Potassium iodide is used as the treatment of overactive thyroid and as protection of the thyroid gland from the influences of radiation from swallowed or inhaled radioactive iodine. It may be used after accidental exposure to radioactive iodine or before and after administration of medicine containing radioactive iodine.

Iodine induces abnormal morphologic changes of cells, inhibited cell proliferation, and increases apoptosis rate in rat aorta endothelial cells. Iodine also reduces the activity of SOD, GSH-Px, and concentrations of GSH and increases the concentrations of MDA and protein carbonyl in a dose-dependent manner. Excess iodine decreased the activity of eNOS and increased the activity of iNOS and the expression of ICAM-1 and VCAM-1 in culture medium. Excess iodine exposure increases oxidative stress, causes damage of vascular endothelial cells, and altered the expression of adhesion factors and the activity of NOS. [1] Potassium iodide increases avidity of some immune reactions including C-mediated cell lysis mediated by altered access of C-binding receptors. [2] Potassium iodide (≥50 mM) increases lipid peroxidation in concentration-dependent manner. Potassium iodide (25 mM) reduces Fenton reaction-induced lipid peroxidation. [3] Potassium iodide is able to eliminate E faecalis from bovine root dentin when used with a 15-minute contact time. [4]

Potassium Iodide decreases Schiff's bases (SB) concentrations in liver and lung homogenates after the administration of PTU but, unexpectedly, the level of SB increases in kidney homogenates of Wistar rats. [5]