Effects of melatonin on the oxidative stress induced by thyrotoxicosis in rats

High concentrations of thyroid hormones can affect the metabolism of oxygen in aerobic conditions and stimulate free radicals generation in mitochondria. Reactive oxygen species are toxic to biomembranes and lead to peroxidation of lipids unless they are not removed by free radical scavengers. A few years ago melatonin (MEL), a pineal hormone, was described as a scavenger of free radicals, especially of hydroxyl and peroxyl radicals. The goal of the study was to examine the parameters of oxidative stress [the levels of conjugated dienes (CD), malondialdehyde (MDA) and Schiff bases (SB)] in male rats with thyrotoxicosis, induced by the injection of L-thyroxine (L-T4) in a dose of 100 &mgr;g/kg B.W. After one week of treatment with L-T4, the animals received MEL in a dose 5 mg/kg B.W., i.p., daily, for 7 days. Diagnosis of thyrotoxicosis was confirmed, using hormonal assays. We observed the increased concentration of free T4 (fT4) and free T3 (fT3) after L-T4 injections. The concentration of fT3 was diminished after MEL in L-T4-injected animals. In the liver, we did not observe any changes in the content of both CD and MDA after L-T4 injections but the content of SB was higher after L-T4 injections when compared to the control group. In the liver, melatonin did not change any parameters of oxidative stress, either alone or after L-T4. The changes in the parameters of oxidative stress were better expressed in the kidney, compared to the liver. Melatonin decreased the concentration of CD and SB in the kidneys of a group of animals with thyrotoxicosis. Additionally, MEL decreased the basal concentrations of CD and SB, when compared to the control group.