Thyroid Hormones, Oxidative Stress, and Inflammation.

Antonio Mancini,Chantal Di Segni,Sebastiano Raimondo,Diego Currò,Giulio Olivieri,Elisabetta Meucci,Andrea Silvestrini

doi:10.1155/2016/6757154

Antonio Mancini, Chantal Di Segni + Show 5 more

Open Access

https://doi.org/10.1155/2016/6757154

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Abstract

Inflammation and oxidative stress (OS) are closely related processes, as well exemplified in obesity and cardiovascular diseases. OS is also related to hormonal derangement in a reciprocal way. Among the various hormonal influences that operate on the antioxidant balance, thyroid hormones play particularly important roles, since both hyperthyroidism and hypothyroidism have been shown to be associated with OS in animals and humans. In this context, the nonthyroidal illness syndrome (NTIS) that typically manifests as reduced conversion of thyroxine (T4) to triiodothyronine (T3) in different acute and chronic systemic conditions is still a debated topic. The pathophysiological mechanisms of this syndrome are reviewed, together with the roles of deiodinases, the enzymes responsible for the conversion of T4 to T3, in both physiological and pathological situations. The presence of OS indexes in NTIS supports the hypothesis that it represents a condition of hypothyroidism at the tissue level and not only an adaptive mechanism to diseases.

Highlights

Oxidative stress (OS) is defined as an unbalance between the production of prooxidant substances and antioxidant defenses
Plasma levels of small antioxidant molecules, such as Vitamin E and coenzyme Q10 (CoQ10), and thyroid hormones are closely related to each other [2, 17]. Both hyperthyroidism and hypothyroidism have been shown to be associated with OS and special cases are the autoimmune thyroiditis or the functional picture of low-T3 syndrome, observed in acute and chronic nonthyroidal illness syndrome (NTIS) [17,18,19]
Monocytes mobilized and attracted by MCP1, together with neutrophils and lymphocytes T present in the adipose tissue, originate an inflammatory response that is reinforced by the stimulation of the synthesis and secretion of tumor necrosis factor (TNF) by macrophages, in turn induced by the increased production of free fatty acids (FFAs) by adipocytes

Summary

Introduction

Oxidative stress (OS) is defined as an unbalance between the production of prooxidant substances and antioxidant defenses. An increased ROS production by the respiratory chain resulting from the rise of the energetic demand or substrate availability [12], as occurs in obesity, or mitochondrial dysfunction or impairment, can produce cell damage and contribute to the pathophysiology of different diseases, such as Mediators of Inflammation inflammatory (e.g., rheumatoid arthritis) and cardiovascular (e.g., myocardial infarction) diseases [2]. Plasma levels of small antioxidant molecules, such as Vitamin E and CoQ10, and thyroid hormones are closely related to each other [2, 17] Both hyperthyroidism and hypothyroidism have been shown to be associated with OS and special cases are the autoimmune thyroiditis or the functional picture of low-T3 syndrome, observed in acute and chronic nonthyroidal illness syndrome (NTIS) [17,18,19]. The aim of our review is to discuss and clarify the relationships between thyroid hormones and parameters of OS in the context of the inflammatory diseases

Oxidative Stress and Inflammation

The Role of Thyroid Hormones in Antioxidant Regulation

The Model of Low-T3 Syndrome

Conclusion