Effect Of Ammonium Perchlorate On Iodine Load And Antioxidant Capacity In Rats

Objective Ammonium Perchlorate （AP） is a kind of white crystalline powder, and isa solid constituent for missile and rockets. It is widely used in aerospace and defenseindustries. In the insustrial production and process of using, the dust of AP could show apotential risk to human body through several different approaches. Studies have found thatAP can alter the structure of thyroid gland and disturb the normal function of thyroid inanimal. Our previous studies have also found that AP can affect the secretion of secretion ofthyroid hormone and the expression of sodium iodide symporter in rats. In this study, weexplored the effect of AP on iodine load and antioxidant capacity, explained the toxicitymechanism of AP on thyroid gland. This could provide some scientific bases for theprevention and controlling from thyroid gland health risks in the occupational groupsexposed to AP.Methods Twenty four SD male rats were randomly divided into three AP treatedgroups and a control group. Rats in AP treated groups were exposed to AP at the dosage of130mg·kg^-1·d^-1（low）,260mg·kg^-1·d^-1（moderate） and520mg·kg^-1·d^-1（high）,（n=6）respectively. The treatments were conducted every day by intragastric administration for13weeks based on the body weight which was weighed once a week. The levels of rat urinaryiodine were detected by manual spectrophotometric measurement of Sandell-Kolthoffreduction in6thweek and13thweek; and after13weeks, rats were sacrificed and dissected.Thyroid gland, heart, liver, spleen, lung, kidney and testis were moved immediately and weighed, and organ coefficient was calculated. Thyroid gland was dissociated to test the totaliodine in thyroid tissue, the iodine relative and the amount of thyroid tissue protein. Takepart of the thyroid gland to test the contents of malondialdehyde （MDA）, and the activities ofsuperoxide dismutase （SOD） and catalase （CAT）.Results Compared with controls,13weeks treatment with low dose （130mg/kg b.wt）of AP did not result in any changes in body weight, but a significant decrease in body weightwas observed in high and moderate（520,260mg/kg b.wt） dose of AP group（P<0.05）. Organcoefficient of each treated group rats were significantly increased（P<0.01）. Compared withthe control group, in the6thweek, urinary iodine levels in high-dose group were significantlyincreased （P <0.05）, in the13thweek the dose of urinary iodine levels were not significantlydifferent（P>0.05）. Compared with the control group, the total iodine and the iodine relativein thyroid tissue of each treated group were significantly decreased （P <0.01）. Comparedwith the control group, the total protein levels in high dose group were significantlydecreased （P <0.05）. Compared with the control group, the contents of MDA and SODactivity in each treated group showed no significant difference. Compared with the controlgroup, the TPO activity was significantly increased in high-dose group （P <0.01）.Conclusion This study showed that AP had a toxic role in SD rats. The target organof AP is thyroid. AP could inhibit thyroid iodine uptake, and increased the urinary iodine andreduce the iodine in thyroid tissue within a certain period of time. AP induced thyroidenlargement and hyperplasia with body weight growth retardation. In addition, AP coulddecrease the protein levels in thyroid. AP could induce oxidative damage in thyroid andincrease the activity of thyroid peroxide. In conclusion, these results show that AP hasobvious toxicity on thyroid and showed the same results of previous studies. It also providesa reliable experimental evidence for the health hazards of AP.