Supplemental selenium alleviates the toxic effects of excessive iodine on thyroid.

As excessive iodine intake is associated with a decrease of the activities of selenocysteine-containing enzymes, supplemental selenium was hypothesized to alleviate the toxic effects of excessive iodine. In order to verify this hypothesis, Balb/C mice were tested by giving tap water with or without potassium iodate and/or sodium selenite for 16 weeks, and the levels of iodine in urine and thyroid, the hepatic selenium level, the activities of glutathione peroxidase (GSHPx), type 1 deiodinase (D1), and thyroid peroxidase (TPO) were assayed. It had been observed in excessive iodine group that hepatic selenium, the activities of GSHPx, D1, and TPO decreased, while in the groups of 0.2 mg/L, 0.3 mg/L and 0.4 mg/L supplemental selenium, the urinary iodine increased significantly. Compared with the group of excessive iodine intake alone, supplemental selenium groups had higher activities of GSHPx, D1, and TPO. We could draw the conclusion that supplemental selenium could alleviate toxic effect of excessive iodine on thyroid. The optimal dosage of selenium ranges from 0.2 to 0.3 mg/L which can protect against thyroid hormone dysfunction induced by excessive iodine intake.

[Intervention of selenium on neurogranin expression in filial cerebrum of mice with excess iodine].

OBJECTIVE: To study the effects of excess iodine intake on neurogranin expression in cerebrum of filial mice and the intervention of selenium. METHODS: 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. RESULTS: 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. CONCLUSION: Excess iodine intake might change the expression of neurogranin in filial cerebrum and the selenium supplementation might alleviate it.

Effect of selenium supplementation on activity and mRNA expression of type 1 deiodinase in mice with excessive iodine intake.

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. CONCLUSION: 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.

Selenium supplement alleviated the toxic effects of excessive iodine in mice.

The relationship between the iodine intake level of a population and the occurrence of thyroid diseases is U-shaped. When excessive iodine is ingested, hypothyroidism or hyperthyroidism associated with goiter might develop. The aim of the study was to evaluate the effect of Se supplementation on the depression of type 1 deiodinase (D1) and glutathione peroxidase (GSHPx) activities caused by excessive iodine. D1 activity was assayed by the method with 125I-rT3 as a substrate. Compared to the effect of iodine alone, iodine in combination with selenium increased the activities of D1 and GSHPx. The addition of selenium alleviated the toxic effects of iodine excess on the activities of D1 and GSHPx.

[Influences of excess iodine on thyroid hormone concentrations in cerebrum of filial mice and intervention of selenium].

OBJECTIVE: To study the influence of excessive iodine intake on thyroid hormones in cerebrum of filial mice and intervention of selenium. METHODS: 60 Balb/c mice were divided randomly into 4 groups: control group, iodine group, selenium group and iodine plus selenium group and given tap water, tap water containing iodine 3000 microg/L, tap water containing selenium 200 microg/L and tap water containing iodine plus selenium 200 microg/L respectively as drinking water. At the end of the fourth month, the mice mated. Thyroid hormones and TSH in serum and in cerebrum of filial mice were determined at the postnatal 0, 14th and 28th day. RESULTS: At the postnatal 14th day, serum TT4 level was lower significantly, and serum TSH was higher in iodine group than those in control group and in the iodine plus selenium group. At the postnatal 0 day and 14th day, thyroid hormone concentrations in the cerebrum of progeny of mice were lower significantly in iodine group than those in control group, selenium group and iodine plus selenium (P < 0.05). No significant difference was observed among the four groups in TT4, TT3 and rT3 concentrations in serum and cerebrum at the postnatal 28th day. CONCLUSION: Excessive iodine intake can change thyroid hormone concentrations in the cerebrum of progeny of mice and selenium supplementation exerted favorable effects on it.

[Effect of selenium supplement on the disordered lipid metabolism induced by the overdose of iodine in mice].

OBJECTIVE: To explore the effect of selenium supplement on the disordered lipid metabolism induced by the overdose of iodine in mice. METHODS: The 80 Balb/c mice were randomly divided into eight groups, the normal control group, the high iodine group (drunk the water containing iodine 3000 microg/L) and six selenium groups (drunk the water containing iodine 3000 microg/L and selenium 0.1, 0.2, 0.3, 0.4, 0.5, 0.75 mg/L). The total cholesterol and triglyceride in serum and liver were determined. RESULTS: The total cholesterol in serum, the total cholesterol and triglyceride in liver of high-iodine group increased significantly compared with normal control group. There is no difference between normal control group and the group drunk the water contained 0.2 mg/L selenium. CONCLUSION: It suggests that it is an effective intervention dosage to drunk water containing 0.2 mg/L selenium.

[Effect of high-iodine intake on MBP mRNA expression in cerebrum of filial mice and selenium intervention].

OBJECTIVE: To study the effect of selenium supplementation on myelin basic protein (MBP) mRNA expression in cerebrum of high-iodine intake filial mice. METHODS: 135 weanling female Balb/C mice were assigned into 3 groups and given drinking water including different doses of iodine and selenium. Normal control (NC, tap water), high iodine intake group (HI, 3.0 mg/L I of drinking water), high iodine intake and selenium supplementation group I (HI + Se, 3.0 mg/L I + 0.5 mg/L Se of drinking water). All the male and female mice were mated after 4 months later, related indicators of filial mice on 14 day were determined. RESULTS: In filial mice, compared with NC group, serum TT4 decreased significantly in HI groups, TT3 also decreased, and mRNA expression of MBP in cerebrum was down-regulated 27%. The selenium suppleme ntation groups inhibited the decrease of TT4 and TT3, up regulated the m RNA expression of MBP in cerebrum. CONCLUSION: High-iodine Intake can decrease thyroxine of filial mice, which maybe is the reason for down-regulated m RNA expression of MBP in cerebrum, and selenium can exert some intervention by thyroxine, but need to verify more.