title: Effect of maternal excessive iodine intake on neurodevelopment and cognitive function in rat offspring.
abstract: BACKGROUND
  Iodine deficiency and iodine excess are both associated with adverse health consequences. Iodine deficiency during pregnancy leads to insufficient maternal thyroid hormone, subsequently causing irreversible adverse effects on the neurological and cognitive functions of the offspring. The results of our previous epidemiological study suggested that mild iodine excess might increase the prevalence of subclinical hypothyroidism. In the present study, female Wistar rats maintained on low-iodine grain were randomly assigned to three groups based on iodated water concentration: low iodine (LI, 1.2 μg/d), normal iodine (NI, 5-6 μg/d), and 3-fold high iodine (3HI, 15-16 μg/d). The present study investigated whether higher-than-normal iodine intake (3HI) by rats from before pregnancy until breastfeeding affects the postnatal (PN) neurodevelopment (PN7 and PN45) of their offspring during particularly sensitive periods in brain development.
  
  
  RESULTS
  After 12 weeks of treatment (before pregnancy), iodine concentrations in urine and thyroid tissue and circulating thyroxine of adult females correlated with iodine intake. Brain-derived neurotrophic factor (BDNF) expression in the hippocampi of pups on PN7 and PN45 was decreased in 3HI group compared to the NI controls (P < 0.05, all) On PN7 and PN45, the BDNF levels of the 3HI pups were 83.5% and 88.8%, respectively, that of the NI pups. In addition, the 3HI group had a higher neuroendocrine-specific protein A (NSP-A) level than the NI controls on PN7 (P < 0.05). NSP-A levels of the 3HI pups were 117.0% that of the NI pups. No significant difference was observed in the expressions of c-Fos or c-Jun in the hippocampal CA1 region of the 3HI group compared to the controls (P > 0.05). Results from the Morris water maze test revealed that pups of the 3HI group had mild learning and spatial memory deficits.
  
  
  CONCLUSIONS
  The neurodevelopmental and cognitive deficits of the 3HI pups were mild and temporary, likely related to the changes in hippocampal protein expressions of BDNF and NSP-A.
authors.affiliation: Department of Endocrinology and Metabolism, First Affiliated Hospital of China Medical University, Shenyang 110001, People's Republic of China.
authors.forename: Le
authors.initials: L
authors.lastname: Zhang
authors.forename: Weiping
authors.initials: W
authors.lastname: Teng
authors.forename: Yuhui
authors.initials: Y
authors.lastname: Liu
authors.forename: Jing
authors.initials: J
authors.lastname: Li
authors.forename: Jinyuan
authors.initials: J
authors.lastname: Mao
authors.forename: Chenling
authors.initials: C
authors.lastname: Fan
authors.forename: Hong
authors.initials: H
authors.lastname: Wang
authors.forename: Hongmei
authors.initials: H
authors.lastname: Zhang
authors.forename: Zhongyan
authors.initials: Z
authors.lastname: Shan
mesh_terms: D000367:Age Factors; D000818:Animals; D000831:Animals, Newborn; D000891:Anti-Infective Agents, Local / Q000009:adverse effects*; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism; D003072:Cognition Disorders / Q000209:etiology*; D002658:Developmental Disabilities / Q000209:etiology*; D005260:Female; D007455:Iodine / Q000009:adverse effects* / Q000378:metabolism / Q000652:urine; D008297:Male; D018782:Maze Learning; D009422:Nervous System Diseases / Q000209:etiology*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000139:chemically induced* / Q000378:metabolism / Q000503:physiopathology*; D051381:Rats; D017208:Rats, Wistar; D013961:Thyroid Gland / Q000378:metabolism; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood
chemical_list: D000891:Anti-Infective Agents, Local; D019208:Brain-Derived Neurotrophic Factor; D013972:Thyrotropin; D007455:Iodine; D013974:Thyroxine