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

Abstract

BackgroundKIO3 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 KIO3in vivo. MethodsThe 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). ResultsHigh 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. ConclusionThe body is able to reduce and utilize high doses of KIO3 ingested through the digestive tract. The metabolism of high KIO3in 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.