Effect of tumor necrosis factor-α with different levels of iodine on expression of Na+/I- symporter in cultured lactating mammary cells

Objective To observe the expression of Na+/I- symporter(NIS) in cultured lactating mammary cells with different levels of iodine and the effect of tumor necrosis factor-α(TNF-α). Methods Original generation of mouse lactating mammary cells cultured in vitro were divided into low iodine group Ⅰ (LI-Ⅰ), low iodine group Ⅱ (LI-Ⅱ), adequate iodine group(AI), high iodine group Ⅰ(HI-Ⅰ), and high iodine group Ⅱ(HI-Ⅱ). Cells were cultured in DEME/F12 culture medium for 24 h with different concentrations of iodine (0,5,50,3000 and 10 000 μg/L, respectively), and TNF-α( 10-2 mg/L) was added to some of cultured cells for 24 h. The expression of NIS mRNA of lactating mammary cells was determined by real-time quantitative PCR and the expression of NIS protein was detected by In-Cell Western. Results In iodine alone group, the expression of NIS mRNA in LI-Ⅰ group [ (64.66 ± 14.99) x 10-4] was higher than that of AI group[ (22.76 ± 7.36) × 10-4, P ＜ 0.01 ]; HI-I group[ (10.18 ±3.53) × 10-4] and HI-Ⅱ group[ (8.59 ± 2.89) × 10-4] were lower than that of AI group(all P ＜ .0.05); With increased iodine concentration, the expression of NIS mRNA decreased. The expression of NIS mRNA in LI-Ⅰ group [(2.72 ± 0.45) × 10-4], LI-Ⅱ group[ (2.69 ± 0.68) × 10-4] and AI group[(1.80 ± 0.67) × 10-4] with iodine plus TNF-o were all lower than that of LI-Ⅰ group, LI-Ⅱ group[ (29.82 ± 4.47 ) × 10-4], and AI group without TNF-α (all P ＜ 0.01). In iodine plus TNF-α, the expression of NIS mRNA in HI-Ⅰ group[(6.58 ± 2.87) × 10-4] and HI-Ⅱ[(7.04 ± 1.36) × 10-4] group were all higher than that of AI group(all P ＜ 0.05); With increased iodine deficiency or iodine excess, the expression of NIS mRNA increased. With increased iodine concentration, the expression of NIS protein decreased in iodine alone group. The expression of NIS protein in iodine plus TNF-α was all lower than that in iodine alone group. In iodine plus TNF-α, the expression of NIS protein increased in both iodine deficiency and iodine excess conditions. Conclusions Iodine may decrease the expression of NIS mRNA and protein of lactating mammary cells. The expression of NIS mRNA and protein of lactating mammary cells was inhibited by TNF-α under different levels of iodine.     

碘过量对NOD和Balb/c鼠甲状腺TRAIL和TRAIL-sR1表达的影响

Objective To investigate the influence of iodine excess on expression of TRAIl/TRAIL-sR1 in NOD and Balb/c mice and to study the effect of TRAIl/TRAIL-sR1 on the pathogenesis of experimental autoimmune thyroiditis(EAT). Methods Both Balb/c and NOD mice were divided randomly into control and iodine excess group by feeding with water containing no NaI or 0.05% Nal. The mice were sacrificed after 8 weeks. TRAIL and TRAIL-sR1 mRNA levels were detected by RT-PCR. The function, morphology and apoptosis of thyroids were also observed by ELISA and Tunnel stain. Results Treated by HI, enlarged follicles and flattened epithelium by accumulation of colloid were found in thyroids of both NOD and Balb/c mice. But significant lymphoid cell infiltration and local fibrosis were only found in thyroids of NOD HI group. The relative weight of thyroids of NOD mice in HI group[(104.8±14.5)mg/kg]was heavier than that of control group [(71.8±20.4)mg/kg]. The level of TT4 declined in HI group[(30.77±3.59)mmol/L]compared with control group[(36.43±2.66)mmol/L], meanwhile, the level of TSH was higher in HI group[(6.98±0.66)μg/L]than that in control group [(5.55±0.56)μg/L]. The difference being statistically significant(t=7.773,-9.526,-4.458, all P < 0.05). The relative weight of thyroids of Balb/c mice of HI group[(155.8±20.8)mg/kg]also heavier than that of control group [(105.1±22.0) mg/kg]. The level of TT4 droped in HI group [(19.75±3.32) mmoL/L]was higher than that in control group[(23.46±6.21)mmoL/L], the level of TSH in HI group[(4.14±1.71)μg/L]was higher than that in control group[(3.55±1.41)μg/L], the difference being statistically significant(t=7.554,-7.239,3.140, all P< 0.05). A great deal of apoptotie ceils observed in NOD (3.97±0.91) and Balb/c mice (1.05±0.45) by Tunnel stain were greater than control groups (0.21±0.15, 0.10±0.03), the difference being statistically significant in beth of the two species(t=-7.167,-17.772, both P < 0.05). The apoptosis index of thyroid follicular epithelium in NOD was obviously higher than Balb/c(t=-7.625, P<0.05). The level of TRAIL mRNA did not remarkably change in Balb/c between control group(0.000 59±0.000 39) and HI group(0.001 24±0.000 46, t=-1.940, P>0.05), but it increased apparently in NOD mice HI group(0.018 88±0.005 77) than that of control group(0.009 61± 0.00591, t=-2.71, P<0.05). The level of the expression of TRAIL-sR1 mRNA increased in HI groups of NOD (0.000 53±0.000 15) and Balb/c mice(0.000 42±0.000 09) than that in control groups of NOD(0.000 28± 0.000 05) and Balb/c mice (0.000 17±0.000 06) and the differences were statistically significant between the two species(t=3.050,3.990, all P<0.05). The differences of the expression of TRAIL and TRAIL-sR1 mRNA between the two species were significant(t=-3.37,-4.76, all P<0.05). Conclusions Iodine excess induces colloid goiter in beth species of mice and thyroiditis in NOD mice. The increase of TRAIL and TRAIL-sR1 influenced by iodine excess is one of the molecular bases of follicular epithelium apoptosis and inflammation in thyroids. Genetic factor is a key factor in the pathogenesis of thyroiditis.     

碘过量对NOD和Balb/c鼠甲状腺TRAIL和TRAIL-sR1表达的影响

Objective To investigate the influence of iodine excess on expression of TRAIl/TRAIL-sR1 in NOD and Balb/c mice and to study the effect of TRAIl/TRAIL-sR1 on the pathogenesis of experimental autoimmune thyroiditis(EAT). Methods Both Balb/c and NOD mice were divided randomly into control and iodine excess group by feeding with water containing no NaI or 0.05% Nal. The mice were sacrificed after 8 weeks. TRAIL and TRAIL-sR1 mRNA levels were detected by RT-PCR. The function, morphology and apoptosis of thyroids were also observed by ELISA and Tunnel stain. Results Treated by HI, enlarged follicles and flattened epithelium by accumulation of colloid were found in thyroids of both NOD and Balb/c mice. But significant lymphoid cell infiltration and local fibrosis were only found in thyroids of NOD HI group. The relative weight of thyroids of NOD mice in HI group[(104.8±14.5)mg/kg]was heavier than that of control group [(71.8±20.4)mg/kg]. The level of TT4 declined in HI group[(30.77±3.59)mmol/L]compared with control group[(36.43±2.66)mmol/L], meanwhile, the level of TSH was higher in HI group[(6.98±0.66)μg/L]than that in control group [(5.55±0.56)μg/L]. The difference being statistically significant(t=7.773,-9.526,-4.458, all P < 0.05). The relative weight of thyroids of Balb/c mice of HI group[(155.8±20.8)mg/kg]also heavier than that of control group [(105.1±22.0) mg/kg]. The level of TT4 droped in HI group [(19.75±3.32) mmoL/L]was higher than that in control group[(23.46±6.21)mmoL/L], the level of TSH in HI group[(4.14±1.71)μg/L]was higher than that in control group[(3.55±1.41)μg/L], the difference being statistically significant(t=7.554,-7.239,3.140, all P< 0.05). A great deal of apoptotie ceils observed in NOD (3.97±0.91) and Balb/c mice (1.05±0.45) by Tunnel stain were greater than control groups (0.21±0.15, 0.10±0.03), the difference being statistically significant in beth of the two species(t=-7.167,-17.772, both P < 0.05). The apoptosis index of thyroid follicular epithelium in NOD was obviously higher than Balb/c(t=-7.625, P<0.05). The level of TRAIL mRNA did not remarkably change in Balb/c between control group(0.000 59±0.000 39) and HI group(0.001 24±0.000 46, t=-1.940, P>0.05), but it increased apparently in NOD mice HI group(0.018 88±0.005 77) than that of control group(0.009 61± 0.00591, t=-2.71, P<0.05). The level of the expression of TRAIL-sR1 mRNA increased in HI groups of NOD (0.000 53±0.000 15) and Balb/c mice(0.000 42±0.000 09) than that in control groups of NOD(0.000 28± 0.000 05) and Balb/c mice (0.000 17±0.000 06) and the differences were statistically significant between the two species(t=3.050,3.990, all P<0.05). The differences of the expression of TRAIL and TRAIL-sR1 mRNA between the two species were significant(t=-3.37,-4.76, all P<0.05). Conclusions Iodine excess induces colloid goiter in beth species of mice and thyroiditis in NOD mice. The increase of TRAIL and TRAIL-sR1 influenced by iodine excess is one of the molecular bases of follicular epithelium apoptosis and inflammation in thyroids. Genetic factor is a key factor in the pathogenesis of thyroiditis.     

碘过量对NOD和Balb/c鼠甲状腺TRAIL和TRAIL-sR1表达的影响

Objective To investigate the influence of iodine excess on expression of TRAIl/TRAIL-sR1 in NOD and Balb/c mice and to study the effect of TRAIl/TRAIL-sR1 on the pathogenesis of experimental autoimmune thyroiditis(EAT). Methods Both Balb/c and NOD mice were divided randomly into control and iodine excess group by feeding with water containing no NaI or 0.05% Nal. The mice were sacrificed after 8 weeks. TRAIL and TRAIL-sR1 mRNA levels were detected by RT-PCR. The function, morphology and apoptosis of thyroids were also observed by ELISA and Tunnel stain. Results Treated by HI, enlarged follicles and flattened epithelium by accumulation of colloid were found in thyroids of both NOD and Balb/c mice. But significant lymphoid cell infiltration and local fibrosis were only found in thyroids of NOD HI group. The relative weight of thyroids of NOD mice in HI group[(104.8±14.5)mg/kg]was heavier than that of control group [(71.8±20.4)mg/kg]. The level of TT4 declined in HI group[(30.77±3.59)mmol/L]compared with control group[(36.43±2.66)mmol/L], meanwhile, the level of TSH was higher in HI group[(6.98±0.66)μg/L]than that in control group [(5.55±0.56)μg/L]. The difference being statistically significant(t=7.773,-9.526,-4.458, all P < 0.05). The relative weight of thyroids of Balb/c mice of HI group[(155.8±20.8)mg/kg]also heavier than that of control group [(105.1±22.0) mg/kg]. The level of TT4 droped in HI group [(19.75±3.32) mmoL/L]was higher than that in control group[(23.46±6.21)mmoL/L], the level of TSH in HI group[(4.14±1.71)μg/L]was higher than that in control group[(3.55±1.41)μg/L], the difference being statistically significant(t=7.554,-7.239,3.140, all P< 0.05). A great deal of apoptotie ceils observed in NOD (3.97±0.91) and Balb/c mice (1.05±0.45) by Tunnel stain were greater than control groups (0.21±0.15, 0.10±0.03), the difference being statistically significant in beth of the two species(t=-7.167,-17.772, both P < 0.05). The apoptosis index of thyroid follicular epithelium in NOD was obviously higher than Balb/c(t=-7.625, P<0.05). The level of TRAIL mRNA did not remarkably change in Balb/c between control group(0.000 59±0.000 39) and HI group(0.001 24±0.000 46, t=-1.940, P>0.05), but it increased apparently in NOD mice HI group(0.018 88±0.005 77) than that of control group(0.009 61± 0.00591, t=-2.71, P<0.05). The level of the expression of TRAIL-sR1 mRNA increased in HI groups of NOD (0.000 53±0.000 15) and Balb/c mice(0.000 42±0.000 09) than that in control groups of NOD(0.000 28± 0.000 05) and Balb/c mice (0.000 17±0.000 06) and the differences were statistically significant between the two species(t=3.050,3.990, all P<0.05). The differences of the expression of TRAIL and TRAIL-sR1 mRNA between the two species were significant(t=-3.37,-4.76, all P<0.05). Conclusions Iodine excess induces colloid goiter in beth species of mice and thyroiditis in NOD mice. The increase of TRAIL and TRAIL-sR1 influenced by iodine excess is one of the molecular bases of follicular epithelium apoptosis and inflammation in thyroids. Genetic factor is a key factor in the pathogenesis of thyroiditis.     

碘过量对NOD和Balb/c鼠甲状腺TRAIL和TRAIL-sR1表达的影响

Objective To investigate the influence of iodine excess on expression of TRAIl/TRAIL-sR1 in NOD and Balb/c mice and to study the effect of TRAIl/TRAIL-sR1 on the pathogenesis of experimental autoimmune thyroiditis(EAT). Methods Both Balb/c and NOD mice were divided randomly into control and iodine excess group by feeding with water containing no NaI or 0.05% Nal. The mice were sacrificed after 8 weeks. TRAIL and TRAIL-sR1 mRNA levels were detected by RT-PCR. The function, morphology and apoptosis of thyroids were also observed by ELISA and Tunnel stain. Results Treated by HI, enlarged follicles and flattened epithelium by accumulation of colloid were found in thyroids of both NOD and Balb/c mice. But significant lymphoid cell infiltration and local fibrosis were only found in thyroids of NOD HI group. The relative weight of thyroids of NOD mice in HI group[(104.8±14.5)mg/kg]was heavier than that of control group [(71.8±20.4)mg/kg]. The level of TT4 declined in HI group[(30.77±3.59)mmol/L]compared with control group[(36.43±2.66)mmol/L], meanwhile, the level of TSH was higher in HI group[(6.98±0.66)μg/L]than that in control group [(5.55±0.56)μg/L]. The difference being statistically significant(t=7.773,-9.526,-4.458, all P < 0.05). The relative weight of thyroids of Balb/c mice of HI group[(155.8±20.8)mg/kg]also heavier than that of control group [(105.1±22.0) mg/kg]. The level of TT4 droped in HI group [(19.75±3.32) mmoL/L]was higher than that in control group[(23.46±6.21)mmoL/L], the level of TSH in HI group[(4.14±1.71)μg/L]was higher than that in control group[(3.55±1.41)μg/L], the difference being statistically significant(t=7.554,-7.239,3.140, all P< 0.05). A great deal of apoptotie ceils observed in NOD (3.97±0.91) and Balb/c mice (1.05±0.45) by Tunnel stain were greater than control groups (0.21±0.15, 0.10±0.03), the difference being statistically significant in beth of the two species(t=-7.167,-17.772, both P < 0.05). The apoptosis index of thyroid follicular epithelium in NOD was obviously higher than Balb/c(t=-7.625, P<0.05). The level of TRAIL mRNA did not remarkably change in Balb/c between control group(0.000 59±0.000 39) and HI group(0.001 24±0.000 46, t=-1.940, P>0.05), but it increased apparently in NOD mice HI group(0.018 88±0.005 77) than that of control group(0.009 61± 0.00591, t=-2.71, P<0.05). The level of the expression of TRAIL-sR1 mRNA increased in HI groups of NOD (0.000 53±0.000 15) and Balb/c mice(0.000 42±0.000 09) than that in control groups of NOD(0.000 28± 0.000 05) and Balb/c mice (0.000 17±0.000 06) and the differences were statistically significant between the two species(t=3.050,3.990, all P<0.05). The differences of the expression of TRAIL and TRAIL-sR1 mRNA between the two species were significant(t=-3.37,-4.76, all P<0.05). Conclusions Iodine excess induces colloid goiter in beth species of mice and thyroiditis in NOD mice. The increase of TRAIL and TRAIL-sR1 influenced by iodine excess is one of the molecular bases of follicular epithelium apoptosis and inflammation in thyroids. Genetic factor is a key factor in the pathogenesis of thyroiditis.     

碘过量对NOD和Balb/c鼠甲状腺TRAIL和TRAIL-sR1表达的影响

Objective To investigate the influence of iodine excess on expression of TRAIl/TRAIL-sR1 in NOD and Balb/c mice and to study the effect of TRAIl/TRAIL-sR1 on the pathogenesis of experimental autoimmune thyroiditis(EAT). Methods Both Balb/c and NOD mice were divided randomly into control and iodine excess group by feeding with water containing no NaI or 0.05% Nal. The mice were sacrificed after 8 weeks. TRAIL and TRAIL-sR1 mRNA levels were detected by RT-PCR. The function, morphology and apoptosis of thyroids were also observed by ELISA and Tunnel stain. Results Treated by HI, enlarged follicles and flattened epithelium by accumulation of colloid were found in thyroids of both NOD and Balb/c mice. But significant lymphoid cell infiltration and local fibrosis were only found in thyroids of NOD HI group. The relative weight of thyroids of NOD mice in HI group[(104.8±14.5)mg/kg]was heavier than that of control group [(71.8±20.4)mg/kg]. The level of TT4 declined in HI group[(30.77±3.59)mmol/L]compared with control group[(36.43±2.66)mmol/L], meanwhile, the level of TSH was higher in HI group[(6.98±0.66)μg/L]than that in control group [(5.55±0.56)μg/L]. The difference being statistically significant(t=7.773,-9.526,-4.458, all P < 0.05). The relative weight of thyroids of Balb/c mice of HI group[(155.8±20.8)mg/kg]also heavier than that of control group [(105.1±22.0) mg/kg]. The level of TT4 droped in HI group [(19.75±3.32) mmoL/L]was higher than that in control group[(23.46±6.21)mmoL/L], the level of TSH in HI group[(4.14±1.71)μg/L]was higher than that in control group[(3.55±1.41)μg/L], the difference being statistically significant(t=7.554,-7.239,3.140, all P< 0.05). A great deal of apoptotie ceils observed in NOD (3.97±0.91) and Balb/c mice (1.05±0.45) by Tunnel stain were greater than control groups (0.21±0.15, 0.10±0.03), the difference being statistically significant in beth of the two species(t=-7.167,-17.772, both P < 0.05). The apoptosis index of thyroid follicular epithelium in NOD was obviously higher than Balb/c(t=-7.625, P<0.05). The level of TRAIL mRNA did not remarkably change in Balb/c between control group(0.000 59±0.000 39) and HI group(0.001 24±0.000 46, t=-1.940, P>0.05), but it increased apparently in NOD mice HI group(0.018 88±0.005 77) than that of control group(0.009 61± 0.00591, t=-2.71, P<0.05). The level of the expression of TRAIL-sR1 mRNA increased in HI groups of NOD (0.000 53±0.000 15) and Balb/c mice(0.000 42±0.000 09) than that in control groups of NOD(0.000 28± 0.000 05) and Balb/c mice (0.000 17±0.000 06) and the differences were statistically significant between the two species(t=3.050,3.990, all P<0.05). The differences of the expression of TRAIL and TRAIL-sR1 mRNA between the two species were significant(t=-3.37,-4.76, all P<0.05). Conclusions Iodine excess induces colloid goiter in beth species of mice and thyroiditis in NOD mice. The increase of TRAIL and TRAIL-sR1 influenced by iodine excess is one of the molecular bases of follicular epithelium apoptosis and inflammation in thyroids. Genetic factor is a key factor in the pathogenesis of thyroiditis.     

碘过量对NOD和Balb/c鼠甲状腺TRAIL和TRAIL-sR1表达的影响

Objective To investigate the influence of iodine excess on expression of TRAIl/TRAIL-sR1 in NOD and Balb/c mice and to study the effect of TRAIl/TRAIL-sR1 on the pathogenesis of experimental autoimmune thyroiditis(EAT). Methods Both Balb/c and NOD mice were divided randomly into control and iodine excess group by feeding with water containing no NaI or 0.05% Nal. The mice were sacrificed after 8 weeks. TRAIL and TRAIL-sR1 mRNA levels were detected by RT-PCR. The function, morphology and apoptosis of thyroids were also observed by ELISA and Tunnel stain. Results Treated by HI, enlarged follicles and flattened epithelium by accumulation of colloid were found in thyroids of both NOD and Balb/c mice. But significant lymphoid cell infiltration and local fibrosis were only found in thyroids of NOD HI group. The relative weight of thyroids of NOD mice in HI group[(104.8±14.5)mg/kg]was heavier than that of control group [(71.8±20.4)mg/kg]. The level of TT4 declined in HI group[(30.77±3.59)mmol/L]compared with control group[(36.43±2.66)mmol/L], meanwhile, the level of TSH was higher in HI group[(6.98±0.66)μg/L]than that in control group [(5.55±0.56)μg/L]. The difference being statistically significant(t=7.773,-9.526,-4.458, all P < 0.05). The relative weight of thyroids of Balb/c mice of HI group[(155.8±20.8)mg/kg]also heavier than that of control group [(105.1±22.0) mg/kg]. The level of TT4 droped in HI group [(19.75±3.32) mmoL/L]was higher than that in control group[(23.46±6.21)mmoL/L], the level of TSH in HI group[(4.14±1.71)μg/L]was higher than that in control group[(3.55±1.41)μg/L], the difference being statistically significant(t=7.554,-7.239,3.140, all P< 0.05). A great deal of apoptotie ceils observed in NOD (3.97±0.91) and Balb/c mice (1.05±0.45) by Tunnel stain were greater than control groups (0.21±0.15, 0.10±0.03), the difference being statistically significant in beth of the two species(t=-7.167,-17.772, both P < 0.05). The apoptosis index of thyroid follicular epithelium in NOD was obviously higher than Balb/c(t=-7.625, P<0.05). The level of TRAIL mRNA did not remarkably change in Balb/c between control group(0.000 59±0.000 39) and HI group(0.001 24±0.000 46, t=-1.940, P>0.05), but it increased apparently in NOD mice HI group(0.018 88±0.005 77) than that of control group(0.009 61± 0.00591, t=-2.71, P<0.05). The level of the expression of TRAIL-sR1 mRNA increased in HI groups of NOD (0.000 53±0.000 15) and Balb/c mice(0.000 42±0.000 09) than that in control groups of NOD(0.000 28± 0.000 05) and Balb/c mice (0.000 17±0.000 06) and the differences were statistically significant between the two species(t=3.050,3.990, all P<0.05). The differences of the expression of TRAIL and TRAIL-sR1 mRNA between the two species were significant(t=-3.37,-4.76, all P<0.05). Conclusions Iodine excess induces colloid goiter in beth species of mice and thyroiditis in NOD mice. The increase of TRAIL and TRAIL-sR1 influenced by iodine excess is one of the molecular bases of follicular epithelium apoptosis and inflammation in thyroids. Genetic factor is a key factor in the pathogenesis of thyroiditis.     

碘过量对NOD和Balb/c鼠甲状腺TRAIL和TRAIL-sR1表达的影响

Objective To investigate the influence of iodine excess on expression of TRAIl/TRAIL-sR1 in NOD and Balb/c mice and to study the effect of TRAIl/TRAIL-sR1 on the pathogenesis of experimental autoimmune thyroiditis(EAT). Methods Both Balb/c and NOD mice were divided randomly into control and iodine excess group by feeding with water containing no NaI or 0.05% Nal. The mice were sacrificed after 8 weeks. TRAIL and TRAIL-sR1 mRNA levels were detected by RT-PCR. The function, morphology and apoptosis of thyroids were also observed by ELISA and Tunnel stain. Results Treated by HI, enlarged follicles and flattened epithelium by accumulation of colloid were found in thyroids of both NOD and Balb/c mice. But significant lymphoid cell infiltration and local fibrosis were only found in thyroids of NOD HI group. The relative weight of thyroids of NOD mice in HI group[(104.8±14.5)mg/kg]was heavier than that of control group [(71.8±20.4)mg/kg]. The level of TT4 declined in HI group[(30.77±3.59)mmol/L]compared with control group[(36.43±2.66)mmol/L], meanwhile, the level of TSH was higher in HI group[(6.98±0.66)μg/L]than that in control group [(5.55±0.56)μg/L]. The difference being statistically significant(t=7.773,-9.526,-4.458, all P < 0.05). The relative weight of thyroids of Balb/c mice of HI group[(155.8±20.8)mg/kg]also heavier than that of control group [(105.1±22.0) mg/kg]. The level of TT4 droped in HI group [(19.75±3.32) mmoL/L]was higher than that in control group[(23.46±6.21)mmoL/L], the level of TSH in HI group[(4.14±1.71)μg/L]was higher than that in control group[(3.55±1.41)μg/L], the difference being statistically significant(t=7.554,-7.239,3.140, all P< 0.05). A great deal of apoptotie ceils observed in NOD (3.97±0.91) and Balb/c mice (1.05±0.45) by Tunnel stain were greater than control groups (0.21±0.15, 0.10±0.03), the difference being statistically significant in beth of the two species(t=-7.167,-17.772, both P < 0.05). The apoptosis index of thyroid follicular epithelium in NOD was obviously higher than Balb/c(t=-7.625, P<0.05). The level of TRAIL mRNA did not remarkably change in Balb/c between control group(0.000 59±0.000 39) and HI group(0.001 24±0.000 46, t=-1.940, P>0.05), but it increased apparently in NOD mice HI group(0.018 88±0.005 77) than that of control group(0.009 61± 0.00591, t=-2.71, P<0.05). The level of the expression of TRAIL-sR1 mRNA increased in HI groups of NOD (0.000 53±0.000 15) and Balb/c mice(0.000 42±0.000 09) than that in control groups of NOD(0.000 28± 0.000 05) and Balb/c mice (0.000 17±0.000 06) and the differences were statistically significant between the two species(t=3.050,3.990, all P<0.05). The differences of the expression of TRAIL and TRAIL-sR1 mRNA between the two species were significant(t=-3.37,-4.76, all P<0.05). Conclusions Iodine excess induces colloid goiter in beth species of mice and thyroiditis in NOD mice. The increase of TRAIL and TRAIL-sR1 influenced by iodine excess is one of the molecular bases of follicular epithelium apoptosis and inflammation in thyroids. Genetic factor is a key factor in the pathogenesis of thyroiditis.     

碘过量对NOD和Balb/c鼠甲状腺TRAIL和TRAIL-sR1表达的影响

Objective To investigate the influence of iodine excess on expression of TRAIl/TRAIL-sR1 in NOD and Balb/c mice and to study the effect of TRAIl/TRAIL-sR1 on the pathogenesis of experimental autoimmune thyroiditis(EAT). Methods Both Balb/c and NOD mice were divided randomly into control and iodine excess group by feeding with water containing no NaI or 0.05% Nal. The mice were sacrificed after 8 weeks. TRAIL and TRAIL-sR1 mRNA levels were detected by RT-PCR. The function, morphology and apoptosis of thyroids were also observed by ELISA and Tunnel stain. Results Treated by HI, enlarged follicles and flattened epithelium by accumulation of colloid were found in thyroids of both NOD and Balb/c mice. But significant lymphoid cell infiltration and local fibrosis were only found in thyroids of NOD HI group. The relative weight of thyroids of NOD mice in HI group[(104.8±14.5)mg/kg]was heavier than that of control group [(71.8±20.4)mg/kg]. The level of TT4 declined in HI group[(30.77±3.59)mmol/L]compared with control group[(36.43±2.66)mmol/L], meanwhile, the level of TSH was higher in HI group[(6.98±0.66)μg/L]than that in control group [(5.55±0.56)μg/L]. The difference being statistically significant(t=7.773,-9.526,-4.458, all P < 0.05). The relative weight of thyroids of Balb/c mice of HI group[(155.8±20.8)mg/kg]also heavier than that of control group [(105.1±22.0) mg/kg]. The level of TT4 droped in HI group [(19.75±3.32) mmoL/L]was higher than that in control group[(23.46±6.21)mmoL/L], the level of TSH in HI group[(4.14±1.71)μg/L]was higher than that in control group[(3.55±1.41)μg/L], the difference being statistically significant(t=7.554,-7.239,3.140, all P< 0.05). A great deal of apoptotie ceils observed in NOD (3.97±0.91) and Balb/c mice (1.05±0.45) by Tunnel stain were greater than control groups (0.21±0.15, 0.10±0.03), the difference being statistically significant in beth of the two species(t=-7.167,-17.772, both P < 0.05). The apoptosis index of thyroid follicular epithelium in NOD was obviously higher than Balb/c(t=-7.625, P<0.05). The level of TRAIL mRNA did not remarkably change in Balb/c between control group(0.000 59±0.000 39) and HI group(0.001 24±0.000 46, t=-1.940, P>0.05), but it increased apparently in NOD mice HI group(0.018 88±0.005 77) than that of control group(0.009 61± 0.00591, t=-2.71, P<0.05). The level of the expression of TRAIL-sR1 mRNA increased in HI groups of NOD (0.000 53±0.000 15) and Balb/c mice(0.000 42±0.000 09) than that in control groups of NOD(0.000 28± 0.000 05) and Balb/c mice (0.000 17±0.000 06) and the differences were statistically significant between the two species(t=3.050,3.990, all P<0.05). The differences of the expression of TRAIL and TRAIL-sR1 mRNA between the two species were significant(t=-3.37,-4.76, all P<0.05). Conclusions Iodine excess induces colloid goiter in beth species of mice and thyroiditis in NOD mice. The increase of TRAIL and TRAIL-sR1 influenced by iodine excess is one of the molecular bases of follicular epithelium apoptosis and inflammation in thyroids. Genetic factor is a key factor in the pathogenesis of thyroiditis.     

碘过量对NOD和Balb/c鼠甲状腺TRAIL和TRAIL-sR1表达的影响

Objective To investigate the influence of iodine excess on expression of TRAIl/TRAIL-sR1 in NOD and Balb/c mice and to study the effect of TRAIl/TRAIL-sR1 on the pathogenesis of experimental autoimmune thyroiditis(EAT). Methods Both Balb/c and NOD mice were divided randomly into control and iodine excess group by feeding with water containing no NaI or 0.05% Nal. The mice were sacrificed after 8 weeks. TRAIL and TRAIL-sR1 mRNA levels were detected by RT-PCR. The function, morphology and apoptosis of thyroids were also observed by ELISA and Tunnel stain. Results Treated by HI, enlarged follicles and flattened epithelium by accumulation of colloid were found in thyroids of both NOD and Balb/c mice. But significant lymphoid cell infiltration and local fibrosis were only found in thyroids of NOD HI group. The relative weight of thyroids of NOD mice in HI group[(104.8±14.5)mg/kg]was heavier than that of control group [(71.8±20.4)mg/kg]. The level of TT4 declined in HI group[(30.77±3.59)mmol/L]compared with control group[(36.43±2.66)mmol/L], meanwhile, the level of TSH was higher in HI group[(6.98±0.66)μg/L]than that in control group [(5.55±0.56)μg/L]. The difference being statistically significant(t=7.773,-9.526,-4.458, all P < 0.05). The relative weight of thyroids of Balb/c mice of HI group[(155.8±20.8)mg/kg]also heavier than that of control group [(105.1±22.0) mg/kg]. The level of TT4 droped in HI group [(19.75±3.32) mmoL/L]was higher than that in control group[(23.46±6.21)mmoL/L], the level of TSH in HI group[(4.14±1.71)μg/L]was higher than that in control group[(3.55±1.41)μg/L], the difference being statistically significant(t=7.554,-7.239,3.140, all P< 0.05). A great deal of apoptotie ceils observed in NOD (3.97±0.91) and Balb/c mice (1.05±0.45) by Tunnel stain were greater than control groups (0.21±0.15, 0.10±0.03), the difference being statistically significant in beth of the two species(t=-7.167,-17.772, both P < 0.05). The apoptosis index of thyroid follicular epithelium in NOD was obviously higher than Balb/c(t=-7.625, P<0.05). The level of TRAIL mRNA did not remarkably change in Balb/c between control group(0.000 59±0.000 39) and HI group(0.001 24±0.000 46, t=-1.940, P>0.05), but it increased apparently in NOD mice HI group(0.018 88±0.005 77) than that of control group(0.009 61± 0.00591, t=-2.71, P<0.05). The level of the expression of TRAIL-sR1 mRNA increased in HI groups of NOD (0.000 53±0.000 15) and Balb/c mice(0.000 42±0.000 09) than that in control groups of NOD(0.000 28± 0.000 05) and Balb/c mice (0.000 17±0.000 06) and the differences were statistically significant between the two species(t=3.050,3.990, all P<0.05). The differences of the expression of TRAIL and TRAIL-sR1 mRNA between the two species were significant(t=-3.37,-4.76, all P<0.05). Conclusions Iodine excess induces colloid goiter in beth species of mice and thyroiditis in NOD mice. The increase of TRAIL and TRAIL-sR1 influenced by iodine excess is one of the molecular bases of follicular epithelium apoptosis and inflammation in thyroids. Genetic factor is a key factor in the pathogenesis of thyroiditis.     

碘过量对NOD和Balb/c鼠甲状腺TRAIL和TRAIL-sR1表达的影响

Objective To investigate the influence of iodine excess on expression of TRAIl/TRAIL-sR1 in NOD and Balb/c mice and to study the effect of TRAIl/TRAIL-sR1 on the pathogenesis of experimental autoimmune thyroiditis(EAT). Methods Both Balb/c and NOD mice were divided randomly into control and iodine excess group by feeding with water containing no NaI or 0.05% Nal. The mice were sacrificed after 8 weeks. TRAIL and TRAIL-sR1 mRNA levels were detected by RT-PCR. The function, morphology and apoptosis of thyroids were also observed by ELISA and Tunnel stain. Results Treated by HI, enlarged follicles and flattened epithelium by accumulation of colloid were found in thyroids of both NOD and Balb/c mice. But significant lymphoid cell infiltration and local fibrosis were only found in thyroids of NOD HI group. The relative weight of thyroids of NOD mice in HI group[(104.8±14.5)mg/kg]was heavier than that of control group [(71.8±20.4)mg/kg]. The level of TT4 declined in HI group[(30.77±3.59)mmol/L]compared with control group[(36.43±2.66)mmol/L], meanwhile, the level of TSH was higher in HI group[(6.98±0.66)μg/L]than that in control group [(5.55±0.56)μg/L]. The difference being statistically significant(t=7.773,-9.526,-4.458, all P < 0.05). The relative weight of thyroids of Balb/c mice of HI group[(155.8±20.8)mg/kg]also heavier than that of control group [(105.1±22.0) mg/kg]. The level of TT4 droped in HI group [(19.75±3.32) mmoL/L]was higher than that in control group[(23.46±6.21)mmoL/L], the level of TSH in HI group[(4.14±1.71)μg/L]was higher than that in control group[(3.55±1.41)μg/L], the difference being statistically significant(t=7.554,-7.239,3.140, all P< 0.05). A great deal of apoptotie ceils observed in NOD (3.97±0.91) and Balb/c mice (1.05±0.45) by Tunnel stain were greater than control groups (0.21±0.15, 0.10±0.03), the difference being statistically significant in beth of the two species(t=-7.167,-17.772, both P < 0.05). The apoptosis index of thyroid follicular epithelium in NOD was obviously higher than Balb/c(t=-7.625, P<0.05). The level of TRAIL mRNA did not remarkably change in Balb/c between control group(0.000 59±0.000 39) and HI group(0.001 24±0.000 46, t=-1.940, P>0.05), but it increased apparently in NOD mice HI group(0.018 88±0.005 77) than that of control group(0.009 61± 0.00591, t=-2.71, P<0.05). The level of the expression of TRAIL-sR1 mRNA increased in HI groups of NOD (0.000 53±0.000 15) and Balb/c mice(0.000 42±0.000 09) than that in control groups of NOD(0.000 28± 0.000 05) and Balb/c mice (0.000 17±0.000 06) and the differences were statistically significant between the two species(t=3.050,3.990, all P<0.05). The differences of the expression of TRAIL and TRAIL-sR1 mRNA between the two species were significant(t=-3.37,-4.76, all P<0.05). Conclusions Iodine excess induces colloid goiter in beth species of mice and thyroiditis in NOD mice. The increase of TRAIL and TRAIL-sR1 influenced by iodine excess is one of the molecular bases of follicular epithelium apoptosis and inflammation in thyroids. Genetic factor is a key factor in the pathogenesis of thyroiditis.     

低碘膳食对大鼠脑组织同源盒基因Nkx-6.1和Nkx-6.2 mRNA表达的影响

Objective To study the influence of low-iodine diet on the expression of homeobox gene Nkx-6.1 and Nkx-6.2 in rat cerebrum tissue, and to explore the possible molecular mechanism of cerebrum development retardation caused by low-iodine. Methods Twenty female Wistar rats were randomly equally divided into two groups: low-iodine group and control group, both fed with low-iodine diet as low as 13.66 μg/kg determinated by spectrophotometry in Tianjin Institute of Endocrinology and the former with deionized water, the later 200 μg/L potassium iodate. Thyroid hormone level was detected using chemiluminescence immunoassay 3 months later and they were mated with male rats normally fed. Rats of 16-day pregnancy, new-born and 20th days old were detected the content of Nkx-6.1 and Nkx-6.2 mRNA in the cerebrum tissue by real-time fluorescence quantitative PCR 0.61), (3.28±0.80)pmol/L] were lower than the control group[(1.04±0.06), (39.42±14.68)nmol/L, (4.83±0.33), day pregnancy, new-born and 20th days old of control group was (1.90±0.23)×10-3,(1.86±0.40)×10-4, (1.11± 0.27)×10-4(F=827.58, P<0.01), Nkx-6.1 mRNA expression level gradually decreased along with aging(all P<0.05). The intra-group difference was significant (F=297.25, P<0.01) and the Nkxr.1 mRNA expression level during 16 days of pregnancy was the highest(P<0.01). It was higher in the control group than in the low-iodine group during 16 days of pregnancy (t=10.14, P<0.01) as well as in the low-iodine group than in the in 16-day pregnancy, new-born and 20th days old of control group was respectively(1.03±0.19)×10-2, (1.33± 0.10)×10-3, (8.79±0,87)×10-3, and that of low-iodine group was (0.31±0.03)×10-2, (1.53±0.13)×10-3, (7.51±0.86)×10-2. The intra-group difference was significant(F=1293.02,1065.83, all P<0.01). Nkx-6.2 expression level during 20th days old was the highest(P<0.01) and that of newborn was the lowest(P<0.01). The Nkx6.2 mRNA expression level in control group were higher than the low-iodine group during 16-day pregnancy and 20th days old(t=14.35, 4.05, all P<0.01). It was higher in the low-iodine group than in the control group during newboru(t=4.78, P<0.01). Conclusions The difference in the expression of Nkx-6.1 and Nkx-62 is highly related to the brain development retardation caused by low-iodine.     

碘过量和多聚肌苷酸-聚胞苷酸及甲状腺球蛋白诱发小鼠甲状腺炎对Toll样受体3表达的影响

Objective To observe the effect of iodine excess(HI),polyinosinic-polycytidylic acid[Poly(I:C),Poly]and thyroglobulin(TG)on the thyroid of mice by the expression of Toll-like receptor 3(TLR3)to reveal the functional role of TLR3 in autoimmune thyroiditis.Methods Forty-two non-obese diabetic mice,body weight (20±3)g,were divided into six groups:control group,HI group,Poly group,TG group,HI+TG group,HI+Poly group. Fed with deionized water and injected intraperitoneally with physiological saline 0.1 ml each day for a week, the mice in control group were injected with physiological saline every other day at the same dose for 1 week before they were sacrificed; HI group drank 0.05% NaI water and were injected intraperitoneally with physiological saline same as control group; Poly group drank deionized water and were injected intraperitoneally with poly 0.1 ml (1 g/L)each day of the week, then the mice were injected with Poly every other day at the same dose for 1 week before they were sacrificed; TG group drank deionized water and were injected intraperitoneally with physiological saline same as control group, immunized with 0.1 mg TG by subcutaneously injecting and the immunization was enhanced after they were fed half dose for 4 and 8 weeks separately. In HI + Poly group, the treatment was the same as HI group and Poly group; HI + TG group: the treatment was the same as HI group and TG group. Eight weeks later, mice were sacrificed and thyroids were taken to make frozen sections, Hematoxylin-Eosin (HE) staining was employed to observe the morphological change of the thyroids. The expression of TLR3 of thyroids was observed under fluorescence microscope after Immumofluorescence using TLR3 antibody and TR3-positive cells were analyzed in the thyroid density. Results HE staining showed thyroids of Poly group had no inflammation under microscope.There were different degrees of inflammatory cell infiltration in HI group and TG group. The inflammatory cell infiltration and the damage of follicular thyroid of HI + TG group and HI + Poly group were serious, and the degrees of inflammation were higher over "++". Thyroid follicular epithelial cell with TLR3 expression could be seen in Poly group and HI group, meanwhile, there were TLR3 strong positive inflammatory cells in HI group under fluorescent microscope. Using stereological analysis of TLR3-positive cell density in the thyroid, the difference between groups was statistically significant(F=7.870, P<0.01 ). TLR3-positive cell density in the thyroid of HI + Poly group was higher[ (9.287 ± 0.522)mm2] than control group[ (0.062 ± 0.025)mm2, P < 0.01] significantly, meanwhile, the density in HI + Poly group was higher than HI group [ (2.574 ± 0.257 )mm2] and Poly group[ (1.361 ± 0.148 )mm2, all P < 0.01]. The density in HI + TG group[ (4.843±0.405)mm2] was higher than HI group and TG group[(1.601 ±0.268)mm2, all P < 0.01 )]. Conclusions Excessive iodine and thyroglobulin can induce thyroiditis, and stimulate the expression of TLR3 in the thyroid follicular epithelial, Poly aggravated thyroiditis induced by iodine excess in NOD mice; TLR3 positive inflammatory cells also appeared in inflammatory region, suggesting that TLR3 is involved in the pathogenesis of autoimmune thyroiditis     

碘过量和多聚肌苷酸-聚胞苷酸及甲状腺球蛋白诱发小鼠甲状腺炎对Toll样受体3表达的影响

Objective To observe the effect of iodine excess(HI),polyinosinic-polycytidylic acid[Poly(I:C),Poly]and thyroglobulin(TG)on the thyroid of mice by the expression of Toll-like receptor 3(TLR3)to reveal the functional role of TLR3 in autoimmune thyroiditis.Methods Forty-two non-obese diabetic mice,body weight (20±3)g,were divided into six groups:control group,HI group,Poly group,TG group,HI+TG group,HI+Poly group. Fed with deionized water and injected intraperitoneally with physiological saline 0.1 ml each day for a week, the mice in control group were injected with physiological saline every other day at the same dose for 1 week before they were sacrificed; HI group drank 0.05% NaI water and were injected intraperitoneally with physiological saline same as control group; Poly group drank deionized water and were injected intraperitoneally with poly 0.1 ml (1 g/L)each day of the week, then the mice were injected with Poly every other day at the same dose for 1 week before they were sacrificed; TG group drank deionized water and were injected intraperitoneally with physiological saline same as control group, immunized with 0.1 mg TG by subcutaneously injecting and the immunization was enhanced after they were fed half dose for 4 and 8 weeks separately. In HI + Poly group, the treatment was the same as HI group and Poly group; HI + TG group: the treatment was the same as HI group and TG group. Eight weeks later, mice were sacrificed and thyroids were taken to make frozen sections, Hematoxylin-Eosin (HE) staining was employed to observe the morphological change of the thyroids. The expression of TLR3 of thyroids was observed under fluorescence microscope after Immumofluorescence using TLR3 antibody and TR3-positive cells were analyzed in the thyroid density. Results HE staining showed thyroids of Poly group had no inflammation under microscope.There were different degrees of inflammatory cell infiltration in HI group and TG group. The inflammatory cell infiltration and the damage of follicular thyroid of HI + TG group and HI + Poly group were serious, and the degrees of inflammation were higher over "++". Thyroid follicular epithelial cell with TLR3 expression could be seen in Poly group and HI group, meanwhile, there were TLR3 strong positive inflammatory cells in HI group under fluorescent microscope. Using stereological analysis of TLR3-positive cell density in the thyroid, the difference between groups was statistically significant(F=7.870, P<0.01 ). TLR3-positive cell density in the thyroid of HI + Poly group was higher[ (9.287 ± 0.522)mm2] than control group[ (0.062 ± 0.025)mm2, P < 0.01] significantly, meanwhile, the density in HI + Poly group was higher than HI group [ (2.574 ± 0.257 )mm2] and Poly group[ (1.361 ± 0.148 )mm2, all P < 0.01]. The density in HI + TG group[ (4.843±0.405)mm2] was higher than HI group and TG group[(1.601 ±0.268)mm2, all P < 0.01 )]. Conclusions Excessive iodine and thyroglobulin can induce thyroiditis, and stimulate the expression of TLR3 in the thyroid follicular epithelial, Poly aggravated thyroiditis induced by iodine excess in NOD mice; TLR3 positive inflammatory cells also appeared in inflammatory region, suggesting that TLR3 is involved in the pathogenesis of autoimmune thyroiditis     

不同碘营养水平对育龄妇女甲状腺功能的影响

Objective To study the effects of different level of iodine nutrition on the thyroid function in women of reproductive age. Methods A total of 100 (50 from each) women of reproductive age but not pregnant were collected from iodine deficient and adequate areas. The questionnaire was obtained individually with items concerning personal history of thyroid diseases, goiters and category of edible salt and drinking water based on the project design. The household salt and drinking water were collected for measuring iodine content, and blood samples were obtained for TSH, FT4 and FT3 testing. Results The coverage of iodized salt and the median level of urinary iodine in iodine deficient women(72.0% and 95.5 μg/L) were obviously lower than that in iodine sufficient women(100.0% and 167.4 μg/L, χ2=16.28, U = 632.00, P < 0.01). Median level of serum TSH in iodine deficient women (2.56 m U/L) appeared in an increasing tendency compared to the iodine sufficient women (1.88 mU/L), but there was no significance (U=990.50, P > 0.05). Serum FT4 mean level in iodine deficient women [(14.7±2.0) pmol/L]was lower than that in iodine sufficient women[(17.0±3.8)pmoI/L, t=3.76, P<0.01]. There was no difference in serum FT3 between two group women[(5.1±1.4), (4.8±0.5)pmoI/L, t = 1.59, P > 0.05]; but FT3/FT4 ratio in iodine deficient women(0.33±0.04) was markedly higher than that in the iodine sufficient women(0.30±0.04, t=3.13, P<0.01). The percentage of thyroid dysfunction in iodine deficient women[20.0% (10/50)]was higher compared with the iodine sufficient women[8.0%(4/50)], but without significance(χ2=2.99, P>0.05). Conclusions Iodine deficiency is a primary cause leading to hypothyroid in women of reproductive age. Long term of iodized salt usage is an efficient way to correct iodine deficiency.     

不同碘营养水平对育龄妇女甲状腺功能的影响

Objective To study the effects of different level of iodine nutrition on the thyroid function in women of reproductive age. Methods A total of 100 (50 from each) women of reproductive age but not pregnant were collected from iodine deficient and adequate areas. The questionnaire was obtained individually with items concerning personal history of thyroid diseases, goiters and category of edible salt and drinking water based on the project design. The household salt and drinking water were collected for measuring iodine content, and blood samples were obtained for TSH, FT4 and FT3 testing. Results The coverage of iodized salt and the median level of urinary iodine in iodine deficient women(72.0% and 95.5 μg/L) were obviously lower than that in iodine sufficient women(100.0% and 167.4 μg/L, χ2=16.28, U = 632.00, P < 0.01). Median level of serum TSH in iodine deficient women (2.56 m U/L) appeared in an increasing tendency compared to the iodine sufficient women (1.88 mU/L), but there was no significance (U=990.50, P > 0.05). Serum FT4 mean level in iodine deficient women [(14.7±2.0) pmol/L]was lower than that in iodine sufficient women[(17.0±3.8)pmoI/L, t=3.76, P<0.01]. There was no difference in serum FT3 between two group women[(5.1±1.4), (4.8±0.5)pmoI/L, t = 1.59, P > 0.05]; but FT3/FT4 ratio in iodine deficient women(0.33±0.04) was markedly higher than that in the iodine sufficient women(0.30±0.04, t=3.13, P<0.01). The percentage of thyroid dysfunction in iodine deficient women[20.0% (10/50)]was higher compared with the iodine sufficient women[8.0%(4/50)], but without significance(χ2=2.99, P>0.05). Conclusions Iodine deficiency is a primary cause leading to hypothyroid in women of reproductive age. Long term of iodized salt usage is an efficient way to correct iodine deficiency.     

不同碘营养水平对育龄妇女甲状腺功能的影响

Objective To study the effects of different level of iodine nutrition on the thyroid function in women of reproductive age. Methods A total of 100 (50 from each) women of reproductive age but not pregnant were collected from iodine deficient and adequate areas. The questionnaire was obtained individually with items concerning personal history of thyroid diseases, goiters and category of edible salt and drinking water based on the project design. The household salt and drinking water were collected for measuring iodine content, and blood samples were obtained for TSH, FT4 and FT3 testing. Results The coverage of iodized salt and the median level of urinary iodine in iodine deficient women(72.0% and 95.5 μg/L) were obviously lower than that in iodine sufficient women(100.0% and 167.4 μg/L, χ2=16.28, U = 632.00, P < 0.01). Median level of serum TSH in iodine deficient women (2.56 m U/L) appeared in an increasing tendency compared to the iodine sufficient women (1.88 mU/L), but there was no significance (U=990.50, P > 0.05). Serum FT4 mean level in iodine deficient women [(14.7±2.0) pmol/L]was lower than that in iodine sufficient women[(17.0±3.8)pmoI/L, t=3.76, P<0.01]. There was no difference in serum FT3 between two group women[(5.1±1.4), (4.8±0.5)pmoI/L, t = 1.59, P > 0.05]; but FT3/FT4 ratio in iodine deficient women(0.33±0.04) was markedly higher than that in the iodine sufficient women(0.30±0.04, t=3.13, P<0.01). The percentage of thyroid dysfunction in iodine deficient women[20.0% (10/50)]was higher compared with the iodine sufficient women[8.0%(4/50)], but without significance(χ2=2.99, P>0.05). Conclusions Iodine deficiency is a primary cause leading to hypothyroid in women of reproductive age. Long term of iodized salt usage is an efficient way to correct iodine deficiency.     

不同碘营养水平对育龄妇女甲状腺功能的影响

Objective To study the effects of different level of iodine nutrition on the thyroid function in women of reproductive age. Methods A total of 100 (50 from each) women of reproductive age but not pregnant were collected from iodine deficient and adequate areas. The questionnaire was obtained individually with items concerning personal history of thyroid diseases, goiters and category of edible salt and drinking water based on the project design. The household salt and drinking water were collected for measuring iodine content, and blood samples were obtained for TSH, FT4 and FT3 testing. Results The coverage of iodized salt and the median level of urinary iodine in iodine deficient women(72.0% and 95.5 μg/L) were obviously lower than that in iodine sufficient women(100.0% and 167.4 μg/L, χ2=16.28, U = 632.00, P < 0.01). Median level of serum TSH in iodine deficient women (2.56 m U/L) appeared in an increasing tendency compared to the iodine sufficient women (1.88 mU/L), but there was no significance (U=990.50, P > 0.05). Serum FT4 mean level in iodine deficient women [(14.7±2.0) pmol/L]was lower than that in iodine sufficient women[(17.0±3.8)pmoI/L, t=3.76, P<0.01]. There was no difference in serum FT3 between two group women[(5.1±1.4), (4.8±0.5)pmoI/L, t = 1.59, P > 0.05]; but FT3/FT4 ratio in iodine deficient women(0.33±0.04) was markedly higher than that in the iodine sufficient women(0.30±0.04, t=3.13, P<0.01). The percentage of thyroid dysfunction in iodine deficient women[20.0% (10/50)]was higher compared with the iodine sufficient women[8.0%(4/50)], but without significance(χ2=2.99, P>0.05). Conclusions Iodine deficiency is a primary cause leading to hypothyroid in women of reproductive age. Long term of iodized salt usage is an efficient way to correct iodine deficiency.     

不同碘营养水平对育龄妇女甲状腺功能的影响

Objective To study the effects of different level of iodine nutrition on the thyroid function in women of reproductive age. Methods A total of 100 (50 from each) women of reproductive age but not pregnant were collected from iodine deficient and adequate areas. The questionnaire was obtained individually with items concerning personal history of thyroid diseases, goiters and category of edible salt and drinking water based on the project design. The household salt and drinking water were collected for measuring iodine content, and blood samples were obtained for TSH, FT4 and FT3 testing. Results The coverage of iodized salt and the median level of urinary iodine in iodine deficient women(72.0% and 95.5 μg/L) were obviously lower than that in iodine sufficient women(100.0% and 167.4 μg/L, χ2=16.28, U = 632.00, P < 0.01). Median level of serum TSH in iodine deficient women (2.56 m U/L) appeared in an increasing tendency compared to the iodine sufficient women (1.88 mU/L), but there was no significance (U=990.50, P > 0.05). Serum FT4 mean level in iodine deficient women [(14.7±2.0) pmol/L]was lower than that in iodine sufficient women[(17.0±3.8)pmoI/L, t=3.76, P<0.01]. There was no difference in serum FT3 between two group women[(5.1±1.4), (4.8±0.5)pmoI/L, t = 1.59, P > 0.05]; but FT3/FT4 ratio in iodine deficient women(0.33±0.04) was markedly higher than that in the iodine sufficient women(0.30±0.04, t=3.13, P<0.01). The percentage of thyroid dysfunction in iodine deficient women[20.0% (10/50)]was higher compared with the iodine sufficient women[8.0%(4/50)], but without significance(χ2=2.99, P>0.05). Conclusions Iodine deficiency is a primary cause leading to hypothyroid in women of reproductive age. Long term of iodized salt usage is an efficient way to correct iodine deficiency.     

不同碘营养水平对育龄妇女甲状腺功能的影响

Objective To study the effects of different level of iodine nutrition on the thyroid function in women of reproductive age. Methods A total of 100 (50 from each) women of reproductive age but not pregnant were collected from iodine deficient and adequate areas. The questionnaire was obtained individually with items concerning personal history of thyroid diseases, goiters and category of edible salt and drinking water based on the project design. The household salt and drinking water were collected for measuring iodine content, and blood samples were obtained for TSH, FT4 and FT3 testing. Results The coverage of iodized salt and the median level of urinary iodine in iodine deficient women(72.0% and 95.5 μg/L) were obviously lower than that in iodine sufficient women(100.0% and 167.4 μg/L, χ2=16.28, U = 632.00, P < 0.01). Median level of serum TSH in iodine deficient women (2.56 m U/L) appeared in an increasing tendency compared to the iodine sufficient women (1.88 mU/L), but there was no significance (U=990.50, P > 0.05). Serum FT4 mean level in iodine deficient women [(14.7±2.0) pmol/L]was lower than that in iodine sufficient women[(17.0±3.8)pmoI/L, t=3.76, P<0.01]. There was no difference in serum FT3 between two group women[(5.1±1.4), (4.8±0.5)pmoI/L, t = 1.59, P > 0.05]; but FT3/FT4 ratio in iodine deficient women(0.33±0.04) was markedly higher than that in the iodine sufficient women(0.30±0.04, t=3.13, P<0.01). The percentage of thyroid dysfunction in iodine deficient women[20.0% (10/50)]was higher compared with the iodine sufficient women[8.0%(4/50)], but without significance(χ2=2.99, P>0.05). Conclusions Iodine deficiency is a primary cause leading to hypothyroid in women of reproductive age. Long term of iodized salt usage is an efficient way to correct iodine deficiency.