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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 ,出现生物膜结构和功能的改变并进一步加重低碘的损伤作用
Objective To further reveal the pathogenesis of low-iodine goiter with free radicals and antioxidant theory. Methods The expression of superoxide dismutase (SOD) in the thyroid tissue of rats with low iodine at different stages was localized by immunohistochemistry and immunoelectron microscopy. The stereological indexes of thyroid follicular epithelial cells were measured by image processing. Results The SOD of thyroid tissue in normal rats was mainly located in the cytoplasm of thyroid follicular epithelial cells and often gathered in the rough endoplasmic reticulum, the cytoplasm of the top of follicular epithelial cells and the border of glial cavity of follicular cavity. Low iodine state, SOD distribution is extremely uneven, low iodine 4 months, most of the cell injury more obvious, SOD was negative reaction, only a few cells were positive; low iodine 6 months, cell injury was significantly increased, SOD content Reduce more. Conclusions Low iodine can reduce the activity of thyroid SOD, decrease the antioxidant capacity, increase the free radicals, change the structure and function of biofilm, and further aggravate the injury of low iodine