title: Effect of selenium supplementation on activity and mRNA expression of type 1 deiodinase in mice with excessive iodine intake.
abstract: OBJECTIVE
  To investigate the effect of selenium supplementation on the selenium status and selenoenzyme, especially the activity and mRNA expression of type 1 deiodinase (D1) in mice with excessive iodine (EI) intake and to explore the mechanism of selenium intervention on iodine-induced abnormities.
  
  
  METHODS
  Weanling female BALB/c mice were given tap water or 3 mg/L of iodine or supplemented with 0.5 mg/L or 1.0 mg/L of selenium in the presence of excessive iodine for 5 months. Selenium status, thyroid hormone level, hepatic and renal D1 activity and mRNA expression were examined.
  
  
  RESULTS
  Excessive iodine intake significantly decreased the selenium concentration in urine and liver, and the activity of glutathione peroxidase (GSH-Px) in liver. Meanwhile, serum total T4 (TT4) increased while serum total T3 (TT3) decreased. Hepatic D1 enzyme activity and mRNA expression were reduced by 33% and 86%, respectively. Renal D1 enzyme activity and mRNA were reduced by 30% and 55%, respectively. Selenium supplementation obviously increased selenium concentration, activity of GSH-Px and Dl as well as mRNA expression of D1. However, increasing the supplementation of Se from 0.5 to 1.0 mg/L did not further increase selenoenzyme activity and expression.
  
  
  CONCLUSIONS
  Relative selenium deficiency caused by excessive iodine plays an essential role in the mechanism of iodine-induced abnormalities. An appropriate dose of selenium supplementation exercises a beneficial intervention.
authors.affiliation: Department of Nutrition and Food Hygiene, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei, China.
authors.forename: Xue-Feng
authors.initials: XF
authors.lastname: Yang
authors.forename: Xiao-Hui
authors.initials: XH
authors.lastname: Hou
authors.forename: Jian
authors.initials: J
authors.lastname: Xu
authors.forename: Huai-Lan
authors.initials: HL
authors.lastname: Guo
authors.forename: Chen-Jiang
authors.initials: CJ
authors.lastname: Yinq
authors.forename: Xiao-Yi
authors.initials: XY
authors.lastname: Chen
authors.forename: Xiu-Fa
authors.initials: XF
authors.lastname: Sun
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D003404:Creatinine / Q000378:metabolism / Q000652:urine; D019587:Dietary Supplements; D005260:Female; D007453:Iodide Peroxidase / Q000235:genetics / Q000378:metabolism*; D007455:Iodine / Q000633:toxicity* / Q000652:urine; D007668:Kidney / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D012333:RNA, Messenger / Q000378:metabolism; D012643:Selenium / Q000494:pharmacology* / Q000652:urine; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood
chemical_list: D000975:Antioxidants; D012333:RNA, Messenger; D014284:Triiodothyronine; D007455:Iodine; D003404:Creatinine; C109812:iodothyronine deiodinase type I; D007453:Iodide Peroxidase; D012643:Selenium; D013974:Thyroxine