Melatonin effects on Schiff's base levels induced by iodide administration in rats

Administration of iodides to animals, living in iodine-deficient areas, can induce necrosis and fibrosis of the thyroid gland. It is believed that structural and functional changes of the thyroid may be related to oxidative processes. Increased lipid peroxidation levels were reported in murine thyroid glands after high doses of iodine. Melatonin (MEL) is believed to exert its effects via electron donation to directly detoxify free radicals, such as, e.g., the highly toxic hydroxyl radical. In numerous reports related to the antioxidative action of MEL, the authors have considered the protective ability of this hormone against peroxidation of lipids. The goal of the study was to evaluate oxidative processes and the protective role of MEL in three organs of the rat (the liver, the brain, and the lungs) during treatment with different doses of iodide.

Schiff's bases (SB) concentrations (a parameter of oxidative stress) were measured in liver, lung and brain homogenates of male Wistar rats. The animals received iodides in their diet in the following concentrations, for 2 weeks: Group 1--Controls (standard normal-iodine diet, containing approx. 0.7 mg of kalium iodide per kg; KI/kg); Group 2--diet containing 0,25 mg KI/kg; Group 3--diet with 4,0 mg KI/kg; Group 4--diet with 8,0 mg KI/kg. Group 5--standard normal-iodine diet and MEL alone in a dose of 1 mg/kg BW i.p. at 3.00 pm, every day for two weeks. Subsequent three groups (6-8) received KI in their diet in doses as above, respectively, together with MEL.

We noted increased levels of SB in the lungs and in the liver, when compared to those observed in controls. We also found decreased SB concentrations in liver and lung homogenates after an administration of MEL but--unexpectedly--the level of SB increased in the group with the highest dose of iodine in diet in lung homogenates. Increased levels of Schiff's bases suggest that iodine is involved in oxidative processes not only in the thyroid but also in other tissues, and MEL protects against the iodine-induced oxidative stress.

Our results confirm the differences in lipid peroxidation among the examined organs. These alterations can possibly be related to different sensitivity rates of examined tissues to oxidative damage.