Background

KIO₃ and KI are the most common salt iodization agents. Coincidentally, iodine exists naturally in high-iodine drinking water in the form of iodide (I⁻) or iodate (IO₃⁻). As an oxidizing substance, IO₃⁻ should be reduced to I⁻ before it can be effectively used by the thyroid. However, there is a lack of systematic studies on the metabolic process of high dose KIO₃ in vivo.

Methods

The iodine metabolism processes in the thyroid and serum of rats after high KIO₃ intake were determined using high-performance liquid chromatography-inductively coupled plasma-mass spectrometry (HPLC/ICP–MS) and arsenic cerium catalytic spectrophotometry. The changes of redox activity in the serum, thyroid, liver, and kidneys were observed by detecting total antioxidative activity (TAA).

Results

High doses of IO₃⁻ were completely reduced to I⁻ in vivo within 0.5 h. The level of organic bound iodine in the serum was stable, while the organic bound iodine in the thyroid increased to a plateau after intake of high-dose KIO₃. The levels of total iodine and I⁻ in serum and thyroid increased quickly, then all decreased after reaching the maximum absorption peak, and I⁻ had two absorption peaks in serum. The thyroid blocking dose of I⁻ was 0.5 mg/kg in rat. Additionally, high KIO₃ intake did not influence the TAA in serum and other tissues.

Conclusion

The body is able to reduce and utilize high doses of KIO₃ ingested through the digestive tract. The metabolism of high KIO₃ in vivo is characterized by two absorption process of I⁻ in serum and the thyroid blocking effect. Moreover, a single intake of high-dose KIO₃ does not affect TAA in vivo. The results suggest that such excess IO₃⁻ may have be reduced in the digestive tract before I⁻ enters the blood.

中文翻译：

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高碘酸钾摄入对大鼠碘代谢和抗氧化能力的影响。

背景

KIO ₃和 KI 是最常见的食盐加碘剂。巧合的是，碘以碘化物（I ^-）或碘酸盐（IO ₃ ^-）的形式天然存在于高碘饮用水中。作为氧化性物质，IO ₃ ^-应还原为I ^-才能被甲状腺有效利用。然而，目前缺乏对高剂量KIO ₃ 体内代谢过程的系统研究。

方法

使用高效液相色谱-电感耦合等离子体质谱 (HPLC/ICP-MS) 和砷铈催化分光光度法测定高 KIO ₃摄入后大鼠甲状腺和血清中的碘代谢过程。通过检测总抗氧化活性（TAA）来观察血清、甲状腺、肝脏和肾脏中氧化还原活性的变化。

结果

高剂量的IO ₃ ^-全部被还原为我^- 在体内在0.5小时内。血清中有机结合碘水平稳定，而甲状腺中有机结合碘在摄入高剂量 KIO ₃后升高至平台期。血清和甲状腺中总碘和I ^-水平迅速升高，达到最大吸收峰后均下降，血清I ^-有两个吸收峰。I ^-的甲状腺阻断剂量在大鼠中为 0.5 mg/kg。此外，高 KIO ₃摄入量不会影响血清和其他组织中的 TAA。

结论

身体能够减少和利用通过消化道摄入的高剂量 KIO ₃。高KIO的代谢₃ 在体内的特征在于余两个吸收过程^-在血清和甲状腺阻滞作用。此外，单次摄入高剂量 KIO ₃不会影响体内TAA 。结果表明，这种过量的IO ₃ ^-可能在I ^- 进入血液之前在消化道中已经减少。