title: Activation of the Nrf2-Keap 1 Pathway in Short-Term Iodide Excess in Thyroid in Rats.
abstract: Wistar rats were randomly divided into groups of varying iodide intake: normal iodide; 10 times high iodide; and 100 times high iodide on Days 7, 14, and 28. Insignificant changes were observed in thyroid hormone levels (p> 0.05). Urinary iodine concentration and iodine content in the thyroid glands increased after high consumption of iodide from NI to 100 HI (p< 0.05). The urinary iodine concentration of the 100 HI group on Days 7, 14, and 28 was 60-80 times that of the NI group. The mitochondrial superoxide production and expressions of Nrf2, Srx, and Prx 3 all significantly increased, while Keap 1 significantly decreased in the 100 HI group when compared to the NI or 10 HI group on Days 7, 14, and 28 (p< 0.05). Immunofluorescence staining results showed that Nrf2 was localized in the cytoplasm in NI group. Although Nrf2 was detected in both cytoplasm and nucleus in 10 HI and 100 HI groups, a stronger positive staining was found in the nucleus. We conclude that the activation of the Nrf2-Keap 1 antioxidative defense mechanism may play a crucial role in protecting thyroid function from short-term iodide excess in rats.
authors.affiliation: Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China.
authors.forename: Tingting
authors.identifier: 0000-0003-0496-2058
authors.initials: T
authors.lastname: Wang
authors.affiliation: Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China.
authors.forename: Xue
authors.initials: X
authors.lastname: Liang
authors.affiliation: Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China.
authors.forename: Iruni Roshanie
authors.identifier: 0000-0002-6284-356X
authors.initials: IR
authors.lastname: Abeysekera
authors.affiliation: Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China.
authors.forename: Umar
authors.identifier: 0000-0003-3641-4187
authors.initials: U
authors.lastname: Iqbal
authors.affiliation: Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China.
authors.forename: Qi
authors.identifier: 0000-0001-6378-5472
authors.initials: Q
authors.lastname: Duan
authors.affiliation: Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China.
authors.forename: Gargi
authors.identifier: 0000-0003-4293-5894
authors.initials: G
authors.lastname: Naha
authors.affiliation: Key Laboratory of Hormones and Development (Ministry of Health), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin 300070, China.
authors.forename: Laixiang
authors.identifier: 0000-0002-0100-4084
authors.initials: L
authors.lastname: Lin
authors.affiliation: Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China.
authors.forename: Xiaomei
authors.identifier: 0000-0001-5725-0690
authors.initials: X
authors.lastname: Yao
mesh_terms: D000818:Animals; D015153:Blotting, Western; D005434:Flow Cytometry; D005455:Fluorescent Antibody Technique; D007454:Iodides / Q000633:toxicity*; D000072019:Kelch-Like ECH-Associated Protein 1 / Q000378:metabolism*; D051267:NF-E2-Related Factor 2 / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D015398:Signal Transduction / Q000187:drug effects; D013961:Thyroid Gland / Q000187:drug effects / Q000378:metabolism*; D013963:Thyroid Hormones / Q000378:metabolism
chemical_list: D007454:Iodides; C486610:KEAP1 protein, rat; D000072019:Kelch-Like ECH-Associated Protein 1; D051267:NF-E2-Related Factor 2; C495637:Nfe2l2 protein, rat; D013963:Thyroid Hormones