2008 - Effects of fluoride on thyroid function and cog. abil

2008 - Effects of fluoride on thyroid function and cog. abil

Postby admin » Sun Dec 22, 2013 9:40 am

51. 邱艳红; 高氟对甲状腺功能和认知能力的影响 (2008)
Effects of fluoride on thyroid function and cognitive abilities
http://d.wanfangdata.com.cn/Thesis_D051085.aspx\\

also:
http://d.wanfangdata.com.cn/Conference_6827134.aspx

目的:研究高氟致甲状腺损害后,对脑的影响具体观察高氟损害甲状腺致甲状腺功能低减后,甲状腺功能低减是否与高氟共同构成脑损害的因素,从而进一步探明氟中毒所致脑损害的发病机理,为更有效地开展氟中毒防治提供理论依据。 方法:将18只Wistar大鼠每组6只随机分为正常组A组高氟甲低组,B组高氟甲低替代组,C组A组饮用自来水,B组C组饮用含NaF100mg/l高氟水,7个月后,C组再予0.04%甲状腺片按1.8ml/kg/d 灌胃替代3周。放免法测定血清TT3TT4TSHHE染色观察甲状腺及海马形态结构,免疫组化方法检测各组海马CA1CA3区谷氨酸受体NMDAR2B亚单位表达的改变。 结果:1.血清TT3TT4TSH改变高氟甲低组,B组TT3TT4明显低于正常对照组P均<0.01,而TSH则呈现高于正常对照组之趋势高氟甲低替代组,C组TT3TT4和TSH均与正常对照组相近P皆>0.05。2HE染色显微镜观察。甲状腺改变,A组大鼠滤泡上皮结构正常排列有序滤胞无增生或萎缩,B组部分滤泡上皮增生数量及层次增加排列紊乱细胞呈柱状或高柱状可向滤泡腔突出,形成乳头部分滤泡萎缩数量减少排列稀疏大小不等部分,滤泡内胶质减少滤泡腔空虚红染均质物减少,C组与B组比较滤泡上皮增生程度明显减轻,滤泡无明显萎缩滤泡内胶质减少程度也明显减轻。2. 海马改变A组大鼠海马神经元细胞排列有序轮廓清晰结构和细胞形态正常细胞核深染尼氏体清楚可见,B组脑组织结构变疏松染色变浅细胞稀疏有水泡空泡形成海马神经元细胞肿胀明显神经元体积较正常增大细胞浆染色变浅细胞核体积较正常增大染色变浅尼氏体消失,其内可有大小不等圆形或类圆空泡神经元排列明显紊乱细胞层次结构,破坏极性消失少量神经元出现坏死结构模糊或破坏突起消失细胞浆染色加深细胞核结构模糊固缩碎裂坏死。C组海马神经元与B组比较脑组织水肿及神经元肿胀明显减轻神经元变性数量减少,神经元排列有序未见神经元坏死。3. NMDA受体亚单位NR2B免疫组化染色测量平均光密度,各组均取海马CA1CA3区进行观察,并测量NMDA受体亚单位NR2B平均光密度,NMDAR2B受体免疫组化,染色呈棕黄色,主要着色在胞膜及胞浆胞核不着色。高氟组NMDAR2B阳性细胞较较正常组和高氟甲低替代组明显减少,各组之间平均光密度均值以B组最高C组居中A组最低P均<0.01。 结论:1. 高氟可导致成年大鼠甲状腺损伤造成其功能低减,表现为甲状腺滤泡上皮增生滤泡萎缩滤泡内胶质减少血清TT3TT4下降和TSH升高。2. 高氟和甲低可导致成年大鼠脑损伤,主要损伤表现在与学习记忆有密切相关的海马区可致海马神经元肿胀变性排列紊乱甚至坏死。3. 高氟和甲低可导致海马CA1CA3区NMDAR2B受体表达减少,可能是高氟脑损伤认知障碍的重要病机。4. 在高氟损伤基础上给予甲状腺制剂替代后大鼠被损伤的甲状腺功能和形态可基本恢复正常在此基础上脑组织海马的损伤,也明显减轻海马CA1CA3区NMDAR2B受体表达虽较正常水平表达减少但较单纯高氟时明显增多,由此表明在慢性氟中毒所致脑损伤中,高氟不是导致脑损伤的唯一因素,高氟损伤所造成的甲状腺功能低减,是高氟所致脑损伤的另一重要参与因素,为此在氟中毒防治中注重甲低的纠正是重要的。
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Objective: To study the fluoride-induced thyroid damage, observe the effect on the brain's specific fluoride thyroid damage caused by low thyroid function, the thyroid function is low and high fluoride reduction factors together constitute the brain damage caused by fluorosis further proved pathogenesis of brain damage, provide a theoretical basis for a more effective implementation of fluoride poisoning prevention. Methods: 18 Wistar rats in each group were randomly divided into six groups A low-fluoride group A, group B hypothyroidism alternative fluoride in group C A group drinking tap water, drinking group with group B C NaF100mg / l fluoride water, seven months later, the group C 再予 0.04% thyroid tablets administered by 1.8ml/kg/d alternative three weeks. Radioimmunoassay of serum thyroid TT3TT4TSHHE staining and hippocampal morphology, immunohistochemistry was used to detect changes in all areas of glutamate receptors in hippocampus CA1CA3 NMDAR2B subunit expression. Results: 1 A low serum fluoride TT3TT4TSH change in group B TT3TT4 significantly lower than the control group, P <0.01, and TSH are showing higher than normal control group of high fluoride trend hypothyroidism alternative in group C TT3TT4 and TSH and the normal control group were similar to P were> 0.05. 2HE staining microscope. Thyroid changes A group of follicular epithelium of rats was normal orderly arrangement of follicular non-proliferation or atrophy, group B part of follicular epithelial hyperplasia increase the number and level of disordered columnar or columnar cells were available to highlight the follicular cavity formed nipple reduce the number of follicles to shrink parts of varying sizes arranged in sparse parts, reducing the follicular colloid follicular cavity empty red dye homogeneous material decrease in group C and group B significantly reduced follicular epithelial hyperplasia, follicular no significant atrophy filter minimize the bubble gum significantly reduced. 2 A change in hippocampal neurons in hippocampal cells arranged in an orderly outline a clear structure and morphology of normal nuclei stained Nissl bodies clearly visible, group B becomes loose organizational structure of the brain cells stained lighter sparse blisters vacuolization hippocampal neurons neuronal cell swelling significantly increased neuronal cytoplasm volume than normal nuclei stained lighter than normal volume increases shallow Nissl staining disappeared, may have different sizes of round or circular inner element vacuoles nerve cells arranged in distinct disorder hierarchy, destruction of a small amount of polar disappearance or destruction of neurons appear fuzzy protrusions disappeared deeper staining cytoplasm condensation nuclei fragmentation structure fuzzy necrosis necrosis structure. Group C hippocampal neurons compared with group B neurons in brain tissue edema and swelling decrease significantly reduce the number of neuronal degeneration of neurons arranged in an orderly and no neuronal necrosis. 3. NMDA receptor subunit NR2B immunohistochemical staining to measure the average optical density of each group were observed hippocampus CA1CA3 area and NMDA receptor subunit NR2B measuring optical density, NMDAR2B receptor immunohistochemical staining showed brown mainly in the membrane and cytoplasm nucleus coloring is not colored. Fluoride group than in the normal group and a low-fluoride alternative group NMDAR2B positive cells was significantly reduced, the average optical density between the groups in mean maximum Group C Group B Group A minimum centered P <0.01. Conclusion: a high fluoride can lead to damage caused by its adult rat thyroid function low cut, showing atrophy of follicular thyroid follicular epithelial hyperplasia follicular colloid reduce serum TSH TT3TT4 fall and rise. 2 and a low fluoride can cause brain injury in adult rats, the main injury manifested in learning and memory are closely related to the hippocampus can cause swelling and degeneration of hippocampal neurons derangement or necrosis. 3 and a low fluoride can cause NMDAR2B receptor expression in hippocampal CA1CA3 area decreased fluoride brain injury may be an important pathogenesis of cognitive impairment. 4. Give thyroid preparations on the basis of fluoride injury in rats after replacement thyroid function and morphology were injuries can damage normal recovered on the basis of the hippocampus of the brain, but also significantly reduced receptor expression in hippocampal CA1CA3 area NMDAR2B although more normal levels decreased expression but significantly increased when compared to pure fluoride, thus indicating that chronic brain injury caused by fluorosis, fluoride is not the only factor leading to brain damage, damage caused by fluoride low thyroid function, is caused by fluoride Another important factor involved in brain injury, for which focus on prevention and treatment of hypothyroidism fluorosis correction is important
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