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]