Xiuwei Li1, Xiaoxiao Cao2, Junyan Li3, Jing Xu1, Wei Ma1, Haiyan Wang1, Jianqiang Wang1, Ying Zhang1. 1. Key Laboratory of Trace Element Nutrition of National Health Commission of China, National Institute for Nutrition and Health, Chinese Center for Disease Control and Prevention, 27 Nanwei Road, Beijing 100050, China. 2. Key Laboratory of Trace Element Nutrition of National Health Commission of China, National Institute for Nutrition and Health, Chinese Center for Disease Control and Prevention, 27 Nanwei Road, Beijing 100050, China. Electronic address: caoxx@ninh.chiancdc.cn. 3. Animal Laboratory, National Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, 29 Nanwei Road, Beijing 100050, China.
Abstract
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 KIO3in 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 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.
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 KIO3in 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 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.