Abstract
Thyroid diseases, including neoplasms, autoimmune diseases and thyroid dysfunctions, are becoming a serious social problem with rapidly increasing prevalence. The latter is increasingly linked to oxidative stress. There are many methods for determining the biomarkers of oxidative stress, making it possible to evaluate the oxidative profile in patients with thyroid diseases compared to the healthy population. This opens up a new perspective for investigating the role of elevated parameters of oxidative stress and damage in people with thyroid diseases, especially of neoplastic nature. An imbalance between oxidants and antioxidants is observed at different stages and in different types of thyroid diseases. The organ, which is part of the endocrine system, uses free radicals (reactive oxygen species, ROS) to produce hormones. Thyroid cells release enzymes that catalyse ROS generation; therefore, a key role is played by the internal defence system and non-enzymatic antioxidants that counteract excess ROS not utilised to produce thyroid hormones, acting as a buffer to neutralise free radicals and ensure whole-body homeostasis. An excess of free radicals causes structural cell damage, undermining genomic stability. Looking at the negative effects of ROS accumulation, oxidative stress appears to be implicated in both the initiation and progression of carcinogenesis. The aim of this review is to investigate the oxidation background of thyroid diseases and to summarise the links between redox imbalance and thyroid dysfunction and disease.
Highlights
Reactive oxygen species (ROS) are molecules capable of independent existence, which contain an oxygen atom and unpaired electrons [1]
Overproduction of thyroid hormones causes oxidative stress through the overproduction of free radicals, unlike in hypothyroidism, where redox imbalance can be attributed to an inefficient antioxidant defence system [74]
Decreased glutathione levels appear to be a distinctive parameter related to the activation and development of oxidative stress in Hashimoto’s thyroiditis, as oxidative stress is associated with thyroid hormone deficiency, inflammation and autoimmune parameters
Summary
Reactive oxygen species (ROS) are molecules capable of independent existence, which contain an oxygen atom and unpaired electrons [1]. The body’s antioxidant defence against the negative effects of ROS works across a number of different platforms. It involves preventing the formation of radicals, scavenging them and repairing ROS-induced damage. Oxidative stress is an effect of redox imbalance between reactive oxygen species and antioxidant defence [9,15]. It may be caused both by the excessive production of ROS and by an inefficient antioxidant system, resulting in molecular damage [16]. Current reports do not distinguish between the causes and consequences of metabolic abnormalities, so there is a need to develop research on the pathogenesis of thyroid disorders
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