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机构地区:[1]重庆医科大学劳动与环境卫生学教研室,重庆400016
出 处:《环境与健康杂志》2010年第3期227-229,F0003,共4页Journal of Environment and Health
基 金:重庆医科大学创新基金资助项目(CX200308)
摘 要:目的研究五溴联苯醚(BDE-99)对大鼠甲状腺结构和功能的影响。方法将健康清洁级4周龄SD大鼠40只随机分为溶剂对照(玉米油)组和低(30mg/kg)、中(60mg/kg)和高(120mg/kg)剂量BDE-99染毒组,每组10只。采用灌胃方式进行染毒,染毒剂量为2.5ml/kg体重,连续染毒15d。采用放射免疫法测定游离三碘甲状腺原氨酸(FT3)、游离四碘甲状腺原氨酸(FT4)和促甲状腺素(TSH)的浓度。分别采用二氨基联苯胺(DAB法)和四唑氮(NBT)法对甲状腺过氧化物酶(thyroperoxidase,TPO)和琥珀酸脱氢酶(succinate dehydro-genase,SDH)的酶组织化学情况进行观察,并采用免疫组化检测和HE染色观察组织病理改变。电镜下观察甲状腺滤泡细胞超微结构改变。结果随着BDE-99染毒剂量的升高,血清FT4、FT3浓度呈降低趋势,而血清TSH浓度则呈升高趋势;甲状腺组织的TPO、SDH活力呈降低趋势,甲状腺组织的PCNA阳性细胞数则呈升高趋势。BDE-99染毒组TPO、SDH显色加深,电镜观察可见甲状腺滤泡细胞胞浆内有大量明显扩张呈囊状的粗面内质网,胞核、胞膜和线粒体未见损伤。结论 BDE-99有可能通过降低甲状腺球蛋白的合成水平而减低甲状腺激素的浓度,反馈性升高TSH浓度,从而导致腺体组织代偿性增生、细胞酶活力增高。Objective To observe the effects of pentabrominated diphenyl ether (BED-99) on the histological structure and function of the thyroid of rats. Methods Forty SPF, SD rats aged 4 weeks, were randomly divided into 4 groups according to the body weight, 10 in each group. The rats were treated with BED-99 at the doses of 30 mg/kg,60 mg/kg, 120 mg/kg,respeetively, through garage. The rats in the control group were received the equal volume of com oil. The levels of serum hormone were determined, the change of histopathology, histochemistry and follicular cells ultramicroscopic structure were observed at 15 days of exposure to BED-99. Results Serum levels of thyroxin (FT4), triiodothyronine (FT3), decreased gradually with dose increase at 15 days of exposure to BED-99.However,thyroid stimulating hormone (TSH) levels increased. The thyroid follicular epithelium hyperplasia was aggravated gradually with dose increase. Proliferating cell nuclear antigen (PCNA) positive cells increased constantly with dose increase. The activities of thyroperoxidase (TPO) and succinate dehydrogenase (SDH) of the treated rats increased significantly compared with the controls, and appeared color darkened. The rough endoplasmic retieulum of the thyroid follicular cells changed to saccate under the electron microscope,whereas nucleolus,cell membrane and mitochondria were not injured. Conclusion BDE-99 may damage the histological structure and function of the thyroid, the mechanism may be that BDE-99 down-regulates the thyroglobulin synthesis and then induces thyroxin level decrease which causes an increase of TSH through feedback.
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