inflammatory stimuli appears to be dependent on functional intracellular TH metabolism. This is illustrated by the fact that the deiodinase enzymes and in some cell types also thyroid hormone receptors appear to be crucial for adequate innate immune cell function. This overview of the literature suggests that TH metabolism plays an important role in the host defence against infection through the modulation of innate immune cell function.

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l-Triiodothyronine and l-Reverse-Triiodothyronine Generation in the Human Polymorphonuclear Leukocyte

Cited by 31 publications

References 29 publications

Thyroid Hormone Relationships in the Fetal and Newborn Lamb

Thyroid Hormone Relationships in the Fetal and Newborn Lamb

Regulation of the Conversion of Thyroxine to Triiodothyronine in the Perfused Rat Liver

Thyroid hormone metabolism in innate immune cells

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