ABSTRACT
<p><b>OBJECTIVE</b>To study the effects of excess iodine intake on neurogranin expression in cerebrum of filial mice and the intervention of selenium.</p><p><b>METHODS</b>Sixty BALB/c mice were divided randomly into four groups with different drinking water: control group (tap water, NC), excess iodine group (3000 microg/L I, EL +), supplementing selenium group (200 microg/L Se, Se +) and the excess iodine plus selenium (3000 microg/L + I 200 microg/L Se, EI + Se +) group. The mice were mated at the end of the fourth month. Serum T4 and T3 were determined on postnatal day 14 and 28. The expression level of neurogranin in filial cerebrum was measured by immunohistochemistry and Western blot.</p><p><b>RESULTS</b>Serum T4 level in EI (68.78 +/- 11.10 nmol/ L) + was lower significantly than that in NC (100.85 +/- 11.47 nmol/ L) and EI + Se + (93.15 +/- 12.10 nmol/ L) on postnatal day 14. Western blot analysis showed that the relative level of neurogranin in EI + (0.621 +/- 0.041) was lower than that in NC (0.841 +/- 0.039) and EI + Se + (0.781 +/- 0.029) on postnatal day 14 (P < 0.05). No significant difference in serum T4 and neurogranin level between four groups on postnatal day 28.</p><p><b>CONCLUSION</b>Excess iodine intake might change the expression of neurogranin in filial cerebrum and the selenium supplementation might alleviate it.</p>
Subject(s)
Animals , Female , Male , Mice , Iodine , Mice, Inbred BALB C , Neurogranin , Selenium , Pharmacology , Telencephalon , Metabolism , Thyroxine , Blood , Triiodothyronine , BloodABSTRACT
<p><b>OBJECTIVE</b>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.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>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.</p>
Subject(s)
Animals , Female , Mice , Antioxidants , Pharmacology , Creatinine , Metabolism , Urine , Dietary Supplements , Iodide Peroxidase , Genetics , Metabolism , Iodine , Toxicity , Urine , Kidney , Metabolism , Liver , Metabolism , Mice, Inbred BALB C , RNA, Messenger , Metabolism , Selenium , Pharmacology , Urine , Thyroxine , Blood , Triiodothyronine , BloodABSTRACT
Long-term excessive iodine intake resulted in an increased TT_4 level and a decreased TT_3 level in maternal serum,meanwhile,hepatic and renal type 1 deiodinase activity decreased dose-dependently.A significant reduction in type 2 deiodinase ( D2 ) activity of 12.5 d placenta was found in 3.0 mg/L or above groups.For 19.5 d uterus,D2 activity decreased and type 3 deiodinase activity increased.The results suggest that excessive iodine has an effect on the embryonic development by regulating maternal-fetal thyroid hormone metabolism.