Potassium iodide, but not potassium iodate, as a potential protective agent against oxidative damage to membrane lipids in porcine thyroid

BACKGROUND: Fenton reaction (Fe(2+)+H(2)O(2)→Fe(3+)+(•)OH+OH(−)) is of special significance in the thyroid gland, as both its substrates, i.e. H(2)O(2) and Fe(2+), are required for thyroid hormone synthesis. Also iodine, an essential element supplied by the diet, is indispensable for thyroid hormone synthesis. It is well known that iodine affects red-ox balance. One of the most frequently examined oxidative processes is lipid peroxidation (LPO), which results from oxidative damage to membrane lipids. Fenton reaction is used to experimentally induce lipid peroxidation. The aim of the study was to evaluate effects of iodine, used as potassium iodide (KI) or potassium iodate (KIO(3)), on lipid peroxidation in porcine thyroid homogenates under basal conditions and in the presence of Fenton reaction substrates. METHODS: Porcine thyroid homogenates were incubated in the presence of either KI (0.00005 – 500 mM) or KIO(3) (0.00005 – 200 mM), without or with addition of FeSO(4) (30 μM) + H(2)O(2) (0.5 mM). Concentration of malondialdehyde + 4-hydroxyalkenals (MDA + 4-HDA) was measured spectrophotometrically, as an index of lipid peroxidation. RESULTS: Potassium iodide, only when used in the highest concentrations (≥50 mM), increased lipid peroxidation in concentration-dependent manner. In the middle range of concentrations (5.0; 10; 25; 50 and 100 mM) KI reduced Fenton reaction-induced lipid peroxidation, with the strongest protective effect observed for the concentration of 25 mM. Potassium iodate increased lipid peroxidation in concentrations ≥2.5 mM. The damaging effect of KIO(3) increased gradually from the concentration of 2.5 mM to 10 mM. The strongest damaging effect was observed at the KIO(3) concentration of 10 mM, corresponding to physiological iodine concentration in the thyroid. Potassium iodate in concentrations of 5–200 mM enhanced Fenton reaction-induced lipid peroxidation with the strongest damaging effect found again for the concentration of 10 mM. CONCLUSIONS: Potassium iodide, used in doses generally recommended in iodide prophylaxis, may prevent oxidative damage to membrane lipids in this gland. Toxic effects of iodide overload may result from its prooxidative action. Potassium iodate does not possess any direct beneficial effects on oxidative damage to membrane lipids in the thyroid, which constitutes an additional argument against its utility in iodine prophylaxis.