Effects of high potassium iodate intake on iodine metabolism and antioxidant capacity in rats.

Background: KIO 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 (IO). As an oxidizing substance, IO 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 KIOin vivo.

Methods: The iodine metabolism processes in the thyroid and serum of rats after high KIO 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 IO were completely reduced to Iin 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 KIO. 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 KIO intake did not influence the TAA in serum and other tissues.

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