ZHOU Xuan , WU Feng-hong , ZHANG Rao , PENG Kai-liang . Effects of Ammonium Perchlorate on Iodine Uptake and Antioxidant Capacity of Thyroid[J]. Journal of Environmental and Occupational Medicine, 2011, 28(6): 347-350.
Citation: ZHOU Xuan , WU Feng-hong , ZHANG Rao , PENG Kai-liang . Effects of Ammonium Perchlorate on Iodine Uptake and Antioxidant Capacity of Thyroid[J]. Journal of Environmental and Occupational Medicine, 2011, 28(6): 347-350.

Effects of Ammonium Perchlorate on Iodine Uptake and Antioxidant Capacity of Thyroid

  • 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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