The thyroid gland is the primary site of sodium/iodide symporter (NIS), an intrinsic plasma membrane protein responsible for the active uptake of iodine, which is indispensable for thyroid hormone synthesis. Since exposure of the thyroid to NIS inhibitors can potentially have harmful effects on the entire organism, it is important to investigate the potential protective effects of known antioxidants, such as melatonin and indole-3-propionic acid (IPA), against pro-oxidative action of classic NIS inhibitors. The study aimed to check if and to what extent melatonin and IPA interact with some confirmed NIS inhibitors regarding their effects on oxidative damage to membrane lipids in the thyroid. For comparison with the thyroid gland, in which NIS is typically present, the liver tissue—not possessing NIS—was applied in the present study. Thyroid and liver homogenates were incubated in the presence of tested NIS inhibitors (i.e., NaClO₃, NH₄SCN, KSeCN, KNO₃, NaF, KClO₄, and BPA) in different ranges of concentrations with/without melatonin (5 mM) or IPA (5 mM). The malondialdehyde+4-hydroxyalkenals (MDA + 4-HDA) concentration (LPO index) was measured spectrophotometrically. NaClO₃ increased LPO in the thyroid and in the liver, but these pro-oxidative effects were not prevented by either melatonin or IPA. Instead, pro-oxidative effects of NH₄SCN observed in both tissues were prevented by both indole substances. KSeCN and NaF increased LPO only in the thyroid, and these pro-oxidative effects were prevented by melatonin and IPA. KNO₃, KClO₄, and BPA did not increase LPO, which can be due to their low concentrations resulting from restricted solubility. In conclusion, as melatonin prevented oxidative damage to membrane lipids in the thyroid caused by some sodium/iodide symporter inhibitors, this indoleamine shoud be considered as a potential protective agent when produced appropriately in living organisms but also as an exogenous substance recommended to individuals overexposed to NIS inhibitors.

We present results on the potential protective antioxidant properties of indole-3-butyric acid. Indole-3-butyric acid is an indole derivative defined as an auxin and widely known as a plant growth regulator. It naturally occurs in Arabidopsis thaliana, which is applied as a model plant in genetic studies. Oxidative damage to membrane lipids (lipid peroxidation; LPO) in porcine thyroid homogenates was induced by Fenton reaction substrates (Fe²⁺ + H₂O₂). Iron (Fe²⁺) was used in very high concentrations of 1200, 600, 300, 150, 75, 37.5, 18.75, 9.375, 4.687, and 2.343 µM. Indole-3-butyric acid (10.0, 5.0, 2.5, 1.25, and 0.625 mM) was applied to check whether it prevents the above process. The LPO level, expressed as malondialdehyde + 4-hydroxyalkenals (MDA + 4-HDA) concentration, was measured spectrophotometrically. Expectedly, Fenton reaction substrates, in a Fe²⁺ concentration-dependent manner, increased LPO level, with the lowest effective concentration of iron being 9.375 µM. In the case of almost all concentrations of indole-3-butyric acid, this auxin has exhibited very promising antioxidant protection, with the most effective concentrations being 10.0 and 5.0 mM; however, as low concentrations of indole-3-butyric acid at 1.25 mM was still effective. Indole-3-butyric acid used alone did not change the basal level of LPO, which is a favourable effect. To summarise, indole-3-butyric acid has protective antioxidant properties against experimentally induced oxidative damage to membrane lipids in the thyroid, and this is for the first time documented in the literature. This compound can be considered a natural protective agent present in plants, which can serve as a dietary nutrient.

Chromium (Cr) is a harmful heavy metal pollutant. Cr(VI) is a group 1 carcinogen (carcinogenic to humans), whereas Cr(III) is a group 3 carcinogen (not classifiable as to its carcinogenicity to humans). Cr is also documented to be an endocrine disrupting chemical. The study aimed to check whether Cr(VI) compound (K₂Cr₂O₇) or Cr(III) compound (CrCl₃·6H₂O) induce oxidative damage to membrane lipids (lipid peroxidation, LPO) in homogenates of two endocrine (the thyroid and the ovary) and two non-endocrine (the kidney and the liver) tissues, and whether antioxidants, such as melatonin, indole-3-propionic acid (IPA) and 17β-estradiol, reveal protective effects. Of note, the healthy thyroid gland is characterized by relatively high oxidative stress. Porcine tissue homogenates were incubated in the presence of Cr(VI) (0.05-10.0 mM) or Cr(III) (5.0-200.0 mM) with/without melatonin (5 mM) or IPA (5 mM) or 17β-estradiol (1 mM). The malondialdehyde+4-hydroxyalkenals (MDA + 4-HDA) concentration (LPO index) was measured spectrophotometrically. Cr(VI) (≥0.1-1.25 mM) significantly increased LPO in all tissues but these damaging effects were not prevented by any antioxidant tested. In turn, Cr(III) (≥25 mM) also significantly increased LPO in all examined tissues. All antioxidants reduced Cr(III)-induced LPO in the ovary, kidney, and liver but had no protective effects in the thyroid. Our findings highlight chromium's strong prooxidative effects, especially in the thyroid. The inability of antioxidants to prevent Cr-induced damage, especially in the thyroid, underscores the need for further research to identify effective protective strategies.

Cadmium is a toxic heavy metal classified by the International Agency for Research on Cancer as a human carcinogen and recognized as an endocrine-disrupting chemical. The present study aimed to evaluate tissue-specific susceptibility to cadmium-induced oxidative damage to membrane lipids (lipid peroxidation, LPO) and to assess the antioxidative effects of melatonin in porcine tissue homogenates representing endocrine (the thyroid and the ovary) and non-endocrine (the liver, the kidney, and the brain) organs. Homogenates were incubated with cadmium chloride (CdCl₂; 2.5–1000 µM) without/with melatonin (0.1–5.0 mM). Lipid peroxidation was assessed spectrophotometrically by measuring malondialdehyde + 4-hydroxyalkenals (MDA + 4-HDA) levels. Cadmium significantly increased LPO in the liver (2.5–1000 μM) and in the kidney (25–1000 μM), whereas no prooxidative effect was observed in endocrine tissues or in the brain. Liver damage was mitigated by melatonin doses as low as 0.1 μM across the 250–1000 μM cadmium range, while protection in the kidney was limited to higher melatonin concentrations (2.5–5.0 mM) against damage induced by 100–1000 μM cadmium concentrations. The findings demonstrate pronounced tissue-specific differences in susceptibility to cadmium-induced oxidative stress and support the potential of melatonin as a preventive agent against heavy metal-induced oxidative stress, particularly in non-endocrine organs.