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.     

碘酸钾对大鼠肝脏抗氧化能力影响

目的 观察Wistar大鼠补充碘酸钾(KIO3)对肝脏抗氧化能力的影响.方法 将Wistar大鼠随机分为6组:低碘组(LI),适碘组(NI),5倍高碘组(5HI),10倍高碘组(10HI),50倍高碘组(50HI),100倍高碘组(100HI).喂养3、6和12个月后,检测肝组织匀浆中的谷胱甘肽过氧化酶(GPx)活性、超氧化物歧化酶(SOD)活性以及丙二醛(MDA)含量.结果 LI组GPx活性低于NI组(P<0.01),但SOD活性较NI组增高(P<0.05),MDA含量则较NI组增高(P<0.01).10HI组的SOD活性在6和12个月时增高(P<0.05),50HI和100HI组的SOD活性在3个月时较NI组显著增高(P<0.01),但在6和12个月时均较NI组显著降低(P<0.01).4个HI组的GPx活性和MDA含量与NI组差异均无统计学意义(P>0.05).结论 低碘导致大鼠肝脏抗氧化损伤;长期摄入高剂量碘酸钾未见对肝脏产生明显过氧化损伤,仅于10倍、50倍和100倍高碘组抗氧化酶活性降低.     

孕妇与婴幼儿碘需要量——世界卫生组织(WHO)技术顾问组拟定新的碘需要量和易感人群监测推荐标准

在2005年瑞士日内瓦召开的会议上,孕妇与婴幼儿碘需要量顾问组成员就几个重要问题达成共识:①全民食盐加碘(USI)仍然是消除碘缺乏病(IDD)的关键策略。②理论上讲,全民食盐加碘有效实施(即食盐充分碘化,人群覆盖范围超过90%)2年以上的地区,饮食提供的碘足以满足育龄、孕期和哺乳期妇女的生理需要,而且储存于甲状腺中的碘能充分保证甲状腺激素的合     

2007年贵州省从江县碘缺乏病健康教育效果评价

Objective To evaluate the effect of health education in controlling the iodine deficiency diserders(IDD) in order to provide reference data for the further prevention and control. Methods Each village of 3 towns in Congjiang County was selected in 2007, where the health education lasting for 10 months had been implemented in the school students of 3-6 grade and the villagers. The school students of 3-6 grade and 30 housewives in the villagers were investigated for their IDD control knowledge, the salt consuming conditions as well as the sales of both rough and fine salt at a salt retail site in each village before and after the health education was implemented. Results The awareness rate of the knowledge of IDD control in the students and housewives was 91.4% (581/636) and 78.3% (282/360), respectively after intervention, which significantly increased (χ2= 532.044, 326.117, both P < 0.01) compared with the rate of 28.2% (184/652) and 11.4% (41/360) before intervention. The proportion of consuming fine salt was 91.8%(146/159) and 95.6%(86/90), significantly inereased(χ2= 236.623, 135.350, both P < 0.01) compared with 6.1%(10/163) and 7.8% (7/90) found before intervention. The selling proportion of fine salt at the salt retail site in the village was 60.0%(900/1500), significantly increased(χ2= 824.176, P < 0.01) compared with 10.0%(150/1500) before intervention. Conclusions Health education and promotion is solid foundation for effectively controlling IDD, through which the students and villagers are actively and voluntarily involved in the program and hence have formed good living and hygiene habits, thus expected effect has been obtained.     

甲状腺激素转运体MCT8的病理生理作用

甲状腺激素(THs)进出细胞需要转运体蛋白的介导.单羧酸转运体(MCT)8是介导T3进入神经元的主要转运体蛋白,是迄今为止唯一具有明确的临床意义、在转运THs入脑中起着重要作用的转运体蛋白,其编码基因(SLC16A2)突变导致了艾伦-赫恩登-达得利综合征(AHDS),以严重的神经运动发育迟滞和高T3、低T4的血清学改变为临床特征.Mct8基因敲除的小鼠模型能够完全复制人MCT8基因突变的血清学改变,但神经症状轻微,部分解释了MCT8缺陷患者的临床表现,为THs转运体病理生理作用的研究提供依据.     

碘缺乏与碘过量对大鼠甲状腺抗氧化能力的影响

目的 观察Wistar大鼠补充不同剂量碘化钾(KI)对甲状腺抗氧化能力的影响.方法 将Wistar大鼠随机分为6组:低碘组(LI),适碘组(NI),5倍高碘组(5HI),10倍高碘组(10HI),50倍高碘组(50HI),100倍高碘组(100HI).每组20只.按每日进食量和饮水量计算的每日总碘摄入量分别为＜1、6.15、30.75、61.5、307.5、615μg/d.喂养6和12个月后,检测甲状腺组织匀浆中的谷胱甘肽过氧化物酶(GPx)活力、超氧化物歧化酶(SOD)活力以及丙二醛(MDA)含量.结果 LI组的GPx活力、SOD活力和MDA含量于摄碘6个月时,均较NI组显著增高,差异均有统计学意义(P＜0.01).5HI、10HI和50HI组的GPx活力和SOD活力在摄碘6个月和12个月时与NI组比较,差异均无统计学意义(P＞0.05);100HI组的GPx活力和SOD活力在6个月时较NI组增高(P＜0.05),但在12个月时较NI组降低,差异均有统计学意义(P＜0.05).在摄碘6个月时,100HI组的MDA含量较NI组有增高趋势(P＞0.05);但在12个月时50HI和100HI组的MDA含量均较NI组降低,差异均有统计学意义(P＜0.05);其他高碘组MDA含量均与NI组差异无统计学意义.结论 低碘导致大鼠甲状腺抗氧化系统失代偿,发生过氧化损伤;长期高碘(100HI)会使甲状腺抗氧化酶活力降低,但未出现明显过氧化损伤;大鼠甲状腺的抗氧化系统对高碘有很强的耐受能力.     

滋肾方和调心方对阿尔茨海默病模型大鼠疗效比较

目的:探讨调心方和滋肾方对阿尔茨海默病(Alzheimer's disease,AD)模型大鼠治疗机制及疗效比较。方法:持续注射D-半乳糖法致亚急性衰老大鼠模型,再用鹅膏蕈氨酸(ibotenic acid,IA)化学损毁大鼠双侧Meynert基底核。造模后,大鼠分为AD模型组、调心方组、滋肾方组、脑复康组。给药治疗前后以"Y"型电迷宫进行学习记忆观察,用分光光度法测定大鼠海马组织胆碱酯酶(cholinesterase,CHE)的活性,并与对照组比较。结果:调心方组大鼠学习能力提高(P<0.05),滋肾方组大鼠学习和记忆能力均提高(P<0.05或P<0.01),调心方组和滋肾方组大鼠海马组织中CHE活性较AD模型组均提高(P<0.01)。结论:调心方和滋肾方均可以提高AD模型大鼠学习记忆能力,其作用机制可能与大鼠海马组织中CHE活性改变有关。     

不同碘摄入水平对仔鼠大脑2型脱碘酶活力与髓鞘碱性蛋白和突触蛋白I表达的影响

目的 研究不同碘摄入水平对仔鼠大脑2型脱碘酶（D2）活力、髓鞘碱性蛋白（MBP）、突触蛋白I表达的影响。方法 将SPA—VAF级Wistar大鼠60只随机分为低碘组（LI组）、正常碘组（NI组）、5、10、50、100倍高碘组（HI组），每组10只，雌、雄各半。经饮水给予碘酸钾，使其每日总碘摄入量分别为1、6．15、30．75、61．5、307．5、615ug。喂养3个月后雌、雄交配，仔鼠在出生后28d处死，以竞争结合放射免疫分析（RIA）法测定血清甲状腺激素（TH），以强阳离子交换层析法测定大脑D2活力，以免疫组化方法检测MBP及突触蛋白I表达的变化。结果 与NI组比较，LI组各血清TH水平均显著降低，差异有统计学意义（P〈0．05，P〈0．01）；各HI组随着碘摄入量的增加各血清TH水平均呈降低趋势，其中TL、FL在615ug，d碘组降低，差异有统计学意义（P〈0．05）。LI组与各HI组的D2活力较NI组有升高的趋势，但均无统计学意义（P〉0．05）。与NI组比较，LI组和各HI组胼胝体MBP蛋白表达均减少，海马CA3区突触蛋白I表达均增多。结论 碘缺乏和重度碘过量（615ug/d碘组）仔鼠表现出甲状腺功能减退，碘缺乏引起的甲状腺功能减退程度和对髓鞘与突触发育的影响比碘过量更为严重。     

碘过量对哺乳期母鼠乳腺钠碘转运体mRNA和蛋白表达的影响

目的 观察碘过量对哺乳期母鼠乳腺钠碘转运体(sodium-iodide symporter,NIS)mRNA及蛋白表达的影响.方法 断乳1个月健康Wistar大鼠60只,雌雄比为2:1.将大鼠按体质量随机分为适碘组(30只)、10倍碘组(15只)、100倍碘组(15只),通过饮食(含碘300μg/ks)和饮水(含碘5、1845、20 295μg/L)摄碘.喂养3个月后交配产仔鼠,在哺乳第10天,采用砷铈催化分光光度法测定母鼠尿碘和乳汁碘.取母鼠乳腺,用反转录聚合酶链反应(RT-PCR)测定NIS mRNA表达;用SABC法进行免疫组化染色观察NIS蛋白表达强度.结果 ①母鼠尿碘:适碘组344.7μg/L、10倍碘组3597.5μg/L、100倍碘组25 404.3μg/L,10倍碘组和100倍碘组分别是适碘组的10.4倍和73.7倍.②母鼠乳汁碘:适碘组6.0×103μg/L、10倍碘组27.1×103μg/L、100倍碘组191.0×103μg/L,10倍碘组和100倍碘组分别是适碘组的4.5倍和31.8倍,母鼠乳汁碘增加倍数低于尿碘.③母鼠乳腺NIS表达:NIS raRNA表达组间比较差异有统计学意义(F=24.19,P＜0.01);其中适碘组(1.532±0.044)较10倍碘组(1.250±0.034)、100倍碘组(1.272±0.039)明显增高(P＜0.01),而且哺乳期母鼠乳腺N1S mRNA表达(1.532±0.044)高于非哺乳期母鼠(0.879±0.018),二者比较差异有统计学意义(t=19.09,P＜0.01);母鼠乳腺NIS蛋白表达强度随碘摄入量增加而减弱.结论 过量碘摄入可抑制乳腺NISmRNA和蛋白表达,限制乳汁中的含碘量随碘摄入量增加的幅度,此机制对下一代有着重要的保护作用.     

我国四地区正常孕妇的尿碘水平分析

Objective To analyze the median urinary iodine(MUI)level in normal pregnant women based on World HeMth Organization(WHO) recommended criterion,and to provide the MUI reference values for monitoring and evaluating iodine nutrition during pregnancy and related studies.Methods Total 604 normal pregnant and 192 non-pregnant women(as a comparison)were selected from a cross-sectional survey.These women were all healthy,iodine sufficient,with normal thyroid function,and negative anti-thyroid antibodies.The iodine content in drinking water,edible salt,and urine was determined by standard methods,and serum TSH,FT4,FT3,thyroid peroxidaseantibody(TPOAb),and thyroglobulin antibody(TgAb)were measured using chemiluminescent immunoassay.Resuits (1)The iodine in drinking water was 3.0μg/L indicating such small amount of iodine could be neglected for daily iodine intake.(2)All women consumed iodized salt with the median iodine in salt of 31.7 mg/kg.The daily iodine intake of at least 240 μg could be roughly estimated if an average of 10 g salt was taken per person per day and further subtracted by 20%iodine lost during cooking,which could meet the iodine needs during pregnancy.(3)The MUI of 173.1μg/L was calculated from 604 pregnant women having 174.5,167.0,and 180.7 μg/L during the first,second,and third trimesters,respectively,reaching the optimal level of 150-249 μg/L recommended by WHO for pregnant women.However,our data showed relatively lower levels,not reaching 200μg/L.The MUI of 240.2μg/L was calculated from 192 non-pregnant women,reaching the level of"above requirement"(200-299μg/L) recommended by WHO for adults.(4)All women were euthyroid and antibody-negative,but the TSH level in pregnant women was lower than that in non-pregnant women,in particular during the first trimester,while FT4 and FT3 were considerably decreased compared with the non-pregnant(with an exception of FT4 in the first trimester),and both gradually declined with the gestational age.Conclusions The optimal MUI level of 150-249 μg/,L recommended by WHO can be applied to pregnant Chinese women,but our data provided a relatively low range of 150-200μ/L throughout pregnancy.The higher MUI of 240.2μg/L in non-pregnant women indicated that iodized salt with different contents should be supplied on market to meet the requirement of different groups of population.