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Biochemistry
Published in Burkhard Madea, Asphyxiation, Suffocation,and Neck Pressure Deaths, 2020
Tg, a homodimeric glycoprotein made up of two 330 kDa chains, plays a fundamental role in the synthesis of thyroid hormones 3,5,3′-triiodo-L-thyronine (T3) and 3,5,3′,5′-tetraiodo-L-thyronine (thyroxine or T4). After synthesis, Tg is transported and stored in the follicular lumen. The thyroid follicles comprise a monolayer of polarized thyrocytes with the baso-lateral surface facing the bloodstream and the apical surface delimiting a central, spherical follicle lumen. The lumen is filled with ‘colloid’ (mainly highly concentrated Tg in different stages of oligomerization). Iodine enters thyroid follicular cells as inorganic iodide and is transformed into its organic form by the iodination of specific tyrosyl residues of Tg to form monoiodotyrosine (3-iodotyrosine, MIT) and 3,5′-diiodotyrosine (DIT). Thyroid peroxidase is the key enzyme in thyroid hormone formation as it catalyzes both the iodination of specific tyrosyl residues of Tg and coupling MIT and DIT to produce T3 and T4. Highly iodinated Tg is removed from the follicular lumen by micropinocytosis and undergoes proteolytic cleavage to release T3 and T4, which are then secreted into the bloodstream [23,25,26,46,58].
Developmental Aspects of the Alveolar Epithelium and the Pulmonary Surfactant System
Published in Jacques R. Bourbon, Pulmonary Surfactant: Biochemical, Functional, Regulatory, and Clinical Concepts, 2019
Jacques R. Bourbon, Caroline Fraslon
The administration of exogenous thyroid hormones or analogs to the fetus or to the pregnant female has been shown to accelerate various aspects of lung development in several species. Thyroxine (T4) thus increased the number of lamellar bodies and induced an early disappearance of glycogen in fetal rabbit370 or rat371 lung. Ballard and co-workers372 injected a pregnant doe with 3,5-dimethyl-3′-isopropyl-L-thyronine, a synthetic analogue of triiodothyronine (T3) which crosses the placenta more readily than the native hormone. They observed increased PC synthesis from labeled choline and increased glycogen utilization by fetal lung as well as increased phospholipid content in lung lavage fluid. Enlarged lung volume, accelerated thinning of alveolar septa, and increased alveolar stability at deflation were also obtained by T4 or T3 treatment of the rabbit fetus.373 Comparable changes in lung morphology were observed in the adult rat treated with dessicated thyroid,374 suggesting an effect of thyroid hormones on alveolar septation. Accelerating effects of T4 on lung maturation have also been observed in fetal lamb375 and chicken embryo.319 A clinical trial of thyroxine treatment in the human fetus376 revealed enhanced fetal lung maturity, as assessed by the microviscosity value of the amniotic fluid lipids.
The Pituitary Thyroid Axis
Published in Istvan Berczi, Pituitary Function and Immunity, 2019
The thyroid gland produces thyroxin (3, 5, 3′, 5′-tetraiodo-L-thyronine or T4), which is metabolized to triiodothyronine (3, 5, 3′-triodo-L-thyronine or T3), which is considered to be the biologically active form of thyroxin. Although thyroid hormones are very important for the normal maintenance of a variety of body functions, their mechanism of action is still in debate. In a recent review, Sterling1 lists six different pathways of thyroid hormone action, for which at least some supportive experimental evidence exists. These are Acting on nuclear transcriptionMitochondrial activationRegulation of the sodium pumpIncorporation of thyroid hormones into thyrosin pathwaysActing through adrenergic receptorsActing on the plasma membrane
Possible Contributions of Nongenomic Actions of Thyroid Hormones to the Vasculopathic Complex of COVID-19 Infection
Published in Endocrine Research, 2022
Paul J. Davis, Hung-Yun Lin, Aleck Hercbergs, Kelly A. Keating, Shaker A. Mousa
A receptor for thyroid hormones has been described on the dimeric plasma membrane structural protein, integrin αvβ3.1–3 The principal ligand of the receptor is L-thyroxine (T4), whose endocrine role had previously been considered exclusively to be that of a prohormone for 3,5,3ʹ-triiodo-L-thyronine (T3), the activator of nuclear receptors for thyroid hormone.4 The nongenomic actions of T4 initiated at the cell surface have been shown in preclinical and clinical studies to be focused on cancer cells and dividing blood vessel cells. In tumor cells, T4 can be a proliferative and anti-apoptotic factor.1 At physiological concentrations, T3 is bound minimally by the integrin.1 In contrast, 3,5ʹ,3ʹ-T3 (reverse T3, rT3) – biologically inactive in the nucleus – is bound by αvβ3 at nanomolar concentrations that can be achieved clinically.5 rT3 initiates several actions at the integrin,5,6 but, like T4, is also known to stimulate actin polymerization,4,7 a process important to the platelet aggregation and angiogenesis that are deranged in the vasculopathy of COVID-19 infection.8,9
Coronaviruses and Integrin αvβ3: Does Thyroid Hormone Modify the Relationship?
Published in Endocrine Research, 2020
Paul J. Davis, Hung-Yun Lin, Aleck Hercbergs, Kelly A. Keating, Shaker A. Mousa
The nonthyroidal illness syndrome (NTIS) is a set of serum thyroid function test results that is often present in systemic illness that does not primarily involve the pituitary-thyroid axis.30 The clinical laboratory findings may include elevated circulating free thyroxine (FT4), reduced total serum 3,5,3-triiodo-L-thyronine (T3), and normal thyrotropin (TSH). Serum reverse T3 (3,3,5-triiodo-L-thyronine, rT3) may also be elevated in the syndrome. NTIS is not seen to be an indication for therapeutic intervention, but elevations of FT4 and rT3 may be factors that promote tumor cell proliferation.14,30,31 We have raised the possibility that clinical cancers complicated by NTIS and that are not responding to conventional therapies may reflect growth-promoting actions of T4 and rT3.30
An assay for screening xenobiotics for inhibition of rat thyroid gland peroxidase activity
Published in Xenobiotica, 2020
Roger J. Price, Rachel Burch, Lynsey R. Chatham, Larry G. Higgins, Richard A. Currie, Brian G. Lake
The thyroid gland produces the hormones L-thyroxine (3,3′,5,5′-tetraiodo-L-thyronine; T4) and triiodo-L-thyronine (3,3′,5-triodo-L-thyronine; T3). Thyroid hormones are involved in important physiological processes including regulation of energy metabolism, growth and differentiation, and development and maintenance of brain function (DeVito et al., 1999; Miller et al., 2009). Chemicals may disrupt thyroid gland function by a number of modes of action including interference with thyroid hormone synthesis or secretion, increased thyroid hormone catabolism and excretion, and disruption of the conversion of T4 to T3 (Capen, 2001; DeVito et al., 1999; Miller et al., 2009). In terms of inhibition of thyroid hormone synthesis, a number of chemicals have been shown to inhibit thyroid peroxidase (TPO) activity (EC 1.11.1.8). TPO catalyses the iodination of tyrosyl residues in thyroglobulin (forming mono- and di-iodinated forms) followed by coupling of the iodotyrosyl residues to form the thyroid hormones (Capen, 2001; Taurog et al., 1996). Known inhibitors of TPO include the antihyperthyroid drugs 6-propyl-2-thiouracil (PTU) and methimazole (MMI), anti-bacterial agents, flavonoids, isoflavones, industrial chemicals and some pesticides (Capen, 2001; Divi & Doerge, 1996; Divi et al., 1997; Doerge & Decker, 1994; Freyberger & Ahr, 2006; Paul et al., 2013, 2014).