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） int...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 D 1 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 D1 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.展开更多
Background Type 1 deiodinase （D1） plays an important role in the metabolism of thyroid hormone and has close relationship with thyroid function. In this study we explore the effects of iodine intake on D1 activity a...Background Type 1 deiodinase （D1） plays an important role in the metabolism of thyroid hormone and has close relationship with thyroid function. In this study we explore the effects of iodine intake on D1 activity and its mRNA expression and its possible mechanism. Methods Forty-eight Wistar rats were randomly divided into six groups with 8 in each： low iodine （LI）, normal iodine （NI）, five-fold iodine （HI5）, ten-fold iodine （HI10）, fifty-fold iodine （HI50）, one hundred-fold iodine （HI100） group. Three months, six months and twelve months after admistration of potassium iodate, they were sacrificed and thyroids were excised. The expression of D1 mRNA in the thyroid tissue was determined by RT-PCR and D1 activity was analyzed by ^125I-rT3 as substrate. The thyroid hormone was measured with radioimmunoassay method. Results Compared with NI group, D1 mRNA expression in LI groups slightly decreased, and D1 activity greatly increased. Both T3 and T4 in thyroid tissue significantly decreased, but the T3/T4 ratio increased. D1 mRNA expression decreased in all HI groups, and D1 activity was significantly lower in HI groups. There was a tendency of decrease in D 1 activity with increased doses of iodine intakes. There was no significant difference in T4 in thyroid tissue between HI groups and NI group, but a tendency of decrease in T3 level was found in all HI groups. Conclusions In the case of iodine deficiency, D 1 activity increased greatly in order to convert more T4 to T3. Excess iodine can inhibit both D1 mRNA expression and its activity to protect organism from being injured by excessive T3.展开更多
基金This work was supported by the National Science Foundation of China (NSFC) (No. 30230330).
文摘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 D 1 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 D1 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.
基金This study was supported by grants from the National Nature Science Foundation of China (No.30230330) and Tianjin Technology Development Project (No.05YFGDSF02700).
文摘Background Type 1 deiodinase （D1） plays an important role in the metabolism of thyroid hormone and has close relationship with thyroid function. In this study we explore the effects of iodine intake on D1 activity and its mRNA expression and its possible mechanism. Methods Forty-eight Wistar rats were randomly divided into six groups with 8 in each： low iodine （LI）, normal iodine （NI）, five-fold iodine （HI5）, ten-fold iodine （HI10）, fifty-fold iodine （HI50）, one hundred-fold iodine （HI100） group. Three months, six months and twelve months after admistration of potassium iodate, they were sacrificed and thyroids were excised. The expression of D1 mRNA in the thyroid tissue was determined by RT-PCR and D1 activity was analyzed by ^125I-rT3 as substrate. The thyroid hormone was measured with radioimmunoassay method. Results Compared with NI group, D1 mRNA expression in LI groups slightly decreased, and D1 activity greatly increased. Both T3 and T4 in thyroid tissue significantly decreased, but the T3/T4 ratio increased. D1 mRNA expression decreased in all HI groups, and D1 activity was significantly lower in HI groups. There was a tendency of decrease in D 1 activity with increased doses of iodine intakes. There was no significant difference in T4 in thyroid tissue between HI groups and NI group, but a tendency of decrease in T3 level was found in all HI groups. Conclusions In the case of iodine deficiency, D 1 activity increased greatly in order to convert more T4 to T3. Excess iodine can inhibit both D1 mRNA expression and its activity to protect organism from being injured by excessive T3.
