ROS Role in the Alterations Induced by Thyroid Dysfunctions

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (15 September 2022) | Viewed by 4323

Special Issue Editors

Special Issue Information

Dear Colleagues,

Thyroid hormones, of which T3 is the main active form, exert numerous physiological effects that influence the growth, development, and metabolism of vertebrates. Therefore, they are considered the main regulators of the homeostasis of the whole organism. However, when their serum level changes, a redox imbalance develops in the target tissues of the hormones, resulting in the development of oxidative stress. In hyperthyroidism and hypothyroidism, a redox imbalance occurs, which can predispose individuals to the onset of dysfunctions affecting tissues, organs, and the whole organism.
With ageing, the incidence of thyroid disorders increases and may be associated with the increased incidence of other pathologies linked to the imbalance of the redox state.
To date, although the main thyroid-hormone-induced oxidative-stress-sensitive signal transduction pathways have been identified, much remains to be understood about their mutual interaction, changes during ageing, pathological states and the impact exerted by antioxidant supplementation.
Given the importance of these topics, it seems appropriate to summarize some of the main recent advances in the role of ROS in alterations due to thyroid dysfunction, by focusing primarily on their impact on thyroid function in health, disease, and ageing.
Authors are encouraged to submit original research and review articles seeking to refine the above topics, potentially including, but not necessarily limited to:
• The role of ROS in thyroid dysfunction;
• Thyroid hormones, ROS, and mitochondrial function;
• Thyroid hormones, ROS, and ageing;
• Thyroid dysfunction, ROS, and chronic diseases;
• Thyroid dysfunction and antioxidant supplementation.

Dr. Paola Venditti
Dr. Gaetana Napolitano
Guest Editors

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Keywords

  • T3
  • thyroid dysfunctions
  • ROS
  • RNS
  • antioxidants

Published Papers (2 papers)

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Research

18 pages, 2447 KiB  
Article
Muscle Oxidative Stress Plays a Role in Hyperthyroidism-Linked Insulin Resistance
by Gianluca Fasciolo, Gaetana Napolitano, Marianna Aprile, Simona Cataldi, Valerio Costa, Maria Teresa Muscari Tomajoli, Assunta Lombardi, Sergio Di Meo and Paola Venditti
Antioxidants 2023, 12(3), 592; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox12030592 - 27 Feb 2023
Cited by 6 | Viewed by 1740
Abstract
While a low level of ROS plays a role in cellular regulatory processes, a high level can lead to oxidative stress and cellular dysfunction. Insulin resistance (IR) is one of the dysfunctions in which oxidative stress occurs and, until now, the factors underlying [...] Read more.
While a low level of ROS plays a role in cellular regulatory processes, a high level can lead to oxidative stress and cellular dysfunction. Insulin resistance (IR) is one of the dysfunctions in which oxidative stress occurs and, until now, the factors underlying the correlation between oxidative stress and IR were unclear and incomplete. This study aims to explore this correlation in skeletal muscle, a tissue relevant to insulin-mediated glucose disposal, using the hyperthyroid rat as a model of oxidative stress. The development of IR in the liver from hyperthyroid animals has been widely reported, whereas data concerning the muscle are quite controversial. Thus, we investigated whether hyperthyroidism induces IR in skeletal muscle and the role of oxidative stress in this process. Particularly, we compared the effects of hyperthyroidism on IR both in the absence and presence of vitamin E (Vit E), acting as an antioxidant. Putative correlations between ROS production, oxidative stress markers, antioxidant capacity and changes in intracellular signalling pathways related to insulin action (AKT) and cellular stress response (EIF2α; JNK; PGC1α; BIP; and NRF1) were investigated. Moreover, we assessed the effects of hyperthyroidism and Vit E on the expression levels of genes encoding for glucose transporters (Slc2a1; Slc2a4), factors involved in lipid homeostasis and insulin signalling (Pparg; Ppara, Cd36), as well as for one of the IR-related inflammatory factors, i.e., interleukin 1b (Il1b). Our results suggest that hyperthyroidism-linked oxidative stress plays a role in IR development in muscle and that an adequate antioxidant status, obtained by vitamin E supplementation, that mitigates oxidative stress, may prevent IR development. Full article
(This article belongs to the Special Issue ROS Role in the Alterations Induced by Thyroid Dysfunctions)
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22 pages, 2436 KiB  
Article
Opposite Effect of Thyroid Hormones on Oxidative Stress and on Mitochondrial Respiration in COVID-19 Patients
by Claudia De Vitis, Carlo Capalbo, Alessandra Torsello, Christian Napoli, Valentina Salvati, Chiara Loffredo, Giovanni Blandino, Giulia Piaggio, Francesca Romana Auciello, Flaminia Pelliccia, Gerardo Salerno, Maurizio Simmaco, Laura Di Magno, Gianluca Canettieri, Flaminia Coluzzi, Rita Mancini, Monica Rocco and Salvatore Sciacchitano
Antioxidants 2022, 11(10), 1998; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11101998 - 08 Oct 2022
Cited by 5 | Viewed by 2135
Abstract
Background: Thyroid hormones (TH)s are master regulators of mitochondrial activity and biogenesis. Nonthyroidal illness syndrome (NTIS) is generally considered an adaptative response to reduced energy that is secondary to critical illness, including COVID-19. COVID-19 has been associated with profound changes in the cell [...] Read more.
Background: Thyroid hormones (TH)s are master regulators of mitochondrial activity and biogenesis. Nonthyroidal illness syndrome (NTIS) is generally considered an adaptative response to reduced energy that is secondary to critical illness, including COVID-19. COVID-19 has been associated with profound changes in the cell energy metabolism, especially in the cells of the immune system, with a central role played by the mitochondria, considered the power units of every cell. Infection by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) affects and alters mitochondrial functions, both to influence its intracellular survival and to evade host immunity. Aim of the study: This study was undertaken to analyze the oxidative balance and mitochondrial respiration in COVID-19 patients with and without NTIS to elucidate the role that thyroid hormones (TH)s play in this context. Methods: In our cohort of 54 COVID-19 patients, admitted to our University Hospital during the COVID-19 pandemic, we evaluated the generation of reactive oxygen species (ROS) by measuring the serum levels of derivatives of reactive oxygen metabolites (dROMs), and we analyzed the antioxidant capacity by measuring the serum biological antioxidant potential (BAP). We then analyzed the mitochondrial respiration in peripheral blood mononuclear cells (PBMC)s of 28 of our COVID-19 patients, using the seahorse instrument (Agilent). Results were correlated with the serum levels of THs and, in particular, of FT3. In addition, the role of T3 on bioelectrical impedance analysis (BIA) and mitochondrial respiration parameters was directly evaluated in two COVID-19 patients with NTIS, in which treatment with synthetic liothyronine (LT3) was given both in vivo and in vitro. Results: In our COVID-19 patients with NTIS, the dROMs values were significantly lower and the BAP values were significantly higher. Consequently, the oxidative stress index (OSi), measured as BAP/dROMs ratio was reduced compared to that observed in COVID-19 patients without NTIS, indicating a protective role exerted by NTIS on oxidative stress. In our COVID-19 patients, the mitochondrial respiration, measured in PBMCs, was reduced compared to healthy controls. Those with NTIS showed a reduced maximal respiratory capacity and a reduced proton leak, compared to those with normal FT3 serum values. Such lowered mitochondrial respiratory capacity makes the cells more vulnerable to bioenergetic exhaustion. In a pilot study involving two COVID-19 patients with NTIS, we could reinforce our previous observation regarding the role of T3 in the maintenance of adequate peripheral hydroelectrolytic balance. In addition, in these two patients, we demonstrated that by treating their PBMCs with LT3, both in vitro and in vivo, all mitochondrial respiration parameters significantly increased. Conclusions: Our results regarding the reduction in the serum levels of the reactive oxygen species (ROS) of COVID-19 patients with NTIS support the hypothesis that NTIS could represent an adaptative response to severe COVID-19. However, beside this beneficial effect, we demonstrate that, in the presence of an acute reduction of FT3 serum levels, the mitochondrial respiration is greatly impaired, with a consequent establishment of a hypoenergetic state of the immune cells that may hamper their capacity to react to massive viral infection. Full article
(This article belongs to the Special Issue ROS Role in the Alterations Induced by Thyroid Dysfunctions)
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