Effects of high potassium iodate intake on iodine metabolism and antioxidant capacity in rats
Introduction
Iodine is a halogen and an essential micronutrient for the synthesis of thyroid hormone. Adequate iodine intake helps maintain stable thyroid hormone levels. Considering that much of the world is iodine-poor, the World Health Organization has proposed universal salt iodization (USI) to solve the public health issue of iodine deficiency. KIO3 and KI were recommended as salt iodization agent in iodine-deficient areas [1]. Coincidentally, iodine exists in natural drinking water in the form of iodate (IO3−) and iodide (I−), and IO3− is present in about 24 % of drinking water sources of water-borne iodine-excess areas in China where the concentration of iodine in water can even be up to 1000 μg/L [2]. IO3− from KIO3 salt is basically reduced to I− during cooking, where the form of IO3− is stable after boiling [3]. Thus, people living in areas with high levels of IO3− in drinking water are more likely to take high-dose IO3− directly.
As an oxidizing substance, IO3− should be reduced to I− before it can be effectively used by the thyroid. Some reports have demonstrated that the bioavailability of KIO3 in vivo was lower than that of KI [4], and the IO3− reduction process in vitro may increase oxidative damage to cell membrane [5]. In our preliminary study, IO3− could be reduced to I− by tissues with decreasing redox abilities in vitro [6]. It is therefore unknown, whether high doses of oral IO3− are completely reduced in vivo. Moreover, the mechanisms of the metabolic processes proceeding in the serum and thyroid after administration of enhanced doses of KIO3 have been studied less, and most related studies are based on intravenous administration of KIO3 rather than digestive tract feeding [[7], [8], [9]]. So, the aim of the present investigation was to evaluate the effects of high KIO3 intake via the digestive tract on the iodine metabolic processes and antioxidant capacity in vivo.
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Animals
In total, 128 female Wistar rats (specific pathogen-free) aged 6 weeks, weighing 140 ± 15 g were fed normally (iodine in the feed can meet the daily physiological needs of rats). The rats were purchased from Vital River Experimental Animal Technology Co. Ltd. (Beijing, China) (SCXK: 2016-0006; SYXK: 2017-00033). All experiments were performed in the Animal Laboratory of National Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention (SYXK:
Determination of IO3− and I− in serum and thyroid
The IO3− and I− in the thyroid and serum were detected using HPLC/ICP–MS after different doses of KIO3 gavage. However, only I− peaks were in the thyroid and serum at each time point in every group (Fig. 2). This indicated that IO3− was completely reduced to I− within 0.5 h in vivo, even when the rats were given 100 times the physiological daily dose of KIO3.
Effects of high KIO3 intake on iodine metabolism process in the serum and thyroid
Considering that blood is the circulating pool of iodine, and thyroid is the storage pool of iodine in vivo, the concentration changes of
Discussion
As previously noted, IO3− can be reduced to I− in vivo after the intravenous injection of high doses of KIO3 [9]. In our study, IO3− can also be totally reduced to I− after KIO3 intake by digestive tract within 0.5 h, even though the dose is up to 100 times the daily physiological requirement for KIO3. However, it is still not entirely clear what is the effect of high KIO3 intake on the iodine metabolism and redox capacity in vivo.
We first explored iodine metabolism in serum and thyroid.
Conclusion
High-dose KIO3 ingested through the digestive tract can be reduced and utilized in rats. During the metabolic process, the concentration of organic bound iodine in the serum was stable, which was rising in the thyroid. The levels of total iodine and I− in the serum or thyroid increased quickly, and then decreased after reaching the maximum absorption peak. Here, I− in the serum had two absorption processes and the thyroid blocking dose of I− was 0.5 mg/kg body weight in rat. Moreover, a
Author contributions
Xiaoxiao Cao designed the study, wrote the manuscript, carried out the detection of IO3− and I−. Xiuwei Li carried out detection of total iodine and the REDOX biomakers. Junyan Li carried out the animal experiments. Jing Xu and Wei Ma carried out all sample pretreatment works. Haiyan Wang and Jianqiang Wang assisted Junyan Li to carry out the animal experiments. Ying Zhang participated in the data statistics of this study. All authors read and approved the manuscript.
CRediT authorship contribution statement
Xiuwei Li: Methodology, Validation. Xiaoxiao Cao: Conceptualization, Methodology, Data curation, Writing - original draft, Writing - review & editing. Junyan Li: Resources, Validation. Jing Xu: Validation. Wei Ma: Validation. Haiyan Wang: Resources. Jianqiang Wang: Resources. Ying Zhang: Formal analysis.
Declaration of Competing Interest
The authors declare that there is no competing financial interests exist.
Acknowledgement
This work was supported by the National Natural Science Foundation of China (No. 81202156).
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