Protective effect of KI in mtDNA in porcine thyroid: comparison with KIO(3) and nDNA

PURPOSE: Iodine, bivalent iron (Fe(2+)), and hydrogen peroxide (H(2)O(2)), all significantly affecting the red-ox balance, are required for thyroid hormone synthesis. Intracellular iodine excess (≥10(−3) M) transiently blocks thyroid hormonogenesis (an adaptive mechanism called Wolff–Chaikoff effect). The aim of the study was to evaluate the effects of iodine, used as potassium iodide (KI) or potassium iodate (KIO(3)), in concentrations corresponding to those typical for Wolff–Chaikoff effect, on the level of oxidative damage to nuclear DNA (nDNA) and mitochondrial DNA (mtDNA) isolated from porcine thyroid under basal conditions and in the presence of Fenton reaction (Fe(2+)+H(2)O(2) → Fe(3+)+(·)OH + OH(−)) substrates. METHODS: Thyroid nDNA and mtDNA were incubated in the presence of either KI or KIO(3) (2.5–50 mM), without/with FeSO(4) (30 µM) + H(2)O(2) (0.5 mM). Index of DNA damage, i.e., 8-oxo-7,8-dihydro-2′-deoxyguanosine, was measured by HPLC. RESULTS: Neither KI nor KIO(3) increased the basal level of 8-oxodG in both nDNA and mtDNA. KI—in all used concentrations—completely prevented the damaging effect of Fenton reaction substrates in mtDNA, and it partially prevented this damage in nDNA. KIO(3) partially prevented Fe(2+)+H(2)O(2)-induced oxidative damage in both DNA only in its highest used concentrations (≥25 mM). CONCLUSIONS: Without additional prooxidative abuse, both iodine compounds, i.e., KI and KIO(3), seem to be safe in terms of their potential oxidative damage to DNA in the thyroid. The superiority of KI over KIO(3) relies on its stronger protective effects against oxidative damage to mtDNA, which constitutes an argument for its preferential utility in iodine prophylaxis.