妊娠大鼠碘缺乏和甲状腺功能减退对仔鼠内嗅皮质cAMP反应元件结合蛋白表达的影响

目的观察碘缺乏和甲状腺功能减退损伤内嗅皮质对cAMP反应元件结合蛋白(cAMP response element-binding protein,CREB)蛋白表达的影响。方法将28只妊娠清洁级Wistar大鼠按体重随机分成对照组、碘缺乏组、甲状腺功能减退1、2组,每组7只。自妊娠第6天(GD6)起,碘缺乏组饲以缺碘地区粮食配制的饲料[碘含量为(14.11±1.96)ng/g],饮用自来水;甲状腺功能减退1、2组分别给予5和15mg/L丙基硫尿嘧啶(propylthiouracil,PTU)溶液作为饮用水,饲喂普通饲料[碘含量为(470.50±46.52)ng/g],直至仔鼠出生后第28天(PN28);对照组饮用自来水,饲喂普通饲料。分别于PN7、PN14、PN21、PN28和PN42时,每组随机取5只仔鼠,观察内嗅皮质CREB的表达。结果 PN7时,各组仔鼠内嗅皮质CREB表达水平间比较,差异无统计学意义。PN14和PN21时,甲状腺功能减退1组、2组和碘缺乏组仔鼠内嗅皮质CREB表达水平低于对照组,差异均有统计学意义(P0.05)。PN14时,甲状腺功能减退2组和碘缺乏组CREB表达水平低于甲状腺功能减退1组,差异均有统计学意义(P0.05)。PN28和PN42时,甲状腺功能减退2组和碘缺乏组仔鼠内嗅皮质CREB表达水平低于对照组,差异均有统计学意义(P0.05);PN28时,碘缺乏组仔鼠内嗅皮质CREB表达水平低于甲状腺功能减退1组,差异有统计学意义(P0.05)。与对照组比较,甲状腺功能减退1、2组和碘缺乏组内嗅皮质CREB染色强度明显降低。结论妊娠大鼠碘缺乏和甲状腺功能减退可降低仔鼠内嗅皮质CREB表达。     

妊娠大鼠碘缺乏和甲状腺功能减退对仔鼠内嗅皮质神经颗粒素表达的影响

目的研究碘缺乏和甲状腺功能减退损伤内嗅皮质对神经颗粒素(neurogranin,Ng/RC3)表达的影响。方法将28只妊娠清洁级Wistar大鼠按体重随机分成对照组、碘缺乏组、甲状腺功能减退1、2组,每组7只。自妊娠第6天(GD6)起,碘缺乏组饲以缺碘地区粮食配制的饲料[碘含量为(14.11±1.96)ng/g],饮用自来水;甲状腺功能减退1、2组分别给予5和15mg/L丙基硫尿嘧啶(propylthiouracil,PTU)溶液作为饮用水,饲喂普通饲料[碘含量为(470.50±46.52)ng/g],直至仔鼠出生后第28天(PN28);对照组饮用自来水,饲喂普通饲料。分别于PN7、PN14、PN21、PN28和PN42时,每组随机取5只仔鼠,观察内嗅皮质Ng的表达。结果 PN7时,各组仔鼠内嗅皮质Ng表达水平间比较,差异无统计学意义。PN14时,甲状腺功能减退2组和碘缺乏组仔鼠内嗅皮质Ng表达水平低于对照组和甲状腺功能减退1组,差异均有统计学意义(P0.05)。PN21,PN28和PN42时,甲状腺功能减退2组和碘缺乏组仔鼠内嗅皮质Ng表达水平低于对照组,差异均有统计学意义(P0.05);PN42时,甲状腺功能减退1组仔鼠内嗅皮质Ng表达水平亦低于对照组,差异有统计学意义(P0.05)。与对照组比较,甲状腺功能减退1、2组和碘缺乏组内嗅皮质Ng染色强度明显降低。结论妊娠大鼠碘缺乏和甲状腺功能减退可降低仔鼠内嗅皮质Ng的表达。     

碘缺乏和甲状腺功能减退对大鼠仔鼠海马ERK1/2表达的影响

目的观察碘缺乏和甲状腺功能减退对大鼠仔鼠海马细胞外信号调节蛋白激酶1及2(ERK1/2)表达的影响。方法健康2月龄孕Wistar大鼠28只,按体重随机分成对照组、甲状腺功能减退组[按饮水中含丙基硫尿嘧啶(PTU)剂量分为5mg/L组和15mg/L组]和碘缺乏组,每组7只。分别于出生后第7、14、21、28和42天每组随机取5只仔鼠,灌流固定大脑,用组织病理切片和免疫组化染色观察分析海马的ERK1/2表达。结果在出生后14、21、28和42天时,海马CA1和CA3区的ERK1/2表达在PTU5mg/L组、PTU15mg/L组和碘缺乏组显著低于对照组(P0.05)。DG区的ERK1/2表达与对照组相比差异无显著性。出生后7天时,各组间ERK1/2表达差异无显著性。结论碘缺乏和甲状腺功能减退可降低海马CA1和CA3区的ERK1/2表达。     

妊娠大鼠碘缺乏和甲状腺功能减退对仔鼠海马神经颗粒素表达的影响

目的观察妊娠大鼠碘缺乏和甲状腺功能减退对仔鼠海马神经颗粒素(neurogranin,Ng/RC3)表达的影响。方法将妊娠清洁级Wistar大鼠28只按体重随机分成对照组、碘缺乏组、甲状腺功能减退1、2组,每组7只。自妊娠第6天(GD6)起,碘缺乏组饲以缺碘地区粮食配制的饲料[碘含量为(14.11±1.96)ng/g],饮用自来水;甲状腺功能减退1、2组分别给予5和15mg/L丙基硫尿嘧啶(propylthiouracil,PTU)溶液作为饮用水,饲喂普通饲料[碘含量为(470.50±46.52)ng/g],直至仔鼠出生后第28天(PN28);对照组饮用自来水,饲喂普通饲料。分别于PN14、PN21、PN28和PN42时,每组随机取5只仔鼠,观察海马CA1、CA3和DG区Ng表达。结果在PN14时,碘缺乏组、甲状腺功能减退1、2组仔鼠海马CA1区Ng蛋白表达水平低于对照组,差异均有统计学意义(P0.05);在PN21时,碘缺乏组、甲状腺功能减退1、2组仔鼠海马CA1区以及碘缺乏组、甲状腺功能减退2组仔鼠海马CA3区Ng蛋白表达水平低于对照组,差异均有统计学意义(P0.05);在PN28时,碘缺乏组、甲状腺功能减退1、2组仔鼠海马CA3区以及碘缺乏组、甲状腺功能减退2组仔鼠海马CA1区Ng蛋白表达水平低于对照组,差异均有统计学意义(P0.05);在PN42时,碘缺乏组、甲状腺功能减退1、2组仔鼠海马CA3区和CA1区Ng蛋白表达水平低于对照组,差异均有统计学意义(P0.05)。结论妊娠大鼠碘缺乏和甲状腺功能减退可降低仔鼠海马CA1和CA3区Ng的表达。     

姜黄素对大鼠肺间质纤维化影响的机制研究

Objective To observe the possible mechanism and inhibitory effects of curcumin on pulmonary fibrosis induced bleomycin in rats at the fibrosing stage. Methods 80 male Sprague-Dawley rats were random divided into 4 groups (20 rats in each group). Rats in the fibrosis model group, the prednisone group and the curcumin group were induced by instilled bleomycin through tracheal, rats in the control group with same volume normal saline. Since the 15th day after bleomycin administration, the curcumin group and prednisone group were given curcumin (300 mg/kg) or prednisone (5mg/kg) per day by intragastric administration, respectively. The normal control group and the model group were given 1% sodium carboxymethyl cellulose ( 10ml/kg). Six rats of each group were random sacrificed on the 21st, 28th, 42nd and 56th days after bleomycin administration. The histological changes of the pulmonary were evaluated by H. E and Masson dyeing. The expressions of transforming growth factor-β1 (TGF-β1), platelet-derived growth factor (PDGF) and hydroxyproline in the tissue of pulmonary were assessed by immunohistochemistry and digestion method. Results Pulmonary fibrosis and hydroxyproline level in the curcumin group were obviously reduced as compared with the model group on the 42nd and 56th day[42 d:1. 28 ±0. 61 vs 2. 28 ±0. 39,P <0. 01 ;(1.73 ±0. 22)mg/g vs (2.50 ±0. 37) mg/g, P <0.01;56 d:1.00 ±0.59 vs 1.73 ±0.36, P< 0. 05; ( 1.57 ± 0. 36) mg/g vs (2. 20 ± 0. 42) mg/g, P < 0. 01 ], and it was also lower than that in prednisone group on the 42nd day( P < 0. 05 ). The expression of TGF-β1 and PDGF in the curcumin group were obviously lower than that in the model group on the 28th, 42nd and 56th day[28 d:TGF-β1 :3642. 05 ±839. 31 vs 5067. 35 ±738. 39, P <0. 05 ;PDGF:2957. 55 ±739. 16 vs 4457. 75 ±568. 39, P <0. 05;42 d: TGF-β1: 2689. 73 ± 529.22 vs 4089. 50 ± 619. 37, P < 0. 01; PDGF: 2834. 46 ± 567. 16 vs 3239. 52 ±628. 26, P <0. 01 ;56 d:TGF-β1: 1968.57 ±408. 36 vs 2968.20 ±498.42, P <0. 01 ;PDGF: 1083.36 ±381.35 vs 2019. 40 ±412. 36, P <0. 01 ], which was lower than that in prednisone group on the 42nd and 56th day (42 d,TGF-β1 :3529. 07 ±981.35,PDGF:2618. 34 ±813. 34;56 d,TGF-β1 :2530. 83 ±439. 37,PDGF: 1738. 35 ±536. 62, Pall <0. 05 ) , and it had no obvious difference compared with control group on the 56th day ( P > 0. 05 ). Conclusion Curcumin could alleviate bleomycin-induced pulmonary fibrosis in rats at the fibrosing stage by inhibiting the expressions of TGF-β1 and PDGF.     

妊娠大鼠碘缺乏和甲状腺功能减退对仔鼠海马脑源性神经营养因子表达的影响

目的观察妊娠大鼠碘缺乏和甲状腺功能减退对仔鼠海马脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)表达的影响。方法将妊娠清洁级Wistar大鼠28只按体重随机分成对照组、碘缺乏组、甲状腺功能减退1、2组,每组7只。自GD6起,碘缺乏组饲以缺碘地区粮食配制的饲料[碘含量为(14.11±1.96)ng/g],饮用自来水;甲状腺功能减退1、2组分别给予5和15mg/L丙基硫尿嘧啶(propylthiouracil,PTU)溶液作为饮用水,饲喂普通饲料[碘含量为(470.50±46.52)ng/g],直至仔鼠出生后第28天(PN28);对照组饮用自来水,饲喂普通饲料。分别于PN14、PN21、PN28和PN42时,每组随机取5只仔鼠,观察海马CA1、CA3和DG区BDNF表达。结果在PN14时,各组仔鼠海马CA1、CA3和DG区BDNF蛋白表达水平间比较,差异均无统计学意义。在PN21时,甲状腺功能减退2组和碘缺乏组仔鼠海马CA1、CA3和DG区BDNF蛋白表达水平低于对照组,差异均有统计学意义(P0.05);碘缺乏组仔鼠海马CA1区以及甲状腺功能减退2组和碘缺乏组仔鼠海马DG区BDNF蛋白水平低于甲状腺功能减退1组,差异均有统计学意义(P0.05)。在PN28时,甲状腺功能减退2组和碘缺乏组仔鼠海马CA1、CA3和DG区以及甲状腺功能减退1组仔鼠海马CA3区BDNF蛋白表达水平低于对照组,差异均有统计学意义(P0.05);甲状腺功能减退2组和碘缺乏组仔鼠海马CA1区BDNF蛋白表达水平低于甲状腺功能减退1组,差异均有统计学意义(P0.05)。在PN42时,甲状腺功能减退1、2组和碘缺乏组仔鼠海马CA1、CA3和DG区BDNF蛋白表达水平低于对照组,差异均有统计学意义(P0.05);甲状腺功能减退2组和碘缺乏组仔鼠海马CA1和DG区BDNF蛋白表达水平低于甲状腺功能减退1组,差异均有统计学意义(P0.05)。结论妊娠大鼠碘缺乏和甲状腺功能减退可降低仔鼠海马BDNF的表达。     

碘缺乏和甲状腺功能减退仔鼠海马CaMKⅡ表达的改变

目的观察多功能钙/钙调蛋白依赖性蛋白激酶Ⅱ(CaMKⅡ)在碘缺乏和甲状腺功能减退的大鼠仔鼠海马中蛋白表达的影响。方法健康2月龄雌性Wistar大鼠,交配妊娠后,取孕鼠28只,按体重随机分成对照组、甲状腺功能减退组和碘缺乏组,甲状腺功能减退组根据饮水中含丙基硫尿嘧啶(PTU)剂量分为5和15mg/L组,每组7只孕鼠。分别于出生后(PN)7、14、和21天时,每组随机取5只仔鼠,灌流固定大脑,进行组织病理切片和免疫组化染色,观察分析海马CaMKⅡ表达。结果对照组仔鼠海马CA1、CA3和DG区均呈强阳性染色,在神经元细胞胞浆内充满CaMKⅡ。5、15mg/L和碘缺乏组仔鼠海马免疫反应产物的分布与对照组一致,但与对照组相比染色强度逐渐降低。PN21和PN14时,仔鼠海马CA1、CA3和DG区平均积分光密度在碘缺乏组[PN21:(26.05±4.98)、(30.79±3.22)、(26.40±2.63);PN14:(25.48±4.87)、(44.17±5.91)、(26.41±3.01)]和15mg/L组[PN21:(17.02±2.68)、(24.57±6.62)、(20.18±4.05);PN14:(20.66±3.51)、(34.94±5.09)、(27.32±4.97)]明显低于对照组[PN21:(57.75±13.22)、(65.03±6.20)、(49.39±8.41),P0.05;PN14:(54.08±12.00)、(71.04±5.07)、(78.52±12.42),P0.05]。PN7时,碘缺乏组和15mg/L组仔鼠海马CA1区平均积分光密度在碘缺乏组(25.74±3.33)和15mg/L组(26.89±5.25)明显低于对照组(40.53±3.65),P0.05。结论碘缺乏和甲状腺功能减退可下调海马组织CaMKⅡ蛋白表达。     

地塞米松预处理对大鼠光气吸入性肺损伤基质金属蛋白酶-9表达的影响

Objective To investigate the effects of dexamethasone on expression of matrix metalloproteinase-9 (MMP-9) in rats with acute lung injury induced by phosgene. Methods The rats were randomly divided into 3 groups: normal control group that consists of the rats with air exposure, phosgene group that consists of the rats with phosgene exposure and dexamethasone group that consists of the rats with phosgene exposure after 2.5 mg/kg dexamethasone being injected. Wet and dry ratio of the lung (W/D) was calculated, and leukocyte count and total protein content of bronchoalveolar lavage fluid (BALF) were recorded at 2 h after exposure. The concentrations of MMP-9 in the serum and BALF were measured by enzyme-linked immunosorbent assay. The pathologic changes of lung tissues were observed under light microscopy. The immunohistochemistry and the RT-PCR were used to detect the contents of MMP-9 in the lung tissue. Results Compared with phosgene group, the lung W/D, protein content and WBC count in of BALF dexamethasone group was significantly decreased (P＜0.01). MMP-9 levels of the serum and BALF in dexamethasone group were (4.799±0.043) μg/L and (15.052±0.029) μg/L, respectively, which were significantly lower than those [(9.439±0.100) and (20.640±0.446) μg/L] in phosgene group (P＜0.01). Compared with phosgene group (2.789±0.282), the expression level(1.183±0.260) of lung M MP-9 mRNA in dexamethasone group was significantly lower than that in phosgene group (P＜0.01).Histological experimental results showed the marked hyperemia and thickening of alveolar wallsand stroma cells infiltrating and more visible alveolar structure damage of alveolar walls in phosgene group while the alveolar structure and the alveolar walls were clear and slightly thickened with inflammatory cells in dexamethasone group. Immunohistochemical results showed that MMP-9 protein expression levels of lung and brochus tissues in normal control group and dexamethasone group were weakly positive, which in phosgene group were strongly positive. Conclusion Dexamethasone has a beneficial effects on acute lung injury induced by phosgene in rats due to the inhibiting MMP-9.     

过氯酸铵对大鼠甲状腺功能及其球蛋白和过氧化物酶mRNA表达的影响

目的 研究过氯酸铵(AP)对大鼠甲状腺功能及甲状腺球蛋白(Tg)、甲状腺过氧化物酶(TPO)基因mRNA表达的影响.方法 将雄性SD大鼠30只随机分为:正常对照组、低碘组(含碘量:50μg/kg)、AP染毒低(130 mg/kg)、中(260 mg/kg)、高剂量组(520 mg/kg)及AP+高碘组[AP:520 mg/kg,高碘饮水(10 mg/L)],每组5只.经口染毒90 d后处死,放射免疫法测定血清游离三碘甲状腺原氨酸(FT3)、游离甲状腺素(FT4)及促甲状腺激素(TSH)的水平;荧光定量PCR法测定甲状腺球蛋白(Tg)、甲状腺过氧化物酶(TPO)基因mRNA表达水平.结果 AP中剂量和AP高剂量组FT4水平[(9.540±1.327)fmol/ml,(6.509±1.949)fmol/ml)明显低于正常对照组[(13.505±1.276)fmol/ml],差异有统计学意义(P＜0.05,P＜0.01).AP高剂量组的TSH水平[(1.227±0.295)mIU/L]明显高于正常对照组[(0.545±0.282)mIU/L],差异有统计学意义(P＜0.05);各AP剂量组Tg的mRNA表达相对值均明显低于正常对照组,差异有统计学意义(P＜0.01),AP高剂量组TPO基因mRNA表达相对值明显低于正常对照组,差异有统计学意义(P＜0.05).结论 AP可降低大鼠FT3、FT4水平,引起TSH反馈性增高,并明显抑制Tg和TPO基因mRNA的表达;而高碘可以在一定程度上拮抗AP对大鼠甲状腺的毒作用.

Abstract：

Objective To investigate the effects of ammonium perchlorate (AP) on thyroid functions and mRNA expression levels of thyroglobulin(Tg) and thyroperoxidase (TPO) genes of rats. Methods Thirty SD male rats were randomly divided into six groups: control group, iodine-deficient group, low dose AP group ( 130 mg/kg), moderate dose AP group (260 mg/kg), high dose AP group (520 mg/kg) and high iodinecombined group. After the rats were exposed orally for 90 days, serum free-thyroxine (FT4), freetriiodothyronine (FT3) and thyroid stimulating hormone (TSH) were measured using radioimmunoassays.mRNA expression levels of thyroglobulin (Tg) and thyroperoxidase (TPO) genes were detected by real-time quantitative PCR. Results Serum FT4 levels in moderate dose AP group and high dose AP group were [(9.540±1.327) fmol/ml] and [(6.509±1.949) fmol/ml] respectively, which were significantly lower than that [ (13.505 ±1.276 ) fmol/ml] in control group (P＜0.05 or P＜0.01). Serum TSH level in high dose AP group was [(1.227±0.295) mIU/L], which was significantly higher than that [(0.545±0.282) mIU/L] in control group (P＜0.05). The mRNA expression levels of thyroglobulin (Tg)gene in all groups exposed to AP were significantly lower than that in control group (P＜0.01). The mRNA expression level of thyroperoxidase (TPO)gene in high dose AP group was significantly higher than that in control group (P＜0.05). Conclusion AP can reduce the serum FT3 and FT4levels of rats, increase the serum TSH level of rats and decrease obviously the mRNA expression levels of Tg and TPO genes. In addition, high iodine can reduce the toxic effects of AP on thyroid gland of rats to some extent.     

碘缺乏对大鼠仔鼠小脑c-fos和c-jun蛋白表达的影响

目的研究碘缺乏对大鼠仔鼠小脑c-fos和c-jun蛋白表达的影响.方法选择健康Wistar大鼠30只(雌性20只,雄性10只),将雌鼠随机分成碘缺乏组及对照组,每组10只.碘缺乏组大鼠于合笼前1周开始喂饲低碘饲料(含碘20～40 ng/g),饮去离子水,直至仔鼠生后30 d;对照组大鼠喂饲标准饲料(含碘145～186 ng/g),饮自来水.取生后第20、30、60天仔鼠,测定体重、血清中游离三碘甲状腺原氨酸(FT3)和游离四碘甲状腺原氨酸(FT4)水平,并取小脑组织进行免疫组织化学链霉菌抗生物素蛋白-过氧化物酶(SP)染色,用图像分析方法分析大鼠仔鼠小脑皮质c-fos和c-jun蛋白表达情况.结果碘缺乏组仔鼠生后第20、30、60天时,体重均低于对照组(均P＜0.01),血清T3、T4水平均低于对照组(均P＜0.01),小脑组织c-fos和c-jun染色强度均低于对照组(均P＜0.05),总积分光密度值均低于对照组(均P＜0.05).结论碘缺乏可降低大鼠仔鼠小脑组织c-fos和c-jun蛋白表达,影响神经系统的发育.     

Cognitive and motor functions of iodine-deficient but euthyroid children in Bangladesh do not benefit from iodized poppy seed oil (Lipiodol)

Iodine supplementation before pregnancy in iodine-deficient women prevents cretinism and neuromotor deficits in their offspring. It is unclear whether iodine supplementation benefits cognitive function in iodine-deficient school-aged children. We therefore conducted a double-blind, randomized, controlled trial of the effects of iodized poppy seed oil (Lipiodol) on cognitive and motor function and weight gain of iodine-deficient school children. The study was conducted with 305 children in grades 1 and 2 from 10 primary schools in two iodine-deficient areas in Bangladesh. The children were stratified by school and grade and randomly assigned to receive 400 mg of oral Lipiodol or a placebo. All children were given a battery of cognitive and motor function tests and had their weights, serum thyroxine (T4) and thyroid-stimulating hormone (TSH) and urinary iodine levels measured before and 4 mo after the intervention. On enrollment, both groups were moderately iodine deficient (median urinary iodine values: placebo group = 3.3 micromol/L, n = 148; iodine group = 3.1 micromol/L, n = 152; goiter prevalence in both groups >95%). However, their T4 and TSH levels were within the normal range. After 4 mo, there was a significant treatment effect on urinary iodine levels (P < 0.0001), but the levels of the treated group were still below normal (median = 7.9 micromol/L). No significant differences were found in T4 and TSH levels, weight gain, cognitive or motor function. The findings suggest that Lipiodol supplementation in moderately iodine-deficient children with normal T4 levels is unlikely to benefit their cognitive function. However, it remains possible that other iodine preparations may have benefits.     

Iodine deficiency mitigates growth retardation and osteopenia in selenium-deficient rats

Selenium deficiency is associated with impaired bone metabolism and osteopenia in rats. However, it is not known how combined selenium and iodine deficiency affects bone metabolism. Therefore, we investigated the effect of selenium and iodine deficiency on bone metabolism in 2nd-generation selenium- and iodine-deficient rats. Selenium-deficient (Se-), iodine-deficient (I-), selenium- and iodine-deficient (Se-/I-), and control rats (Se+/I+), were pair-fed their respective diets until they were 74 d old. Each pair-fed rat was fed a selenium-adequate diet in the same amount as that consumed the day before by its selenium-deficient counterpart, taking food spillage into account. The skeletal phenotype was analyzed by dual energy X-ray absorptiometry, histomorphometry, and bone metabolism markers. Erythrocyte glutathione peroxidase activity (Gpx) and plasma thyroid hormones were measured to assess selenium and iodine status, respectively. In both Se-/I+ and Se-/I- rats, Gpx was reduced by 99% compared with pair-fed Se+/I+ and Se+/I- rats (P < 0.001). Iodine deficiency reduced plasma thyroxine by 64% in the 2 iodine-deficient groups (P < 0.001). Body weight, tail length, plasma insulin-like growth factor, pituitary growth hormone concentration, and femur and tibia bone mineral density were significantly greater in the Se-/I- rats than in the Se-/I+ rats. This study shows that iodine deficiency mitigated growth retardation and osteopenia in 2nd-generation selenium-deficient rats and suggests that adequate selenium status should be ensured before measures are taken to correct iodine deficiency.     

Iodine Supplementation in Pregnancy in an Iodine-Deficient Region: A Cross-Sectional Survey

Iodine deficiency is a common problem in pregnant women and may have implications for maternal and child health. Iodine supplementation during pregnancy has been recommended by several scientific societies. We undertook a cross-sectional survey to assess the efficacy of these recommendations in a European iodine-deficient region. Urinary iodine concentrations (UIC) were determined in pregnant women before (n = 203) and after (n = 136) the implementation of guidelines for iodine supplementation in pregnancy. Iodine supplementation (200 μg/day) reduced the proportion of pregnant women with severe iodine deficiency (37.4% to 18.0%, p = 0.0002). The median UIC increased from 67.6 µg/L to 106.8 µg/L but remained below the recommended target level (>150 µg/L) for pregnant women. In conclusion, iodine supplementation in pregnant women improved iodine status in this iodine-deficient region but was insufficient to achieve recommended iodine levels in pregnancy. Additional measures, such as the adjustment of the dose or timing of supplementation, or universal salt iodization, may be needed.     

孕妇缺碘对婴儿智能的影响

报道了孕妇碘缺乏病（ＩＤＤ）于妊娠早期补碘成不补碘对其所生婴儿智能发育的影响。根据尿碘、血清促甲状腺激素（ＴＳＨ）值、Ｔ４值、甲状腺肿等指标诊断，缺碘孕妇于初孕１～４个月补碘一次（碘油丸含碘４００ｍｇ／丸为Ｃ组），另设缺碘不补碘组（Ｂ组）和正常对照组（Ａ组）。跟踪孕妇，产后每月测婴儿身长、体重、智能（采用ＣＤＣＣ测试法）。结果证明补碘孕妇所生婴儿的身长、体重、智能均高于缺碘对照组（Ｐ＜０．０１或０．０５），并发现母亲缺碘其婴儿智力发育明显迟缓。孕妇缺碘如能早期补碘可预防新生儿的智力发育不良。     

硒对小鼠高碘性氧化损伤的干预作用研究

目的:研究高碘性甲状腺肿形成的机制并寻求合适的硒干预剂量。方法:140只Balb/c小鼠分为7组:正常组、高碘组(饮水含碘3000μg/L)和5个补硒组(饮水含碘3000μg/L,硒分别为0.1、0.2、0.3、0.4、0.5mg/L),共喂养16w。放射免疫法测定甲状腺激素水平,测定血浆、肝脏、肾脏和甲状腺组织谷胱甘肽过氧化物酶(GSH-Px)和超氧化物歧化酶(SOD)活性,丙二醛(MDA)水平。结果:高碘组GSH-Px、SOD活性下降,MDA含量升高,而经饮水补充0.2~0.3mg/L硒组各项指标与正常组无显著性差异。结论:高碘会导致小鼠抗氧化能力下降,而经饮水补充0.2~0.3mg/L硒是有效的干预剂量。     

不同地区饮用水碘水平居民碘营养状况调查研究

目的:研究不同外环境碘水平地区人群碘营养状况,探讨高碘地区停供碘盐及"适碘"地区的水碘切点值,为制定预防策略提供依据。方法:沿黄河下游山东段选择不同地理位置的调查点13个,根据水碘含量分将其为0～(A)、50～(B)、100～(C)、150～(D)、300～(E)和800～μg/L(F)6个组,检测居民户饮用水和食盐碘含量,并对6～61岁居民进行尿碘测定和甲状腺肿大检查。结果:6个组的水碘中位数分别为20.3、91.4、143.2、203.6、341.9和812.3μg/L,盐碘中位数为0、25.7、25.8、30.4、36.4和33.0mg/kg,尿碘中位数为116.8、354.2、400.4、607.9、881.3和1213.8μg/L,甲状腺肿大率为10.8、8.6、15.0、14.2、14.9和25.0%。尿碘<100μg/L的样本占8.2%、100～300μg/L的占18.2%、>300μg/L的占73.6%。水碘>90μg/L的5组的尿碘频数分布都明显向高值偏移,其尿碘>300μg/L的比例随着水碘的升高而逐渐增加。水碘与尿碘的相关系数为0.449。水碘与尿碘和甲状腺肿大率均呈正相关,尿碘和甲状腺肿大率随水碘含量增加而升高,高碘地区明显高于低碘和"适碘"地区。结论:水碘20μg/L的地区须供应合格碘盐以使多数居民的碘营养水平适宜,而水碘在90μg/L以上地区居民的碘营养明显过量。建议:停供USI的水碘切点值为90μg/L,水碘在20～90μg/L之间的地区可暂界定为适碘地区。     

Iodine supplementation improves cognition in iodine-deficient schoolchildren in Albania: a randomized, controlled, double-blind study

BACKGROUND: Iodine is required for the production of thyroid hormones, which are necessary for normal brain development and cognition. Although several randomized trials examined the effect of iodine supplementation on cognitive performance in schoolchildren, the results were equivocal. OBJECTIVE: We aimed to ascertain whether providing iodized oil to iodine-deficient children would affect their cognitive and motor performance. DESIGN: In a double-blind intervention trial, 10-12-y-old children (n = 310) in primary schools in rural southeastern Albania were randomly assigned to receive 400 mg I (as oral iodized oil) or placebo. We measured urinary iodine (UI), thyroid-stimulating hormone (TSH), and total thyroxine (TT4) concentrations and thyroid gland volume (by ultrasound). The children were given a battery of 7 cognitive and motor tests, which included measures of information processing, working memory, visual problem solving, visual search, and fine motor skills. Thyroid ultrasound and the biochemical and psychological tests were repeated after 24 wk. RESULTS: At baseline, the children's median UI concentration was 43 microg/L; 87% were goitrous, and nearly one-third had low concentrations of circulating TT4. Treatment with iodine markedly improved iodine and thyroid status: at 24 wk, median UI in the treated group was 172 microg/L, mean TT4 was approximately 40% higher, and the prevalence of hypothyroxinemia was < 1%. In the placebo group after the intervention, these variables did not differ significantly from baseline. Compared with placebo, iodine treatment significantly improved performance on 4 of 7 tests: rapid target marking, symbol search, rapid object naming, and Raven's Coloured Progressive Matrices (P < 0.0001). CONCLUSION: Information processing, fine motor skills, and visual problem solving are improved by iodine repletion in moderately iodine-deficient schoolchildren.