Thyroid hormones increase ROS release in the mitochondrial respiratory chain ( Figure 1 ) ( 5.1 Thyroid dysfunctions and OxS 5.1.1 Hypothyroidism Even in its subclinical form, hypothyroidism reduces antioxidant system activity, which promotes OxS, causing oxidative damage and altered lipid metabolism in thyroid cells ( 5.1.2 Hyperthyroidism ROS generation is increased by hyperthyroidism ( 5.2 Thyroid disorders and OxS 5.2.1 Nodular goitre OxS promotes thyroid cell proliferation ( Additionally, rare loss-of-function germline mutations of Kelch-like ECH-associated protein 1 (KEAP1) could be detected in nodular goitre leading to Nrf2 pathway activation that favours transcription of cytoprotective and antioxidant enzymes ( 5.2.2 Autoimmune thyroid diseases 5.2.2.1 Hashimoto thyroiditis By interacting with TPO and thyroglobulin (TG) and promoting immunogenicity by altering their morphology and function, NADPH-oxidases (NOXs) involvement in the production of hydrogen peroxide (H 2 O 2 ) regarding thyroid hormone synthesis may be related to the pathophysiology of AITD ( Because it increases ROS production and lowers antioxidant levels, excessive iodine consumption is considered an additional risk factor for developing AITD
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Several lines of evidence including TERT promoter mutations in benign or pre-malignant phases of evolution suggest that the cells of common and dysplastic naevi are more proliferative and not entirely senescent, as some models of naevi propose
