抄録
<jats:p>Thyroid diseases, such as autoimmune disease and benign and malignant nodules, are more prevalent in women than in men, but the mechanisms involved in this sex difference is still poorly defined. H<jats:sub>2</jats:sub>O<jats:sub>2</jats:sub>is produced at high levels in the thyroid gland and regulates parameters such as cell proliferation, migration, survival, and death; an imbalance in the cellular oxidant–antioxidant system in the thyroid may contribute to the greater incidence of thyroid disease among women. Recently, we demonstrated the existence of a sexual dimorphism in the thyrocyte redox balance, characterized by higher H<jats:sub>2</jats:sub>O<jats:sub>2</jats:sub>production, due to higher NOX4 and Poldip2 expression, and weakened enzymatic antioxidant defense in the thyroid of adult female rats compared with male rats. In addition, 17β-estradiol administration increased<jats:italic>NOX4</jats:italic>mRNA expression and H<jats:sub>2</jats:sub>O<jats:sub>2</jats:sub>production in thyroid PCCL3 cells. In this review, we discuss the possible involvement of oxidative stress in estrogen-related thyroid pathophysiology. Our current hypothesis suggests that a redox imbalance elicited by estrogen could be involved in the sex differences found in the prevalence of thyroid dysfunctions.</jats:p>
収録刊行物
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- Journal of Endocrinology
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Journal of Endocrinology 221 (2), R31-R40, 2014-02-27
Bioscientifica