过氯酸铵对甲状腺摄碘与抗氧化能力的影响
Effects of Ammonium Perchlorate on Iodine Uptake and Antioxidant Capacity of Thyroid
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摘要:
目的 探讨过氯酸铵(AP)对大鼠甲状腺摄碘和抗氧化能力的影响。阐述AP对甲状腺的毒作用机理,为预防和控制其职业危害提供科学依据。 方法 将20只SD雄性大鼠随机分为AP低(130 mg/kg)、中(260 mg/kg)、高(520 mg/kg)剂量组以及对照组(0 mg/kg),每组5只,染毒13周后,检测血清中甲状腺激素、甲状腺摄碘(131I)率、钠碘转运体(NIS)mRNA表达、甲状腺组织丙二醛(MDA)和超氧化物歧化酶(SOD)等指标,并观察甲状腺超微结构。 结果 与对照组相比, AP各剂量组血清中游离甲状腺素(FT4)均明显降低(P<0.01);高剂量促甲状腺激素(TSH)明显性高于对照组,差异有统计学意义(P<0.01);各剂量组甲状腺摄131I率均明显低于对照组(P<0.01);高剂量NIS mRNA表达高于对照组,差异有统计学意义(P<0.05); AP中、高剂量组MDA含量明显高于对照组(P<0.01);各剂量组SOD活力也均比对照组明显升高(P<0.05)。电镜观察显示,各剂量组甲状腺滤泡腔变小,基底膜增厚,滤泡上皮细胞中的线粒体和内质网严重肿胀或扩张。 结论 AP可抑制甲状腺摄碘,以致甲状腺激素水平改变,并使NIS mRNA表达代偿性增高。AP可对甲状腺产生氧化损伤,超微病理表现为上皮细胞中的线粒体和内质网明显变化。 Abstract:Objective To explore the effect of ammonium perchlorate (AP) on iodine uptake and antioxidant capacity of thyroid and to explain thyroid toxicity mechanism of AP, providing a scientific basis for possible thyroid relatedhealth issues prevention among AP exposed workers. Methods Twenty SD male rats were randomly divided into three AP treated groups and a control group with five rats in each group. The three AP treated groups were exposed to AP at the dosage of 130mg/kg (low), 260mg/kg (moderate) and 520 mg/kg (high). The rats were exposed to AP by an intragastric administration for 13 weeks. Thyroid hormones concentrations in serum, thyroid radioiodine uptake rate, the expressions of sodium iodide sympoter (NIS)mRNA, the contents of malondialdehyde (MDA)and the activities of super oxide dimutese (SOD)in thyroid were tested. The alteration of thyroidal ultrastructure was also observed. Results Compared with the control group, serum free thyroxine (FT4) level of each treated group was significantly deceased (P<0.01). The thyrotropin (TSH)level in the high dose group was significantly increased (P<0.01). The thyroid radioiodine uptake rate of each treated group was significantly depressed (P < 0.01). The expression of NIS mRNA in the high dose group was significantly increased (P < 0.01). The contents of MDA in the moderate and high dose groups were significantly increased (P < 0.01), while the activities of SOD in all treated groups were significantly increased (P<0.05). The ultrastructural images of thyroid in all treated groups showed shrunk follicular lumen, thicken basement membrane, mitochondrion and endoplasmic reticulum swelling and extension severely in the epithelial cells. Conclusion AP could inhibit thyroid iodine uptake and altered thyroid hormone homeostasis, which le ad to a expression increasing of NIS mRNA as a result of compensation. AP could induce oxidative damage in thyroid indicated by obvious swelling and extension of mitochondrion and endoplasmic reticulum in epithelial cells in ultrastructural images.
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