The thyroid hormones, triiodothyronine (T3) and its prohormone, thyroxine (T4), are tyrosine-based hormones produced by the thyroid gland that are primarily responsible for regulation of metabolism. Iodine is necessary for the production of T3 and T4. A deficiency of iodine leads to decreased production of T3 and T4, enlarges the thyroid tissue and will cause the disease known as simple goitre. The major form of thyroid hormone in the blood is thyroxine (T4), which has a longer half-life than T3. The ratio of T4 to T3 released into the blood is roughly 20 to 1. T4 is converted to the active T3 (three to four times more potent than T4) within cells by deiodinases (5'-iodinase). These are further processed by decarboxylation and deiodination to produce iodothyronamine (T1a) and thyronamine (T0a). All three isoforms of the deiodinases are selenium-containing enzymes, thus dietary selenium is essential for T3 production.
Keywords
Thyroxine
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Portable Chemiluminescence-Based Lateral Flow Assay Platform for the Detection of Cortisol in Human Serum
Applications: LFAReactive species: Human
"Abstract: In this study, we developed the portable chemiluminescence (CL)-based lateral flow assay (LFA) platform for the detection of cortisol in human serum. Cortisol is well-known as a stress hormone due to its high relevancy for human mental and physical health, such as hypertension or depression. To date, a number of optical devices have provided the sensitive determination of levels of analytes. However, this modality type still requires costly optical modules. The developed CL platform is simply composed of two detection modules along with a loading part for the LFA strip. The LFA membrane contains gold nanoparticle probes conjugated with antibodies against cortisol and horseradish peroxidase (HRP), which can also efficiently increase the luminescent signal by providing many areas for anti-cortisol antibody and HRP. The measured voltage signals coming from the photodiode in a CL reader were compared with a standard microplate reader for the evaluation of accuracy. The linear range observed for cortisol was measured to be 0.78-12.5 μg/dL (R2 = 0.99) with a limit of detection (LOD) of 0.342 μg/dL. In addition, the CL-LFA reader showed a high correlation (R2 = 0.96) with the standard cortisol console (COBAS 8000, Roche), suggesting that our developed CL-based LFA platform can be usable in situ."Article snippet: Thyroxine (T4)-BSA was purchased from Creative Diagnostics.
Figure 1. The measured chemiluminescence intensity shows the selectivity of cortisol from other interferent analytes (T3, T4, TSH, PTH).
Background
Thyroxine is produced and secreted by the thyroid gland and is involved in the regulation of growth, development and energy metabolism in almost all tissues and organs of the body. It consists of two main forms: tetraiodothyronine (T4) and the more biologically active triiodothyronine (T3). The main thing produced and secreted by the thyroid gland is T4, which reaches different tissues and organs through blood circulation. Deiodinase (DIO) converts intracellular T4 to T3, but because its expression varies widely in different tissues and cells, the level of T3 varies from cell to cell. DIO1 is expressed predominantly in the liver, thyroid, and kidneys and maximizes thyroxine activity by converting T4 to T3.
Thyroid hormone (TH) biosynthesis and secretion are tightly controlled by the hypothalamic-pituitary-thyroid (HPT) axis. Iodine is necessary for the synthesis of thyroid hormones; the thyroid gland produces T4 at a rate of 80-100 μg per day, and T3 is produced primarily by extra-thyroidal deiodination. THs circulate in the body primarily in bound form, and changes in serum levels of bound proteins alter serum concentrations of total T4 and T3 but do not affect free hormone concentrations.
Figure 1. TH biosynthesis (Source: Somasundaram N, et al. 2020)
Thyroxine acts in the cell in two main ways; on the one hand, thyroxine binds to both thyroxine nuclear receptors (TRs) and thyroid hormone response elements (TREs) and affects the expression of downstream genes at the transcriptional level, which is referred to as the gene function of thyroxine. On the other hand, thyroxine affects downstream cellular signaling by binding to receptors on cell membranes, thereby affecting downstream cellular signaling or interacting with different signaling pathways, which is referred to as the nongenetic function of thyroxine. In the physiological state, thyroxine is involved in the regulation of a wide range of cellular life activities, including cell growth and development, inflammation, respiratory metabolism, etc., and is essential for the maintenance of normal cellular activities. If there is an abnormality in thyroxine and its signaling pathways, such as in the case of hyperthyroidism, substantial damage can be done to the organism. Thyroid disease can manifest as hypothyroidism or hyperthyroidism, as well as benign or malignant thyroid nodules.
Alternative Names
T4 [BSA] tetraiodothyronine (T4) [BSA]
References
1. Mateo RCI, et al. Thyroxine and treatment of hypothyroidism: seven decades of experience. Endocrine. 2019 Oct;66(1):10-17.
2. Somasundaram N, et al. Thyroid Disorders. Sri Lanka Journal of Diabetes Endocrinology and Metabolism. 2020 Jun;10:41.
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References
Maternal serum perfluoroalkyl substance mixtures and thyroid hormone concentrations in maternal and cord sera: The HOME Study
ENVIRONMENTAL RESEARCH
Authors: Lebeaux, Rebecca M.; Doherty, Brett T.; Gallagher, Lisa G.; Zoeller, R. Thomas; Hoofnagle, Andrew N.; Calafat, Antonia M.; Karagas, Margaret R.; Yolton, Kimberly; Chen, Aimin; Lanphear, Bruce P.; Braun, Joseph M.; Romano, Megan E.
Background: Per- and polyfluoroalkyl substances (PFAS) are ubiquitous. Previous studies have found associations between PFAS and thyroid hormones in maternal and cord sera, but the results are inconsistent. To further address this research question, we used mixture modeling to assess the associations with individual PFAS, interactions among PFAS chemicals, and the overall mixture. Methods: We collected data through the Health Outcomes and Measures of the Environment (HOME) Study, a prospective cohort study that between 2003 and 2006 enrolled 468 pregnant women and their children in the greater Cincinnati, Ohio region. We assessed the associations of maternal serum PFAS concentrations measured during pregnancy with maternal (n = 185) and cord (n = 256) sera thyroid stimulating hormone (TSH), total thyroxine (TT4), total triiodothyronine (TT3), free thyroxine (FT4), and free triiodothyronine (FT3) using two mixture modeling approaches (Bayesian kernel machine regression (BKMR) and quantile g-computation) and multivariable linear regression. Additional models considered thyroid autoantibodies, other non-PFAS chemicals, and iodine deficiency as potential confounders or effect measure modifiers. Results: PFAS, considered individually or as mixtures, were generally not associated with any thyroid hormones. A doubling of perfluorooctanesulfonic acid (PFOS) had a positive association with cord serum TSH in BKMR models but the 95% Credible Interval included the null (beta = 0.09; 95% CrI: -0.08, 0.27). Using BKMR and multivariable models, we found that among children born to mothers with higher thyroid peroxidase antibody (TPOAb), perfluorooctanoic acid (PFOA), PFOS, and perfluorohexanesulfonic acid (PFHxS) were associated with decreased cord FT4 suggesting modification by maternal TPOAb status. Conclusions: These findings suggest that maternal serum PFAS concentrations measured in the second trimester of pregnancy are not strongly associated with thyroid hormones in maternal and cord sera. Further analyses using robust mixture models in other cohorts are required to corroborate these findings.
L-Thyroxine Therapy for Older Adults With Subclinical Hypothyroidism and Hypothyroid Symptoms Secondary Analysis of a Randomized Trial
ANNALS OF INTERNAL MEDICINE
Authors: de Montmollin, Maria; Feller, Martin; Beglinger, Shanthi; McConnachie, Alex; Aujesky, Drahomir; Collet, Tinh-Hai; Ford, Ian; Gussekloo, Jacobijn; Kearney, Patricia M.; McCarthy, Vera J. C.; Mooijaart, Simon; Poortvliet, Rosalinde K. E.; Quinn, Terence; Stott, David J.; Watt, Torquil; Westendorp, Rudi; Rodondi, Nicolas; Bauer, Douglas C.
Background: L-thyroxine does not improve hypothyroid symptoms among adults with subclinical hypothyroidism (SCH). However, those with greater symptom burden before treatment may still benefit. Objective: To determine whether L-thyroxine improves hypothyroid symptoms and tiredness among older adults with SCH and greater symptom burden. Design: Secondary analysis of the randomized, placebocontrolled trial TRUST (Thyroid Hormone Replacement for Untreated Older Adults with Subclinical Hypothyroidism Trial). (ClinicalTrials.gov: NCT01660126) Setting: Switzerland, Ireland, the Netherlands, and Scotland. Participants: 638 persons aged 65 years or older with persistent SCH (thyroid-stimulating hormone level of 4.60 to 19.9 mIU/L for >3 months and normal free thyroxine level) and complete outcome data. Intervention: L-thyroxine or matching placebo with mock dose titration. Measurements: 1-year change in Hypothyroid Symptoms and Tiredness scores (range, 0 to 100; higher scores indicate more symptoms) on the Thyroid-Related Quality-of-Life Patient-Reported Outcome Questionnaire among participants with high symptom burden (baseline Hypothyroid Symptoms score >30 or Tiredness score >40) versus lower symptom burden. Results: 132 participants had Hypothyroid Symptoms scores greater than 30, and 133 had Tiredness scores greater than 40. Among the group with high symptom burden, the Hypothyroid Symptoms score improved similarly between those receiving L-thyroxine (mean within-group change, -12.3 [95% CI, -16.6 to -8.0]) and those receiving placebo (mean within-group change, -10.4 [CI, -15.3 to -5.4]) at 1 year; the adjusted between-group difference was -2.0 (CI, -5.5 to 1.5; P = 0.27). Improvements in Tiredness scores were also similar between those receiving L-thyroxine (mean within-group change, -8.9 [CI, -14.5 to -3.3]) and those receiving placebo (mean within-group change, -10.9 [CI, -16.0 to -5.8]); the adjusted between-group difference was 0.0 (CI, -4.1 to 4.0; P = 0.99). There was no evidence that baseline Hypothyroid Symptoms score or Tiredness score modified the effects of L-thyroxine versus placebo (P for interaction = 0.20 and 0.82, respectively). Limitation: Post hoc analysis, small sample size, and examination of only patients with 1-year outcome data. Conclusion: In older adults with SCH and high symptom burden at baseline, L-thyroxine did not improve hypothyroid symptoms or tiredness compared with placebo.
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Figure 1. The measured chemiluminescence intensity shows the selectivity of cortisol from other interferent analytes (T3, T4, TSH, PTH). 
Figure 1. TH biosynthesis
