Oxidative stress as a key feature of autoimmune thyroiditis: an update

Abstract

iNTrodUcTioN: oxidative stress has been proposed as one of the factors concurring in the pathophysiology of autoimmune thyroid diseases. reactive oxygen species are the main expression of oxidative stress in biological systems, and their production can overcome antioxidant defenses ultimately leading to cell damage, apoptosis, and death. The present review was aimed at describing the state of the art of the relationships between oxidative stress and autoimmune thyroiditis. The most used biomarkers of oxidative stress and their correlation with thyroid function are reported. eVideNce acQUiSiTioN: We conducted a search of the literature in the english language starting from 2000, using the following search terms: "Hashimoto thyroiditis," "autoimmune thyroiditis," "hypothyroidism," "hyperthyroidism," "oxidative stress," "oxidants," "antioxidant," "advanced glycation end products." Both clinical studies and animal models were evaluated. eVideNce SYNTHeSiS: data form clinical studies clearly indicate that the balance between oxidants and antioxidants is shifted towards the oxidative side in patients with autoimmune thyroiditis, suggesting that oxidative stress may be a key event in the pathophysiology of the disease, irrespective of thyroid function. Studies in animal models, such as the NOD.H2h4 mouse, confirm that thyroidal accumulation of ROS plays a role in the initiation and progression of autoimmune thyroiditis. coNclUSioNS: oxidant/antioxidant imbalance represent a key feature of thyroid autoimmunity. oxidative stress parameters could be used as biochemical markers of chronic inflammation, to better predict the disease evolution along its natural history. dietary habits and antioxidant supplements may provide protection from autoimmunity, opening new perspectives in the development of more tailored therapies.

Serum Levels of Soluble Receptor for Advanced Glycation End Products Are Reduced in Euthyroid Children with Newly Diagnosed Hashimoto’s Thyroiditis: A Pilot Study

“…Release of pro-inflammatory cytokines by the infiltrating T and B cells, as well as by the thyrocytes themselves, further contributes to promoting and amplifying tissue damage and inflammation [12]. In this context, an imbalance between the endogenous production of reactive oxygen species (ROS) and the antioxidant defenses has been emerging as a relevant event to the development and progression of the autoimmune process and related glandular dysfunction [13, 14]. Under pathological conditions, including exposure to several environmental triggers (excess iodine, radiation, pollutants, drugs, etc.)…”

“…Under pathological conditions, including exposure to several environmental triggers (excess iodine, radiation, pollutants, drugs, etc.) and autoimmune inflammation itself (T and B lymphocyte activation and pro-inflammatory cytokine release), excess ROS accumulates in thyroid tissue and causes oxidative modifications of proteins, lipids, and DNA, resulting in cell damage and death and tissue inflammation and destruction [14-16]. Moreover, when thyroid dysfunction occurs, it further enhances oxidative stress, since alterations in thyroid hormone concentrations may affect either the generation of ROS or the synthesis of antioxidants, or both [14].…”

“…and autoimmune inflammation itself (T and B lymphocyte activation and pro-inflammatory cytokine release), excess ROS accumulates in thyroid tissue and causes oxidative modifications of proteins, lipids, and DNA, resulting in cell damage and death and tissue inflammation and destruction [14-16]. Moreover, when thyroid dysfunction occurs, it further enhances oxidative stress, since alterations in thyroid hormone concentrations may affect either the generation of ROS or the synthesis of antioxidants, or both [14]. Several studies examined the relation between oxidative stress and HT, by means of several different enzymatic or nonenzymatic molecules, which reflect the oxidant-antioxidant status of the body, sometimes with conflicting results [13, 14, 17-22].…”

“…Moreover, when thyroid dysfunction occurs, it further enhances oxidative stress, since alterations in thyroid hormone concentrations may affect either the generation of ROS or the synthesis of antioxidants, or both [14]. Several studies examined the relation between oxidative stress and HT, by means of several different enzymatic or nonenzymatic molecules, which reflect the oxidant-antioxidant status of the body, sometimes with conflicting results [13, 14, 17-22].…”

Thyroid sequelae of COVID-19: a systematic review of reviews

“…Indeed, the cytokine storm occurring during SARS-CoV-2 infection often results in an uncontrolled inflammatory response that is detrimental to host cells [17,22]. As far as the thyroid gland is concerned, it should be highlighted that several models, including the chronic low-level inflammation associated with aging, the so-called "inflammaging" [28], and the oxidant/antioxidant imbalance associated with thyroid chronic inflammation [29], proved to have a role in the pathogenesis of thyroid diseases. From this point of view, there is potential to consider a thyroid role in the long-term effects of COVID-19.…”