促甲状腺激素β-亚基的基因表达与调控

垂体前叶五类细胞的功能特化受普遍存在和细胞特异性转录因子的控制。细胞特异性转录因子Ｐｉｔ－１对生长激素（ＧＨ）、泌乳素（ＰＲＬ）基因的基础表达和对促甲状腺激素（ＴＳＨ）β－亚基基因的调节表达是必要的。转录因子截然不同的结合位点和某些转录控制机制，清楚地显示出以ＴＳＨ基因为例的垂体激素基因表达调节的复杂性。人Ｐｉｔ－１基因的不同突变证实，这个蛋白质的作用与以ＧＨ、ＰＲＬ和ＴＳＨ缺陷为特征的联合性垂体激素缺陷有关     

正常甲状腺功能人群血清促甲状腺激素变化的五年随访研究

目的 探讨正常甲状腺功能者5年随访时促甲状腺激素(TSH)的异常率和影响这一人群TSH发生异常的因素.方法 3个不同碘营养背景的农村社区的3403例甲状腺功能正常者中,80.1%(2727例)接受了筛查后的5年随访,测定其血清TSH和甲状腺自身抗体水平.结果 随访对象中,68例(2.5%)TSH异常降低(<0.3 mU/L),64例(2.4%)TSH异常增高(>4.8 mU/L).logistic回归分析显示,初访时甲状腺过氧化物酶抗体(TPOAb)阴性而随访时阳性(OR=5.5)、初访和随访TPOAb均阳件(OR=4.0)、随访时甲状腺球蛋白抗体(TgAb)阳性(OR=3.7)和初访时TSH<1.0 mU/L(OR=2.6)是TSH异常降低的危险因素;而缺碘基础上补碘至碘足量(OR=4.8)、长期碘过量(OR=3.9)、随访时TgAb阳性(OR=3.7)、初访和随访TPOAb均阳性(OR=3.6)、初访时TPOAb阴性而随访时阳性(OR=2.7)和TSH>1.9 mU/L(OR=2.6)是TSH异常增高的危险因素.结论 与轻度碘缺乏相比,碘足量和碘过量足TSH由正常转为异常升高的危险因素,缺碘基础上补碘至碘足量导致TSH转为异常升高的危险性更高于长期碘过量.初访TSH处于1.0～1.9 mU/L时,5年随访时发生TSH异常的几率最小.     

人促甲状腺激素受体膜外区N端基因免疫诱导Balb/c小鼠实验性格雷夫斯病

目的 观察人促甲状腺激素受体(human thyrotropin receptor,hTSHR)膜外区N端(氨基酸29～280区域)的抗原性及其与格雷夫斯病(Graves病)发病的关系.方法 提取人正常甲状腺组织总RNA,反转录后进行PCR,扩增产物与表达载体pcDNA3.1进行连接得到重组质粒pcDNA3.1/hTSHR188-940bp.用重组质粒免疫Balb/c小鼠,检测小鼠血清中甲状腺素(thyroxin,T4)、抗TsHR抗体(anti-TSHR antibody,TRAb)、甲状腺刺激抗体(thyroid stimulating antibody,TSAb)水平的变化,光镜下观察甲状腺组织的结构变化.结果 PCR扩增得到hTSHR膜外区N端753 bp的基因片段hTSHRl88-940bp,该片段与表达载体pcDNA3.1连接后,经HindⅢ酶切和核苷酸序列测定方法鉴定证实hTSHR188～940bp片段插入序列和方向正确.用pcDNA3.1/hTSHR188～940 bp免疫Balb/c小鼠后发现,血清TRAb水平从第6周(0.148±0.018)开始升高,到第10周(0.134±0.011)一直维持在比较高的水平,与第0周(0.106±0.006)比较,差异均有统计学意义(P＜0.01).血清T4、TSAb水平在第10周[(62.20±12.77)μg/L、1.392±0.615]出现明显升高,与第0周[(41.02±7.97)μg/L、0.864±0.076]比较,差异均有统计学意义(P＜0.01).甲状腺病理学检查发现大部分小鼠甲状腺滤泡上皮增生,滤泡腔增大,偶见炎细胞浸润.结论 TSHR188～940bp编码的hTSHR膜外区N端氨基酸29～280区域抗原决定簇使机体产生TSAb,从而导致甲状腺功能亢进,出现类Graves病表现,说明TSHR的这个区域与Graves病密切相关,可能是导致该病的重要因素.     

睡眠剥夺对大鼠血清促肾上腺皮质激素、促甲状腺激素及皮质醇的影响

目的观察不同睡眠剥夺时间对大鼠血清促肾上腺皮质激素（ACTH）、促甲状腺激素（TSH）及皮质醇（CORT）的影响。方法将大鼠随机分为正常笼养组（CC）,大平台实验组（TC）,睡眠剥夺1d、3d、5d和7d组,采用改良多平台睡眠剥夺法（MMPM）建立睡眠剥夺模型,取大鼠下腔静脉血,采用化学发光免疫法测定血清中ACTH、TSH、CORT的含量。结果选60只大鼠进行实验,最后纳入48只大鼠进入结果分析。与CC组、TC组相比较,随着睡眠剥夺时间的延长,大鼠血清ACTH、TSH及CORT含量先呈升高趋势,随后分别在剥夺睡眠第3、5、5天时达到峰值,然后呈逐渐降低趋势。结论睡眠剥夺能够应激性地激活大鼠下丘脑-垂体肾上腺皮质轴,使大鼠血清中ACTH、TSH、CORT的含量随睡眠剥夺时间的变化产生波动。     

甲亢患者β_2-微球蛋白与甲状腺激素相关性研究

目的探讨甲亢患者β2-微球蛋白含量与甲状腺激素间的关系及其可能具有的临床价值。方法 40例甲亢患者作为观察组,40例健康体检人群为对照组。对比分析不同组间和不同疗效间各项实验室指标的差异,并进行血清和尿β2-微球蛋白与FT3、FT4、TSH的相关性分析。结果治疗前,甲亢患者FT3、FT4、TSH及血清和尿β2-微球蛋白含量与对照组比较均有统计学差异（P〈0.01）,治疗后,无统计学差异（P〉0.05）;治愈组患者血清和尿β2-微球蛋白、FT3、FT4、TSH含量与好转组及无效组间的差异均有统计学意义（P〈0.01）;治疗前,血清和尿β2-微球蛋白与FT3、FT4呈正相关,与TSH呈负相关。结论甲亢患者β2-微球蛋白含量与甲状腺激素关系密切,可作为判断病情变化和疗效观察的重要指标。     

甲亢患者血、尿β2-MG水平及其与甲状腺激素水平的相关性分析

目的探讨甲状腺功能亢进症（下称甲亢）患者血、尿β2-微球蛋白（MG）水平变化及与病情的相关性。方法对40例甲亢患者（观察组）及40例健康查体者（对照组）血清、尿β2-MG及血清游离甲状腺素（FT3）、游离三碘甲状腺原氨酸（FT4）、促甲状腺素（TSH）水平进行检测,并分析其相关性。结果治疗前甲亢患者FT3、FT4水平均高于对照组（P均〈0.01）,TSH水平显著低于对照组（P均〈0.01）,血清和尿β2-MG水平均高于对照组（P〈0.01）;治疗后甲亢患者FT3、FT4水平与治疗前相比明显下降（P〈0.01）,TSH水平有所升高（P〈0.01）,血清和尿β2-MG水平均有明显下降（P〈0.01）。治疗前血清β2-MG水平与FT3、FT4呈正相关,与TSH呈负相关;尿β2-MG水平与FT3、FT4亦呈正相关,与TSH呈负相关。结论甲亢患者血和尿β2-MG水平显著升高,两者均可灵敏反映病情变化,可作为临床疗效评价的重要指标。     

补碘对缺碘人群促甲状腺激素受体抗体的影响

为探讨补碘对缺碘机体甲状腺自身免疫的影响，采用酶联免疫分析方法测定了缺碘地区人群口服碘油前后的促甲状腺激素受体抗体(TRAb)和甲状腺刺激抗体(TSAb)水平变化。结果发现，缺碘机体补碘后的TRAb和TSAb水平均明显高于补碘前;TRAb从阳性检出率增高，12个月时其阳性检出率高达24．44％。表明缺碘地区人群补碘后其自身抗体水平增高且抗体阳性率增多。提示补碘可诱导缺碘机体发生甲状腺自身免疫反应，易产生自身免疫性甲状腺疾病。     

TSH和高碘对FRTL细胞甲状腺激素合成相关基因表达的影响

目的观察不同浓度TSH和高碘对FRTL细胞钠/碘转运体(NIS)mRNA、甲状腺过氧化物酶(TPO)和甲状腺球蛋白(Tg)基因表达的影响。方法采用FRTL细胞系,用不含有TSH的培养基培养7d后,用不同水平TSH(0.1、0.5、1、10、50、100U/L)刺激。培养24h后,检测3种基因NIS、TPO、Tg的mRNA水平。高碘组按照10-7、10-6、10-5、10-4、10-3mol/L的碘离子浓度加入培养基,在第24和48小时,收集细胞,检测3种基因NIS、TPO、Tg的mRNA水平。结果TSH刺激24h后,FRTL细胞内NIS、TPO、Tg基因表达都伴随TSH水平的升高而上升。TSH从0.1U/L开始就对NIS基因表达增加有显著性影响(P<0.05),TSH对TPO基因表达的刺激从1U/L开始有显著性影响。TSH对Tg基因表达的作用从0.1U/L开始就有刺激作用(P<0.05)。高碘组对细胞这3种基因的表达没有刺激作用。结论TSH对FRTL细胞系产生甲状腺激素具有明显的刺激上调的作用。但高碘对该细胞3种基因的表达没有上调的作用。     

泡球蚴感染BALB/c小鼠肝脏TGF-β1表达的动态变化

目的观察泡球蚴感染BALB/c小鼠肝脏转化生长因子β1（TGF-β1）的动态变化。方法将60只BALB/c小鼠随机分为实验组和对照组,肉眼直视下肝脏穿刺感染泡球蚴。分别于感染后2 d8、d、4周、12周、24周、36周采取小鼠肝脏组织,通过HE和Masson染色观察小鼠肝脏病理改变,免疫组织化学法观察泡球蚴感染不同阶段的TGF-β1动态变化。结果泡球蚴感染小鼠肝脏汇管周围出现炎细胞浸润、脂肪变性、坏死、钙化和肝泡球蚴纤维囊壁形成等多种病理改变;TGF-β1表达水平呈先升高再下降趋势,感染4周、12周、24周、36周时的阳性率分别为（1.44±3.22）%、（18.83±4.03）%（、9.44±4.71）%和（8.13±3.65）%,其中感染12周和36周与对照组相比差异有统计学意义（P〈0.05）。结论泡球蚴感染BALB/c小鼠TGF-β1表达上调,可能与感染小鼠肝纤维化的发展有关。     

妊娠期大鼠不同程度碘缺乏对胎鼠碘代谢和甲状腺功能的影响

目的 研究妊娠期大鼠不同程度碘缺乏对胎鼠碘代谢和甲状腺功能的影响.方法 40只Wistar雌性大鼠按体质量随机分为4组,每组10只,均食用低碘饲料(含碘量为50μg/kg);重、中、轻度缺碘(SID、MoID、MiID)组和正常碘(NI)组饮用含不同剂量碘化钾(0、54.9、163.8、381.7μg/L)的自来水(含碘量为8μg/L),每日总碘供给量分别为1.24、2.50、5.00、10.00μg.喂养3月后与按NI组条件饲养的Wistar雄性鼠交配,以妊娠20 d孕鼠和胎鼠为研究对象,过硫酸铵消化砷铈催化分光光度法测定孕鼠尿碘和胎鼠羊水含碘量,碱灰化砷铈催化分光光度法测定孕鼠血碘和胎盘组织含碘量,化学发光法测定孕鼠血清及胎鼠羊水甲状腺激素水平,检测并观察孕鼠和胎鼠的甲状腺质量及大体变化.结果 ①孕鼠尿碘、血碘,胎鼠羊水碘均随碘供给量减少呈降低趋势.NI、MiID、MoID、SID组孕鼠尿碘中位数分别为353.7、115.9、26.9、0μg/L,组间比较差异有统计学意义(χ2=32.884,P<0.01);MoID、SID组[(29.4±18.6)、(11.7±7.0)μg/L]孕鼠血碘明显低于NI组[(49.1±23.0)μg/L,P<0.05或<0.01).与NI组[(65.4±41.2)μg/L,(0.35±0.14)μg/g]比较,MiID、MoID、SID组胎鼠羊水碘[(48.3±23.1)、(29.2±14.7)、(19.5±6.7)μg/L]呈降低趋势,胎盘组织碘[(0.57±0.26)、(0.53±0.34)、(0.53±0.15)μg/g]呈升高趋势,但组间比较差异均无统计学意义(P>0.05).②SID组孕鼠血清TT4[(14.3±4.1)mmol/L]和FT4[(10.8±3.6)pmol/L]明显低于NI组[(28.4±19.3)nmol/L,(20.2±8.0)pmol/L,P<0.05或<0.01],而FT3/FT4比值(0.34±0.16),甲状腺绝对质量[(48.4±22.7)mg]和相对质量[(144±76)mg/kg]明显高于NI组[(0.16±0.02)、(19.5±3.1)mg,(66±10)mg/kg,P<0.01];MiID、MoID组TT4[(25.5±13.1)、(22.1±6.1)nmoL/L]和FT4[(18.6±8.4)、(18.5±4.1)pmol/L]与NI组比较,有降低趋势,FT3/FT4比值(0.17±0.06、0.19±0.04),甲状腺绝对质量[(25.0±8.9)、(27.0±5.7)mg]和相对质量[(78±25)、(84±19)mg/kg]与NI组比较,有增高趋势,但组间比较差异均无统计学意义(P>0.05);SID组孕鼠甲状腺明显充血肿大,MiID、MoID组轻度肿大.③SID组胎鼠羊水FT4[(1.07±0.87)pmol/L]低于NI组[(2.38±1.55)pmoVL],FT3/FT4比值(1.96±0.61)高于NI组(0.50±0.18),组间比较差异均有统计学意义(P<0.05或<0.01);MiID、MoID组FT4[(2.77±0.90)、(2.35±0.76)pmol/L]、FT3/FT4比值(0.46±0.15、0.61±0.21)与NI组比较,差异均无统计学意义(P>0.05);SID组胎鼠甲状腺有明显充血肿大,MiID、MoID组仅见轻度充血,其大小与NI组相似.结论 重度碘缺乏使孕鼠及其胎鼠均发生了明显甲状腺功能减退症,而轻度碘缺乏通过代偿可使胎儿甲状腺激素维持正常水平,中度碘缺乏对母亲和胎儿均有不同程度的负面影响.     

BALB/c小鼠衰老过程中大脑皮质组织基因表达的改变

目的 鉴别和克隆小鼠衰老相关基因，为揭示人体衰老机制提供线索。方法 利用改进逆转录-多聚酶链反应(DDRT-PCR)技术分析了4月龄和24月龄BALB／c小鼠大脑皮质组织中mRNA的差异表达。结果 确定了42个差异表达cDNA片段，在衰老小鼠中表达上调和下调者各21个。其中17个为已知编码蛋白功能的基因片段，12个为已知基因序列但未知功能的基因片段，13个可能为新基因片段。在已知蛋白功能的基因中，与氧化应激、能量产生和蛋白质代谢等相关的基因分别为2个、3个和4个，此外还有参与细胞凋亡、神经退行性变和生长发育调节等基因表达的改变。结论 小鼠衰老可能与机体氧化应激状态、能量产生和蛋白质代谢等的改变有关。     

妊娠期大鼠不同程度碘缺乏对胎鼠碘代谢和甲状腺功能的影响

Objective To study the effects of iodine deficiency during pregnancy on fetal iodine metabolism and thyroid function. Methods Wistar dams were randomly divided into four groups: severe iodine deficiency(SID), moderate iodine deficiency(MoID), mild iodine deficiency(MiID) and normal iodine(NI). All the dams were fed with iodine deficient food(iodine contents: 50 μg/kg) and drinking water with different doses of KI (0,54.9,163.8,381.7 μg/L) for 3 months till mating. Iodine was supplied at the dose of 1.24 μg/d(SID), 2.50 μg/d(MoID), 5.00 μg/d(MiID) and 10.00 μg/d(NI), respectively. The dams and their fetuses on gestation of 20 days were studied. Urine iodine of dams and iodine contents in fetal amniotic fluid were measured by As3+-Ce4+catalytic spectrophotometry using ammonium persulfate digestion. And blood iodine in pregnant rats and iodine contents in placental tissue were measured by As3+-Ce4+catalytic spectrophotometry in dry ash of samples in KClO3-ZnSO4-K2CO3-NaCl. Thyroid hormone levels in mother serum and in fetal amniotic fluid were detected by chemiluminascent assay, and their thyroid glands were weighted and carefully observed. Results ①Iodine content in urine and blood of pregnant rats and amniotic fluid of fetal rats reduced along with their decrease of iodine supply. Urine iodine median of rats in 4 groups(NI: 353.7 μg/L; MiID: 115.9 μg/L; MoID: 26.9 μg/L; SID: 0 μg/L) were statistically significant(χ2=32.884, P < 0.01). Blood iodine level in MoID and SID[(29.4±18.6), (11.7± 7.0)μg/L]was significantly lower than that in NI[(49.1±23.0)μg/L, P < 0.05 or < 0.01]. In iodine deficiency groups, there was a decreasing trend in iodine contents of fetal amniotic fluid[MiID: (48.3±23.1)μg/L; MoID: (29.2±14.7)μ/L; SID:(19.5±6.7)μg/L]and an increasing tendency in iodine contents of placental tissue [MiID: (0.57±0.26)μg/g, MoID: (0.53±0.34)μg/g; SID: (0.53±0.15)μg/g], but there was no statistical significance(P>0.05). ②In SID, TT4[(14.3±4.1)nmol/L]and FT4[(10.8±3.6)pmol/L]were lower than that in NI[(28.4±19.3)nmol/L, (20.2±8.0)pmol/L, P < 0.05 or < 0.01], while that in MoID[(22.1±6.1)nmol/L, (18.5±4.1)pmol/L]and MiID[(25.5±13.1)nmol/L, (18.6±8.4)pmol/L]were decreased without statistical significance(P > 0.05). And FT3/FT4 ratio(0.34±0.16), absolute[(48.4±22.7)mg]and relative weights[(144± 76)mg/kg]of thyroid gland in pregnant rats were respectively higher than that in NI[0.16±0.02, (19.5±3.1)mg, (66±10)mg/kg, P<0.01]. But that in MoID[0.19±0.04, (27.0±5.7)mg, (84±19)mg/kg]and MiID[0.17± 0.06, (25.0±8.9)mg, (78±25)mg/kg]were increased without statistical significance(P > 0.05). A visibly congestive enlargement thyroid was found in SID, while thyroid mildly enlarged in MoID and MiID. ③Compared with NI [(2.38±1.55)pmol/L,0.50±0.18], the FT4 levels [(1.07±0.87) pmol/L]in amniotic fluid were significantly decreased (P < 0.05) and the FT3/FT4 ratio (1.96±0.61) was significantly increased (P < 0.01) in SID. There were no statistical significances(P > 0.05) in other 3 groups[MiID: (2.77±0.90)pmol/L,0.46±0.15; MoID: (2.35±0.76)pmoL/L,0.61±0.21]. A visible thyroid enlargement with hyperemia was observed in SID fetus while in other 2 experiment groups their thyroids were only mildly congested. Conclusions Severe iodine deficiency during pregnancy can result in both mother and fetus overt hypothyroidism. The fetal thyroid hormone levels in mild iodine deficiency status is close to normal levels because of maternal and placental compensation. Moreover, both the dam and the fetus suffer from the negative effects in moderate iodine deficiency during pregnancy.     

妊娠期大鼠不同程度碘缺乏对胎鼠碘代谢和甲状腺功能的影响

Objective To study the effects of iodine deficiency during pregnancy on fetal iodine metabolism and thyroid function. Methods Wistar dams were randomly divided into four groups: severe iodine deficiency(SID), moderate iodine deficiency(MoID), mild iodine deficiency(MiID) and normal iodine(NI). All the dams were fed with iodine deficient food(iodine contents: 50 μg/kg) and drinking water with different doses of KI (0,54.9,163.8,381.7 μg/L) for 3 months till mating. Iodine was supplied at the dose of 1.24 μg/d(SID), 2.50 μg/d(MoID), 5.00 μg/d(MiID) and 10.00 μg/d(NI), respectively. The dams and their fetuses on gestation of 20 days were studied. Urine iodine of dams and iodine contents in fetal amniotic fluid were measured by As3+-Ce4+catalytic spectrophotometry using ammonium persulfate digestion. And blood iodine in pregnant rats and iodine contents in placental tissue were measured by As3+-Ce4+catalytic spectrophotometry in dry ash of samples in KClO3-ZnSO4-K2CO3-NaCl. Thyroid hormone levels in mother serum and in fetal amniotic fluid were detected by chemiluminascent assay, and their thyroid glands were weighted and carefully observed. Results ①Iodine content in urine and blood of pregnant rats and amniotic fluid of fetal rats reduced along with their decrease of iodine supply. Urine iodine median of rats in 4 groups(NI: 353.7 μg/L; MiID: 115.9 μg/L; MoID: 26.9 μg/L; SID: 0 μg/L) were statistically significant(χ2=32.884, P < 0.01). Blood iodine level in MoID and SID[(29.4±18.6), (11.7± 7.0)μg/L]was significantly lower than that in NI[(49.1±23.0)μg/L, P < 0.05 or < 0.01]. In iodine deficiency groups, there was a decreasing trend in iodine contents of fetal amniotic fluid[MiID: (48.3±23.1)μg/L; MoID: (29.2±14.7)μ/L; SID:(19.5±6.7)μg/L]and an increasing tendency in iodine contents of placental tissue [MiID: (0.57±0.26)μg/g, MoID: (0.53±0.34)μg/g; SID: (0.53±0.15)μg/g], but there was no statistical significance(P>0.05). ②In SID, TT4[(14.3±4.1)nmol/L]and FT4[(10.8±3.6)pmol/L]were lower than that in NI[(28.4±19.3)nmol/L, (20.2±8.0)pmol/L, P < 0.05 or < 0.01], while that in MoID[(22.1±6.1)nmol/L, (18.5±4.1)pmol/L]and MiID[(25.5±13.1)nmol/L, (18.6±8.4)pmol/L]were decreased without statistical significance(P > 0.05). And FT3/FT4 ratio(0.34±0.16), absolute[(48.4±22.7)mg]and relative weights[(144± 76)mg/kg]of thyroid gland in pregnant rats were respectively higher than that in NI[0.16±0.02, (19.5±3.1)mg, (66±10)mg/kg, P<0.01]. But that in MoID[0.19±0.04, (27.0±5.7)mg, (84±19)mg/kg]and MiID[0.17± 0.06, (25.0±8.9)mg, (78±25)mg/kg]were increased without statistical significance(P > 0.05). A visibly congestive enlargement thyroid was found in SID, while thyroid mildly enlarged in MoID and MiID. ③Compared with NI [(2.38±1.55)pmol/L,0.50±0.18], the FT4 levels [(1.07±0.87) pmol/L]in amniotic fluid were significantly decreased (P < 0.05) and the FT3/FT4 ratio (1.96±0.61) was significantly increased (P < 0.01) in SID. There were no statistical significances(P > 0.05) in other 3 groups[MiID: (2.77±0.90)pmol/L,0.46±0.15; MoID: (2.35±0.76)pmoL/L,0.61±0.21]. A visible thyroid enlargement with hyperemia was observed in SID fetus while in other 2 experiment groups their thyroids were only mildly congested. Conclusions Severe iodine deficiency during pregnancy can result in both mother and fetus overt hypothyroidism. The fetal thyroid hormone levels in mild iodine deficiency status is close to normal levels because of maternal and placental compensation. Moreover, both the dam and the fetus suffer from the negative effects in moderate iodine deficiency during pregnancy.     

妊娠期大鼠不同程度碘缺乏对胎鼠碘代谢和甲状腺功能的影响

Objective To study the effects of iodine deficiency during pregnancy on fetal iodine metabolism and thyroid function. Methods Wistar dams were randomly divided into four groups: severe iodine deficiency(SID), moderate iodine deficiency(MoID), mild iodine deficiency(MiID) and normal iodine(NI). All the dams were fed with iodine deficient food(iodine contents: 50 μg/kg) and drinking water with different doses of KI (0,54.9,163.8,381.7 μg/L) for 3 months till mating. Iodine was supplied at the dose of 1.24 μg/d(SID), 2.50 μg/d(MoID), 5.00 μg/d(MiID) and 10.00 μg/d(NI), respectively. The dams and their fetuses on gestation of 20 days were studied. Urine iodine of dams and iodine contents in fetal amniotic fluid were measured by As3+-Ce4+catalytic spectrophotometry using ammonium persulfate digestion. And blood iodine in pregnant rats and iodine contents in placental tissue were measured by As3+-Ce4+catalytic spectrophotometry in dry ash of samples in KClO3-ZnSO4-K2CO3-NaCl. Thyroid hormone levels in mother serum and in fetal amniotic fluid were detected by chemiluminascent assay, and their thyroid glands were weighted and carefully observed. Results ①Iodine content in urine and blood of pregnant rats and amniotic fluid of fetal rats reduced along with their decrease of iodine supply. Urine iodine median of rats in 4 groups(NI: 353.7 μg/L; MiID: 115.9 μg/L; MoID: 26.9 μg/L; SID: 0 μg/L) were statistically significant(χ2=32.884, P < 0.01). Blood iodine level in MoID and SID[(29.4±18.6), (11.7± 7.0)μg/L]was significantly lower than that in NI[(49.1±23.0)μg/L, P < 0.05 or < 0.01]. In iodine deficiency groups, there was a decreasing trend in iodine contents of fetal amniotic fluid[MiID: (48.3±23.1)μg/L; MoID: (29.2±14.7)μ/L; SID:(19.5±6.7)μg/L]and an increasing tendency in iodine contents of placental tissue [MiID: (0.57±0.26)μg/g, MoID: (0.53±0.34)μg/g; SID: (0.53±0.15)μg/g], but there was no statistical significance(P>0.05). ②In SID, TT4[(14.3±4.1)nmol/L]and FT4[(10.8±3.6)pmol/L]were lower than that in NI[(28.4±19.3)nmol/L, (20.2±8.0)pmol/L, P < 0.05 or < 0.01], while that in MoID[(22.1±6.1)nmol/L, (18.5±4.1)pmol/L]and MiID[(25.5±13.1)nmol/L, (18.6±8.4)pmol/L]were decreased without statistical significance(P > 0.05). And FT3/FT4 ratio(0.34±0.16), absolute[(48.4±22.7)mg]and relative weights[(144± 76)mg/kg]of thyroid gland in pregnant rats were respectively higher than that in NI[0.16±0.02, (19.5±3.1)mg, (66±10)mg/kg, P<0.01]. But that in MoID[0.19±0.04, (27.0±5.7)mg, (84±19)mg/kg]and MiID[0.17± 0.06, (25.0±8.9)mg, (78±25)mg/kg]were increased without statistical significance(P > 0.05). A visibly congestive enlargement thyroid was found in SID, while thyroid mildly enlarged in MoID and MiID. ③Compared with NI [(2.38±1.55)pmol/L,0.50±0.18], the FT4 levels [(1.07±0.87) pmol/L]in amniotic fluid were significantly decreased (P < 0.05) and the FT3/FT4 ratio (1.96±0.61) was significantly increased (P < 0.01) in SID. There were no statistical significances(P > 0.05) in other 3 groups[MiID: (2.77±0.90)pmol/L,0.46±0.15; MoID: (2.35±0.76)pmoL/L,0.61±0.21]. A visible thyroid enlargement with hyperemia was observed in SID fetus while in other 2 experiment groups their thyroids were only mildly congested. Conclusions Severe iodine deficiency during pregnancy can result in both mother and fetus overt hypothyroidism. The fetal thyroid hormone levels in mild iodine deficiency status is close to normal levels because of maternal and placental compensation. Moreover, both the dam and the fetus suffer from the negative effects in moderate iodine deficiency during pregnancy.     

妊娠期大鼠不同程度碘缺乏对胎鼠碘代谢和甲状腺功能的影响

Objective To study the effects of iodine deficiency during pregnancy on fetal iodine metabolism and thyroid function. Methods Wistar dams were randomly divided into four groups: severe iodine deficiency(SID), moderate iodine deficiency(MoID), mild iodine deficiency(MiID) and normal iodine(NI). All the dams were fed with iodine deficient food(iodine contents: 50 μg/kg) and drinking water with different doses of KI (0,54.9,163.8,381.7 μg/L) for 3 months till mating. Iodine was supplied at the dose of 1.24 μg/d(SID), 2.50 μg/d(MoID), 5.00 μg/d(MiID) and 10.00 μg/d(NI), respectively. The dams and their fetuses on gestation of 20 days were studied. Urine iodine of dams and iodine contents in fetal amniotic fluid were measured by As3+-Ce4+catalytic spectrophotometry using ammonium persulfate digestion. And blood iodine in pregnant rats and iodine contents in placental tissue were measured by As3+-Ce4+catalytic spectrophotometry in dry ash of samples in KClO3-ZnSO4-K2CO3-NaCl. Thyroid hormone levels in mother serum and in fetal amniotic fluid were detected by chemiluminascent assay, and their thyroid glands were weighted and carefully observed. Results ①Iodine content in urine and blood of pregnant rats and amniotic fluid of fetal rats reduced along with their decrease of iodine supply. Urine iodine median of rats in 4 groups(NI: 353.7 μg/L; MiID: 115.9 μg/L; MoID: 26.9 μg/L; SID: 0 μg/L) were statistically significant(χ2=32.884, P < 0.01). Blood iodine level in MoID and SID[(29.4±18.6), (11.7± 7.0)μg/L]was significantly lower than that in NI[(49.1±23.0)μg/L, P < 0.05 or < 0.01]. In iodine deficiency groups, there was a decreasing trend in iodine contents of fetal amniotic fluid[MiID: (48.3±23.1)μg/L; MoID: (29.2±14.7)μ/L; SID:(19.5±6.7)μg/L]and an increasing tendency in iodine contents of placental tissue [MiID: (0.57±0.26)μg/g, MoID: (0.53±0.34)μg/g; SID: (0.53±0.15)μg/g], but there was no statistical significance(P>0.05). ②In SID, TT4[(14.3±4.1)nmol/L]and FT4[(10.8±3.6)pmol/L]were lower than that in NI[(28.4±19.3)nmol/L, (20.2±8.0)pmol/L, P < 0.05 or < 0.01], while that in MoID[(22.1±6.1)nmol/L, (18.5±4.1)pmol/L]and MiID[(25.5±13.1)nmol/L, (18.6±8.4)pmol/L]were decreased without statistical significance(P > 0.05). And FT3/FT4 ratio(0.34±0.16), absolute[(48.4±22.7)mg]and relative weights[(144± 76)mg/kg]of thyroid gland in pregnant rats were respectively higher than that in NI[0.16±0.02, (19.5±3.1)mg, (66±10)mg/kg, P<0.01]. But that in MoID[0.19±0.04, (27.0±5.7)mg, (84±19)mg/kg]and MiID[0.17± 0.06, (25.0±8.9)mg, (78±25)mg/kg]were increased without statistical significance(P > 0.05). A visibly congestive enlargement thyroid was found in SID, while thyroid mildly enlarged in MoID and MiID. ③Compared with NI [(2.38±1.55)pmol/L,0.50±0.18], the FT4 levels [(1.07±0.87) pmol/L]in amniotic fluid were significantly decreased (P < 0.05) and the FT3/FT4 ratio (1.96±0.61) was significantly increased (P < 0.01) in SID. There were no statistical significances(P > 0.05) in other 3 groups[MiID: (2.77±0.90)pmol/L,0.46±0.15; MoID: (2.35±0.76)pmoL/L,0.61±0.21]. A visible thyroid enlargement with hyperemia was observed in SID fetus while in other 2 experiment groups their thyroids were only mildly congested. Conclusions Severe iodine deficiency during pregnancy can result in both mother and fetus overt hypothyroidism. The fetal thyroid hormone levels in mild iodine deficiency status is close to normal levels because of maternal and placental compensation. Moreover, both the dam and the fetus suffer from the negative effects in moderate iodine deficiency during pregnancy.     

妊娠期大鼠不同程度碘缺乏对胎鼠碘代谢和甲状腺功能的影响

Objective To study the effects of iodine deficiency during pregnancy on fetal iodine metabolism and thyroid function. Methods Wistar dams were randomly divided into four groups: severe iodine deficiency(SID), moderate iodine deficiency(MoID), mild iodine deficiency(MiID) and normal iodine(NI). All the dams were fed with iodine deficient food(iodine contents: 50 μg/kg) and drinking water with different doses of KI (0,54.9,163.8,381.7 μg/L) for 3 months till mating. Iodine was supplied at the dose of 1.24 μg/d(SID), 2.50 μg/d(MoID), 5.00 μg/d(MiID) and 10.00 μg/d(NI), respectively. The dams and their fetuses on gestation of 20 days were studied. Urine iodine of dams and iodine contents in fetal amniotic fluid were measured by As3+-Ce4+catalytic spectrophotometry using ammonium persulfate digestion. And blood iodine in pregnant rats and iodine contents in placental tissue were measured by As3+-Ce4+catalytic spectrophotometry in dry ash of samples in KClO3-ZnSO4-K2CO3-NaCl. Thyroid hormone levels in mother serum and in fetal amniotic fluid were detected by chemiluminascent assay, and their thyroid glands were weighted and carefully observed. Results ①Iodine content in urine and blood of pregnant rats and amniotic fluid of fetal rats reduced along with their decrease of iodine supply. Urine iodine median of rats in 4 groups(NI: 353.7 μg/L; MiID: 115.9 μg/L; MoID: 26.9 μg/L; SID: 0 μg/L) were statistically significant(χ2=32.884, P < 0.01). Blood iodine level in MoID and SID[(29.4±18.6), (11.7± 7.0)μg/L]was significantly lower than that in NI[(49.1±23.0)μg/L, P < 0.05 or < 0.01]. In iodine deficiency groups, there was a decreasing trend in iodine contents of fetal amniotic fluid[MiID: (48.3±23.1)μg/L; MoID: (29.2±14.7)μ/L; SID:(19.5±6.7)μg/L]and an increasing tendency in iodine contents of placental tissue [MiID: (0.57±0.26)μg/g, MoID: (0.53±0.34)μg/g; SID: (0.53±0.15)μg/g], but there was no statistical significance(P>0.05). ②In SID, TT4[(14.3±4.1)nmol/L]and FT4[(10.8±3.6)pmol/L]were lower than that in NI[(28.4±19.3)nmol/L, (20.2±8.0)pmol/L, P < 0.05 or < 0.01], while that in MoID[(22.1±6.1)nmol/L, (18.5±4.1)pmol/L]and MiID[(25.5±13.1)nmol/L, (18.6±8.4)pmol/L]were decreased without statistical significance(P > 0.05). And FT3/FT4 ratio(0.34±0.16), absolute[(48.4±22.7)mg]and relative weights[(144± 76)mg/kg]of thyroid gland in pregnant rats were respectively higher than that in NI[0.16±0.02, (19.5±3.1)mg, (66±10)mg/kg, P<0.01]. But that in MoID[0.19±0.04, (27.0±5.7)mg, (84±19)mg/kg]and MiID[0.17± 0.06, (25.0±8.9)mg, (78±25)mg/kg]were increased without statistical significance(P > 0.05). A visibly congestive enlargement thyroid was found in SID, while thyroid mildly enlarged in MoID and MiID. ③Compared with NI [(2.38±1.55)pmol/L,0.50±0.18], the FT4 levels [(1.07±0.87) pmol/L]in amniotic fluid were significantly decreased (P < 0.05) and the FT3/FT4 ratio (1.96±0.61) was significantly increased (P < 0.01) in SID. There were no statistical significances(P > 0.05) in other 3 groups[MiID: (2.77±0.90)pmol/L,0.46±0.15; MoID: (2.35±0.76)pmoL/L,0.61±0.21]. A visible thyroid enlargement with hyperemia was observed in SID fetus while in other 2 experiment groups their thyroids were only mildly congested. Conclusions Severe iodine deficiency during pregnancy can result in both mother and fetus overt hypothyroidism. The fetal thyroid hormone levels in mild iodine deficiency status is close to normal levels because of maternal and placental compensation. Moreover, both the dam and the fetus suffer from the negative effects in moderate iodine deficiency during pregnancy.     

妊娠期大鼠不同程度碘缺乏对胎鼠碘代谢和甲状腺功能的影响

Objective To study the effects of iodine deficiency during pregnancy on fetal iodine metabolism and thyroid function. Methods Wistar dams were randomly divided into four groups: severe iodine deficiency(SID), moderate iodine deficiency(MoID), mild iodine deficiency(MiID) and normal iodine(NI). All the dams were fed with iodine deficient food(iodine contents: 50 μg/kg) and drinking water with different doses of KI (0,54.9,163.8,381.7 μg/L) for 3 months till mating. Iodine was supplied at the dose of 1.24 μg/d(SID), 2.50 μg/d(MoID), 5.00 μg/d(MiID) and 10.00 μg/d(NI), respectively. The dams and their fetuses on gestation of 20 days were studied. Urine iodine of dams and iodine contents in fetal amniotic fluid were measured by As3+-Ce4+catalytic spectrophotometry using ammonium persulfate digestion. And blood iodine in pregnant rats and iodine contents in placental tissue were measured by As3+-Ce4+catalytic spectrophotometry in dry ash of samples in KClO3-ZnSO4-K2CO3-NaCl. Thyroid hormone levels in mother serum and in fetal amniotic fluid were detected by chemiluminascent assay, and their thyroid glands were weighted and carefully observed. Results ①Iodine content in urine and blood of pregnant rats and amniotic fluid of fetal rats reduced along with their decrease of iodine supply. Urine iodine median of rats in 4 groups(NI: 353.7 μg/L; MiID: 115.9 μg/L; MoID: 26.9 μg/L; SID: 0 μg/L) were statistically significant(χ2=32.884, P < 0.01). Blood iodine level in MoID and SID[(29.4±18.6), (11.7± 7.0)μg/L]was significantly lower than that in NI[(49.1±23.0)μg/L, P < 0.05 or < 0.01]. In iodine deficiency groups, there was a decreasing trend in iodine contents of fetal amniotic fluid[MiID: (48.3±23.1)μg/L; MoID: (29.2±14.7)μ/L; SID:(19.5±6.7)μg/L]and an increasing tendency in iodine contents of placental tissue [MiID: (0.57±0.26)μg/g, MoID: (0.53±0.34)μg/g; SID: (0.53±0.15)μg/g], but there was no statistical significance(P>0.05). ②In SID, TT4[(14.3±4.1)nmol/L]and FT4[(10.8±3.6)pmol/L]were lower than that in NI[(28.4±19.3)nmol/L, (20.2±8.0)pmol/L, P < 0.05 or < 0.01], while that in MoID[(22.1±6.1)nmol/L, (18.5±4.1)pmol/L]and MiID[(25.5±13.1)nmol/L, (18.6±8.4)pmol/L]were decreased without statistical significance(P > 0.05). And FT3/FT4 ratio(0.34±0.16), absolute[(48.4±22.7)mg]and relative weights[(144± 76)mg/kg]of thyroid gland in pregnant rats were respectively higher than that in NI[0.16±0.02, (19.5±3.1)mg, (66±10)mg/kg, P<0.01]. But that in MoID[0.19±0.04, (27.0±5.7)mg, (84±19)mg/kg]and MiID[0.17± 0.06, (25.0±8.9)mg, (78±25)mg/kg]were increased without statistical significance(P > 0.05). A visibly congestive enlargement thyroid was found in SID, while thyroid mildly enlarged in MoID and MiID. ③Compared with NI [(2.38±1.55)pmol/L,0.50±0.18], the FT4 levels [(1.07±0.87) pmol/L]in amniotic fluid were significantly decreased (P < 0.05) and the FT3/FT4 ratio (1.96±0.61) was significantly increased (P < 0.01) in SID. There were no statistical significances(P > 0.05) in other 3 groups[MiID: (2.77±0.90)pmol/L,0.46±0.15; MoID: (2.35±0.76)pmoL/L,0.61±0.21]. A visible thyroid enlargement with hyperemia was observed in SID fetus while in other 2 experiment groups their thyroids were only mildly congested. Conclusions Severe iodine deficiency during pregnancy can result in both mother and fetus overt hypothyroidism. The fetal thyroid hormone levels in mild iodine deficiency status is close to normal levels because of maternal and placental compensation. Moreover, both the dam and the fetus suffer from the negative effects in moderate iodine deficiency during pregnancy.     

妊娠期大鼠不同程度碘缺乏对胎鼠碘代谢和甲状腺功能的影响

Objective To study the effects of iodine deficiency during pregnancy on fetal iodine metabolism and thyroid function. Methods Wistar dams were randomly divided into four groups: severe iodine deficiency(SID), moderate iodine deficiency(MoID), mild iodine deficiency(MiID) and normal iodine(NI). All the dams were fed with iodine deficient food(iodine contents: 50 μg/kg) and drinking water with different doses of KI (0,54.9,163.8,381.7 μg/L) for 3 months till mating. Iodine was supplied at the dose of 1.24 μg/d(SID), 2.50 μg/d(MoID), 5.00 μg/d(MiID) and 10.00 μg/d(NI), respectively. The dams and their fetuses on gestation of 20 days were studied. Urine iodine of dams and iodine contents in fetal amniotic fluid were measured by As3+-Ce4+catalytic spectrophotometry using ammonium persulfate digestion. And blood iodine in pregnant rats and iodine contents in placental tissue were measured by As3+-Ce4+catalytic spectrophotometry in dry ash of samples in KClO3-ZnSO4-K2CO3-NaCl. Thyroid hormone levels in mother serum and in fetal amniotic fluid were detected by chemiluminascent assay, and their thyroid glands were weighted and carefully observed. Results ①Iodine content in urine and blood of pregnant rats and amniotic fluid of fetal rats reduced along with their decrease of iodine supply. Urine iodine median of rats in 4 groups(NI: 353.7 μg/L; MiID: 115.9 μg/L; MoID: 26.9 μg/L; SID: 0 μg/L) were statistically significant(χ2=32.884, P < 0.01). Blood iodine level in MoID and SID[(29.4±18.6), (11.7± 7.0)μg/L]was significantly lower than that in NI[(49.1±23.0)μg/L, P < 0.05 or < 0.01]. In iodine deficiency groups, there was a decreasing trend in iodine contents of fetal amniotic fluid[MiID: (48.3±23.1)μg/L; MoID: (29.2±14.7)μ/L; SID:(19.5±6.7)μg/L]and an increasing tendency in iodine contents of placental tissue [MiID: (0.57±0.26)μg/g, MoID: (0.53±0.34)μg/g; SID: (0.53±0.15)μg/g], but there was no statistical significance(P>0.05). ②In SID, TT4[(14.3±4.1)nmol/L]and FT4[(10.8±3.6)pmol/L]were lower than that in NI[(28.4±19.3)nmol/L, (20.2±8.0)pmol/L, P < 0.05 or < 0.01], while that in MoID[(22.1±6.1)nmol/L, (18.5±4.1)pmol/L]and MiID[(25.5±13.1)nmol/L, (18.6±8.4)pmol/L]were decreased without statistical significance(P > 0.05). And FT3/FT4 ratio(0.34±0.16), absolute[(48.4±22.7)mg]and relative weights[(144± 76)mg/kg]of thyroid gland in pregnant rats were respectively higher than that in NI[0.16±0.02, (19.5±3.1)mg, (66±10)mg/kg, P<0.01]. But that in MoID[0.19±0.04, (27.0±5.7)mg, (84±19)mg/kg]and MiID[0.17± 0.06, (25.0±8.9)mg, (78±25)mg/kg]were increased without statistical significance(P > 0.05). A visibly congestive enlargement thyroid was found in SID, while thyroid mildly enlarged in MoID and MiID. ③Compared with NI [(2.38±1.55)pmol/L,0.50±0.18], the FT4 levels [(1.07±0.87) pmol/L]in amniotic fluid were significantly decreased (P < 0.05) and the FT3/FT4 ratio (1.96±0.61) was significantly increased (P < 0.01) in SID. There were no statistical significances(P > 0.05) in other 3 groups[MiID: (2.77±0.90)pmol/L,0.46±0.15; MoID: (2.35±0.76)pmoL/L,0.61±0.21]. A visible thyroid enlargement with hyperemia was observed in SID fetus while in other 2 experiment groups their thyroids were only mildly congested. Conclusions Severe iodine deficiency during pregnancy can result in both mother and fetus overt hypothyroidism. The fetal thyroid hormone levels in mild iodine deficiency status is close to normal levels because of maternal and placental compensation. Moreover, both the dam and the fetus suffer from the negative effects in moderate iodine deficiency during pregnancy.     

妊娠期大鼠不同程度碘缺乏对胎鼠碘代谢和甲状腺功能的影响

Objective To study the effects of iodine deficiency during pregnancy on fetal iodine metabolism and thyroid function. Methods Wistar dams were randomly divided into four groups: severe iodine deficiency(SID), moderate iodine deficiency(MoID), mild iodine deficiency(MiID) and normal iodine(NI). All the dams were fed with iodine deficient food(iodine contents: 50 μg/kg) and drinking water with different doses of KI (0,54.9,163.8,381.7 μg/L) for 3 months till mating. Iodine was supplied at the dose of 1.24 μg/d(SID), 2.50 μg/d(MoID), 5.00 μg/d(MiID) and 10.00 μg/d(NI), respectively. The dams and their fetuses on gestation of 20 days were studied. Urine iodine of dams and iodine contents in fetal amniotic fluid were measured by As3+-Ce4+catalytic spectrophotometry using ammonium persulfate digestion. And blood iodine in pregnant rats and iodine contents in placental tissue were measured by As3+-Ce4+catalytic spectrophotometry in dry ash of samples in KClO3-ZnSO4-K2CO3-NaCl. Thyroid hormone levels in mother serum and in fetal amniotic fluid were detected by chemiluminascent assay, and their thyroid glands were weighted and carefully observed. Results ①Iodine content in urine and blood of pregnant rats and amniotic fluid of fetal rats reduced along with their decrease of iodine supply. Urine iodine median of rats in 4 groups(NI: 353.7 μg/L; MiID: 115.9 μg/L; MoID: 26.9 μg/L; SID: 0 μg/L) were statistically significant(χ2=32.884, P < 0.01). Blood iodine level in MoID and SID[(29.4±18.6), (11.7± 7.0)μg/L]was significantly lower than that in NI[(49.1±23.0)μg/L, P < 0.05 or < 0.01]. In iodine deficiency groups, there was a decreasing trend in iodine contents of fetal amniotic fluid[MiID: (48.3±23.1)μg/L; MoID: (29.2±14.7)μ/L; SID:(19.5±6.7)μg/L]and an increasing tendency in iodine contents of placental tissue [MiID: (0.57±0.26)μg/g, MoID: (0.53±0.34)μg/g; SID: (0.53±0.15)μg/g], but there was no statistical significance(P>0.05). ②In SID, TT4[(14.3±4.1)nmol/L]and FT4[(10.8±3.6)pmol/L]were lower than that in NI[(28.4±19.3)nmol/L, (20.2±8.0)pmol/L, P < 0.05 or < 0.01], while that in MoID[(22.1±6.1)nmol/L, (18.5±4.1)pmol/L]and MiID[(25.5±13.1)nmol/L, (18.6±8.4)pmol/L]were decreased without statistical significance(P > 0.05). And FT3/FT4 ratio(0.34±0.16), absolute[(48.4±22.7)mg]and relative weights[(144± 76)mg/kg]of thyroid gland in pregnant rats were respectively higher than that in NI[0.16±0.02, (19.5±3.1)mg, (66±10)mg/kg, P<0.01]. But that in MoID[0.19±0.04, (27.0±5.7)mg, (84±19)mg/kg]and MiID[0.17± 0.06, (25.0±8.9)mg, (78±25)mg/kg]were increased without statistical significance(P > 0.05). A visibly congestive enlargement thyroid was found in SID, while thyroid mildly enlarged in MoID and MiID. ③Compared with NI [(2.38±1.55)pmol/L,0.50±0.18], the FT4 levels [(1.07±0.87) pmol/L]in amniotic fluid were significantly decreased (P < 0.05) and the FT3/FT4 ratio (1.96±0.61) was significantly increased (P < 0.01) in SID. There were no statistical significances(P > 0.05) in other 3 groups[MiID: (2.77±0.90)pmol/L,0.46±0.15; MoID: (2.35±0.76)pmoL/L,0.61±0.21]. A visible thyroid enlargement with hyperemia was observed in SID fetus while in other 2 experiment groups their thyroids were only mildly congested. Conclusions Severe iodine deficiency during pregnancy can result in both mother and fetus overt hypothyroidism. The fetal thyroid hormone levels in mild iodine deficiency status is close to normal levels because of maternal and placental compensation. Moreover, both the dam and the fetus suffer from the negative effects in moderate iodine deficiency during pregnancy.     

妊娠期大鼠不同程度碘缺乏对胎鼠碘代谢和甲状腺功能的影响

Objective To study the effects of iodine deficiency during pregnancy on fetal iodine metabolism and thyroid function. Methods Wistar dams were randomly divided into four groups: severe iodine deficiency(SID), moderate iodine deficiency(MoID), mild iodine deficiency(MiID) and normal iodine(NI). All the dams were fed with iodine deficient food(iodine contents: 50 μg/kg) and drinking water with different doses of KI (0,54.9,163.8,381.7 μg/L) for 3 months till mating. Iodine was supplied at the dose of 1.24 μg/d(SID), 2.50 μg/d(MoID), 5.00 μg/d(MiID) and 10.00 μg/d(NI), respectively. The dams and their fetuses on gestation of 20 days were studied. Urine iodine of dams and iodine contents in fetal amniotic fluid were measured by As3+-Ce4+catalytic spectrophotometry using ammonium persulfate digestion. And blood iodine in pregnant rats and iodine contents in placental tissue were measured by As3+-Ce4+catalytic spectrophotometry in dry ash of samples in KClO3-ZnSO4-K2CO3-NaCl. Thyroid hormone levels in mother serum and in fetal amniotic fluid were detected by chemiluminascent assay, and their thyroid glands were weighted and carefully observed. Results ①Iodine content in urine and blood of pregnant rats and amniotic fluid of fetal rats reduced along with their decrease of iodine supply. Urine iodine median of rats in 4 groups(NI: 353.7 μg/L; MiID: 115.9 μg/L; MoID: 26.9 μg/L; SID: 0 μg/L) were statistically significant(χ2=32.884, P < 0.01). Blood iodine level in MoID and SID[(29.4±18.6), (11.7± 7.0)μg/L]was significantly lower than that in NI[(49.1±23.0)μg/L, P < 0.05 or < 0.01]. In iodine deficiency groups, there was a decreasing trend in iodine contents of fetal amniotic fluid[MiID: (48.3±23.1)μg/L; MoID: (29.2±14.7)μ/L; SID:(19.5±6.7)μg/L]and an increasing tendency in iodine contents of placental tissue [MiID: (0.57±0.26)μg/g, MoID: (0.53±0.34)μg/g; SID: (0.53±0.15)μg/g], but there was no statistical significance(P>0.05). ②In SID, TT4[(14.3±4.1)nmol/L]and FT4[(10.8±3.6)pmol/L]were lower than that in NI[(28.4±19.3)nmol/L, (20.2±8.0)pmol/L, P < 0.05 or < 0.01], while that in MoID[(22.1±6.1)nmol/L, (18.5±4.1)pmol/L]and MiID[(25.5±13.1)nmol/L, (18.6±8.4)pmol/L]were decreased without statistical significance(P > 0.05). And FT3/FT4 ratio(0.34±0.16), absolute[(48.4±22.7)mg]and relative weights[(144± 76)mg/kg]of thyroid gland in pregnant rats were respectively higher than that in NI[0.16±0.02, (19.5±3.1)mg, (66±10)mg/kg, P<0.01]. But that in MoID[0.19±0.04, (27.0±5.7)mg, (84±19)mg/kg]and MiID[0.17± 0.06, (25.0±8.9)mg, (78±25)mg/kg]were increased without statistical significance(P > 0.05). A visibly congestive enlargement thyroid was found in SID, while thyroid mildly enlarged in MoID and MiID. ③Compared with NI [(2.38±1.55)pmol/L,0.50±0.18], the FT4 levels [(1.07±0.87) pmol/L]in amniotic fluid were significantly decreased (P < 0.05) and the FT3/FT4 ratio (1.96±0.61) was significantly increased (P < 0.01) in SID. There were no statistical significances(P > 0.05) in other 3 groups[MiID: (2.77±0.90)pmol/L,0.46±0.15; MoID: (2.35±0.76)pmoL/L,0.61±0.21]. A visible thyroid enlargement with hyperemia was observed in SID fetus while in other 2 experiment groups their thyroids were only mildly congested. Conclusions Severe iodine deficiency during pregnancy can result in both mother and fetus overt hypothyroidism. The fetal thyroid hormone levels in mild iodine deficiency status is close to normal levels because of maternal and placental compensation. Moreover, both the dam and the fetus suffer from the negative effects in moderate iodine deficiency during pregnancy.