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机构地区:[1]天津医科大学组织学和胚胎学教研室,300070
出 处:《中华内分泌代谢杂志》2000年第2期112-114,共3页Chinese Journal of Endocrinology and Metabolism
摘 要:目的 以自由基及抗氧化理论进一步揭示低碘性甲状腺肿的发病机制。方法 采用免疫组织化学和免疫电镜技术对低碘不同时期大鼠甲状腺组织的超氧化物歧化酶 (SOD)进行定位 ,经图像处理技术测量了甲状腺滤泡上皮细胞的体视学指标。结果 正常大鼠甲状腺组织的SOD主要位于甲状腺滤泡上皮细胞的胞浆中 ,常聚集在粗面内质网、滤泡上皮细胞顶端胞质及微绒毛与滤泡腔胶质接壤区 ;而在低碘状态下 ,SOD分布极不均匀 ,低碘 4个月 ,大多数细胞损伤较明显 ,SOD呈阴性反应 ,只有少数细胞呈阳性反应 ;低碘 6个月 ,细胞损伤明显加重 ,SOD的含量更加减少。结论低碘造成甲状腺细胞SOD减少、抗氧化能力下降、自由基增多 。Objective To study the relationship between free radical and iodine deficiency by means of observing iodine deficiency, morphological damage and superoxide dismutase (SOD) in rat thyroid. Methods Immunohistochemical and immunoelectron microscopy techniques were performed to show the location of SOD and the ultrastructure of the epithelial cell of thyroid in rats with different iodine deficiency. Stereological parametes were obtained by image processing. Results SOD of thyroid in normal rats was located in the rough endoplasmicreticulum,theboundaryofmicrovilliandcolloid lumin, and cytoplasm of top of follicular epithelia. The thyroid of iodine deficiency showed the poor distribution of SOD. In the group of low iodine intake for 4 months (LI 4), many epithelial cells were obviously damaged, and the content of SOD was significantly lower. Only very few epithelial cells had a positive reaction of SOD. In the group of low iodine intake for 6 months, SOD was very poor and the structure was damaged seriously following the process of iodine deficiency. Conclusions Iodine deficiency induces the reduction of SOD, the increase of free radicals and damaging structure and function of membrane and results in the further aggravation of damage by iodine deficiency.
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