The article reviewed dietary iodine reference intakes for different populations constituted by major countries and international organizations. Lowor high iodine intake can renderrisks to human health and there are different cut-points of iodineexcess for susceptible population. Universal salt iodization demonstratedthe influence on the spectrum of thyroid diseases and its benefitsoutweighrisks since its significant benefits on human potential and quality of life. This article has suggested practical evaluation indicators for certification of sufficient iodine intaketo keep adequate iodine intake for population.

The choline acetyltransferase (CHAT) and the molecular forms of acetyl-cholinesterase (ACHE) activites in various brain regions of 20-day-old hypothyroid and hyper-thyroid rats were measured. The results provided the following information: 1) CHAT and ACHE activities were directly interrelated with thyroid hormones. 2) In both hypothyroid and hyperthyroid rats the nonextractable ACHE activity was distinctly decreased in every brain region, suggesting that both conditions were affected in the critical period of cholinergic synaptic development. 3) The ratio of membrane-bound ACHE to soluble ACHE decreased;it showed that thyroid hormone deficiency might distrub development and maturation of cholinergic neurons. 4) In most regions of the central nervous system,the CHAT seemed to be more affected than ACHE by thyroid hormones.

The effects of different iodide intakes on the thyroid sodium iodide symporter (NIS) mRNA expression, thyroid hormones, urinary iodine and tissue iodine in thyroid were observed. NIS mRNA expression was elevated; and urinary iodine, thyroid tissue iodine and thyroid hormones were significantly lowered in low iodine group. In high iodine group, NIS mRNA expression was inhibited and thyroid hormones decreased. The results show that NIS is the important component of this autoregulatory mechanism. Both low and high iodine intakes can lead to hypothyroidism.

Objective:To study the master iodine nutrition status of population living in areas with different iodine in drinking water and the cut-off point of stopping iodized salt supply and the range of adequate iodine intake for the strategy of prevention from iodine deficiency or excess. Method:Thirteen townships points along the Yellow River downstream in Shandong were investigated and divided into six groups(A-F) based on water iodine concentrations of 0-50,50-100,100-150,150-300,300-800 and over 800 ?g/L. The indicators of water iodine,edible salt iodine,urinary iodine(UI) and thyroid goiter were observed. Results:From A,B,C,D,E and F group,the medians of water iodine concentration were 20.3,91.4,143.2,203.6,341.9 and 812.3 ?g/L,of edible salt iodine were 0,25.7,25.8,30.4,36.4 and 33.0 mg/kg,and of UI were 116.8,354.2,400.4,607.9,881.3 and 1 213.8 ?g/L respectively. The goiter rates were 10.8,8.6,15.0,14.2,14.9 and 25.0 % respectively . The sample proportion of UI below 100 ?g/L was 8.2%,of 100-300 ?g/L was 18.2% and of over 300 ?g/L was 73.6%. Frequency excursion of UI had a high trend towards water iodine concentration over 90?g/L in 5 groups. The proportion of UI over 300 ?g/L increased,consistent with higher water iodine level. Median UI of all groups with iodized salt decreased significantly,especially group F. There were significant correlations between UI and water iodine. Iodine nutrition status was markedly excessive in group B,C,D,E and F. Conclusions:Iodine nutrition status of most residents consuming drinking water with iodine concentration about 20 ?g/L should be adequately supplied with eligible iodized salt. Iodine intakes in groups B-F were excessive,and iodized salt supply should be stopped there. The cut-point of water iodine level where iodized salt stopped could possibly be 90 ?g/L,and the range of adequate iodine intake,in terms of drinking water,could be defined at range of over 20 to 90 ?g/L in iodine concentration.

Objective:To investigate the effects of exogenous hydrogen peroxide(H_2O_2)on mitochondrial superoxide production and mitochondrial membrane potential changes(△ψ)in fisher rat thyroid cell line(FRTL).Methods:Following 1 mmol/L H_2O_2 exposure in FRTL cells for 10 min,30 min and 24 h,mitochondrial superoxide production was measured by living cell imaging and flow cytometry using MitoSOX.The mitochondrial membrane potential was assayed by spectrofluorimeter and fluorescent microscopy using rhodamine 123(rh123).The cell viability was detected by MTT colorimetric method.Morphological changes were observed by invert microscope.Apoptosis assay was performed by acridine orange staining.Results:Quantitative measurements of the mean intensities of MitoSOX demonstrated significant increase with 1 mmol/L H_2O_2 following 10 min,30 min and 24 h treatment in FRTL cells compared with that of control.Fluorescence intensity of rh123 and optical density of MTr were significantly decreased in FRTL ceils with 1 mmol/L H_2O_2 following 30 min and 24 h treatment(P ＜ 0.01).Under light microscope and fluorescence microscope the characteristic morphological features of programmed cell death,pickuosis,karyorrhexis,and cell shrinkage were observed after acridine orange staining.Conclusion:Acute and chronic exogenous H_2O_2 exposure cause oxide stress in FRTL cells,which result in the increase of mitochondrial superoxide production,△ψdecline,cell necrosis and apoptosis.

BACKGROUND: Triiodothyronine (T3) is an important regulation factor at the critical period of brain development. It maybe control the successive differentiation during the development of central nervous system (CNS).OBJECTIVE: To monitor the differentiation of neural stem cells (NSCs) induced by T3 and the thyroid hormone receptor (TR) mRNA expression changes.DESIGN: Open experiment.SETTING: Department of Pathology, Tianjin Medical College of Chinese People's Armed Police Force; Institute of Endocrinology of Tianjin Medical University.MATERIALS: This study was carried out in the Tianjin Medical University between January 2003 and March 2005.Ten-to-twelve-week-old aborted fetuses were obtained from the General Hospital of Tianjin Medical University with the approval of the local ethical committee. Informed consents were obtained from the mothers and their relatives.METHODS: ①Under the aseptic condition, the bilateral cortex of human fetal brain was removed and dissociated by brief mechanical trituration in D-Hanks. Then, 20 μg/L bFGF and 30 nmol/L T3 were used to induce the proliferation of NSCs and inoculated to poly-L-lysine-coated 24-well plate and 25 mL culture flask for routine culture at 1 ×109 L-1. The culture medium was DMEM/F12 serum-free complemented with N2. Half of the culture medium was changed every 48 hours.Seven days later, bFGF was discarded, only T3 was used for induction and differentiation. ② At 1, 2 and 3 weeks of culture, cells were collected, and RT-PCR was semiquantitatively used to detect TR mRNA expression changes at different stages of differentiation of NSCs. Isoforms were identified by immuocytochemistry.MAIN OUTCOME MEASURES: ①Cellular morphology observation and isoforms identification before and after differentiation of NSCs induced by T3. ② TR mRNA expression changes during the differentiation of NSCs.RESULTS: ①The hNSCs were round and had a smooth surface and gradually gathered to neurospheres. The proliferative hNSCs were nestin-positive and incorporated BrdU. When NSCs were induced by T3 for one week, most of the cells took on monopole or double poles, and had long and thin processes. The differentiated cells were neurofilament protein (NFP)-positive, galactocerebroside (GC)-positive or glial fibrillary acidic protein (GFAP)-positive. When NSCs were induced by T3 for three weeks, most of the cells were big, with unclear cell membrane, round nucleus, many thick processes which had many branches. The spider-like cells were scattered, and 80% of the cells were myelin basic protein-positive. ② TRα1 mRNA expression level was the highest before inducing NSCs. With the induction of T3, the expression level was decreased gradually, and was the lowest at 2 weeks, and then was rebounded gradually, but the final level was still lower than that of NSC (F =32.49, P =0.008). The tendency of TRα2 mRNA expression alteration was identical with that of TRα1 mRNA. TRβ1 mRNA expression level was the lowest in NSC, was increased gradually with the induction of T3 and attained the highest level at 2 weeks of induction of T3. Furthermore, the expression level of TRβ1 mRNA was also higher than that of TRα1 at the same time (t =15.64,P =0.001), and it reached the lowest level at 3 weeks of the induction. TRα3 expression level was firstly decreased after the differentiation induced by T3, and was close to the expression level of NSC at 2 weeks of induction (F =51.94, P =0.378), then was decreased to lower lever.CONCLUSION: T3 can induce NSC to differentiate into neurons, oligodendrocyte and astrocytes. TR mRNAs are expressed in different time intervals during the differentiation of NSCs.

Thyroid function ultimately depends on appropriate iodine supply to the gland. Thyroid hormone deiodination is an intrinsic component of the thyroid hormone homeostasis. Type Ⅰ iodothyronine deiodinase (D1) plays an important role in thyroid hormone metabolism and has close relationship with thyroid function. Based on successfully establishing animal models of iodine deficiency and iodine excess in Babl/c mice (Babl/c mice were randomly divided into five groups: low iodine (LI), normal iodine (NI), five-fold iodine (5HI) , ten-fold iodine (10HI) and fifty-fold iodine (50HI) group. Three months and six months after admistration, they were sacrificed and thyroids were excised), the expression level of D1 mRNA were examined by using real time quantitative PCR method. D1 activity was analyzed by 125I-rT3 as substrate combined with ion-exchange chromatography. The thyroid hormone was measured with radioimmunoassay method. The data revealed that in the case of iodine deficiency, both D1 mRNA expression and D1 activity was greatly increased(compared with NI groups, P

FRTL cells were incubated in the culture medium containing 10 -6 -10-3 mol/L KI for 24, 48 and 72 h, and the levels of sodium iodide symporter (NIS) mRNA and protein were measured using RT-PCR and Western blot. The levels of NIS mRNA in FRTL cells incubated with different concentrations of iodide for 24 and 48 h showed no significant difference as compared with the control group, however, NIS protein was reduced gradually in FRTL cells incubated with different concentrations of iodide for 48 and 72 h as compared with that in control group. The higher the iodide concentration, the lower the levels of NIS protein. The results show that acute iodine excess does not affect the expression of NIS mRNA, but down-regulates NIS protein expression. Iodine excess may regulate the expression of NIS through post-transcription.

Objective To observe the effects of different iodine intake on the thyroid tumor growth and thyroid function in the orthotopic nude mice model of human papillary thyroid carcinoma (PTC) cell line TPC-1.Methods Human PTC cell line TPC-1 (2 × 105) was injected into the left thyroid gland of nude mice.After the operation,the nude mice were randomly divided into three groups:low iodine group (LI),normal iodine group (NI),and high iodine group(HI,50 folds of normal iodine) based on the iodine levels contained in their diet.4 and 12 weeks later,the nude mice were executed,then their thyroid tumors were removed and weighted.The levels of urinary iodine were measured with As3+-Ce4+ catalytic spectrophotometry using ammonium persulfate digestion method.The thyroid hormone level was detected using chemiluminescent immunoassay.The morphology and structure of thyroid tumor tissue was observed by microscope.Results The iodine intervention feeding was successful according to urinary iodine level of LI,NI,and HI groups,paralleled to their iodine intakes.However,the difference of the weight of thyroid tumor in three groups had no statistical significance(P＞0.05).At 4 weeks,compared with control group,the levels of thyroid hormones were normal in NI group,while lower T4 and normal T3 were found in LI group.However,T4 was higher and T3 was lower in HI group (P＜0.05).At 12 weeks,the levels of thyroid hormones all were decreased due to the enlargement of thyroid gland tumor in NI,LI and HI groups.T4 and T3 in LI group were the lowest among three groups,even T4 was below detection limit.T4 was normal and T3 was lower in HI group as compared to control group.Conclusion Iodine intake may not significantly affect tumor growth in the orthotopic nude mice model of human PTC cell line TPC-1,but it has a significant effect on the synthesis of thyroid hormones.

Objective To study mother and infant's iodine metabolism and thyroid function during lactation with different iodine intakes. Methods Wistar rats were randomly assigned to four groups with severe iodine deficiency (SID), mild iodine deficiency (MiID), normal iodine (NI), and excessive iodine (ExI) intake respectively. All rats were fed on an iodine deficient food and drinking water with different quantities of potassium iodide for 3 months until mating. The urinary iodine, milk iodine, blood iodine, and thyroid hormones (TH) were detected in lactating mother and the offspring rats 14 days after birth. Thyroid weight of mother rats was determined. Thyroid morphology of mother and their offsprings was observed. Results ( 1) Iodine contents in urine, milk, and blood of lactating rats and the offsprings were increased with the increase of iodine supplied in diet. But the change in amplitude between groups was decreased in the other; urine iodine > milk iodine > blood iodine. (2) Serum TT4[ (16. 7±12. 0 vs 36.4±15. 0) nmol/L, P<0.05] was significantly decreased, but TSH [(5.73±2.90vs 1. 38±0.30)mIU/L, P<0.01]and TT3/TT4(6.6±2.7 vs 2. l±0.3,P<0.01) were increased in lactating rats of SID group compared with NI, so as TT4( 10.6±2. 3 vs 16.4±4. 7) nmol/L, P<0.05 ] of offspring rats in SID, but were not in MiID and ExI groups. (3 ) Histological studies showed that small follicular thyroid nodules with follicular hyperplasia occurred in both lactating rats and their offsprings in the SID group, mild swelling in MiID group and polymorphism changes appeared in mother rats of ExI group, but no significant difference appeared in offsprings compared with NI group. Conclusions Severe iodine deficiency will lead to hypothyroidism in mother and infant, but normal iodine nutrition and thyroid function in mother and offspring were maintained through the compensatory action of mother and child in mild iodine deficiency and iodine excess.