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Citation
Tags
HERO ID
4345517
Reference Type
Journal Article
Subtype
Review
Title
Sexual dimorphism and thyroid dysfunction: a matter of oxidative stress?
Author(s)
Fortunato, RS; Ferreira, AC; Hecht, F; Dupuy, C; Carvalho, DP
Year
2014
Is Peer Reviewed?
Yes
Journal
Journal of Endocrinology
ISSN:
0022-0795
EISSN:
1479-6805
Volume
221
Issue
2
Page Numbers
R31-R40
Language
English
PMID
24578296
DOI
10.1530/JOE-13-0588
Abstract
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. H₂O₂ 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 H₂O₂ 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 NOX4 mRNA expression and H₂O₂ 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.
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