Gładysz Aleksandra K, Stępniak Jan, Karbownik-Lewińska Małgorzata
Department of Oncological Endocrinology, Medical University of Lodz, 7/9 Zeligowski St., 90-752 Lodz, Poland.
Polish Mother's Memorial Hospital-Research Institute, 281/289 Rzgowska St., 93-338 Lodz, Poland.
Antioxidants (Basel). 2023 Aug 29;12(9):1688. doi: 10.3390/antiox12091688.
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., NaClO, NHSCN, KSeCN, KNO, NaF, KClO, 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. NaClO 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 NHSCN 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. KNO, KClO, 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.
甲状腺是钠/碘同向转运体（NIS）的主要存在部位，NIS是一种内在的质膜蛋白，负责碘的主动摄取，而碘是甲状腺激素合成所必需的。由于甲状腺暴露于NIS抑制剂可能会对整个机体产生潜在的有害影响，因此研究已知的抗氧化剂（如褪黑素和吲哚-3-丙酸（IPA））对经典NIS抑制剂的促氧化作用的潜在保护作用具有重要意义。该研究旨在检验褪黑素和IPA是否以及在何种程度上与某些已证实的NIS抑制剂相互作用，及其对甲状腺膜脂质氧化损伤的影响。为了与通常存在NIS的甲状腺进行比较，本研究采用了不具有NIS的肝脏组织。将甲状腺和肝脏匀浆在不同浓度范围的受试NIS抑制剂（即NaClO、NHSCN、KSeCN、KNO、NaF、KClO和BPA）存在下孵育，同时加入/不加入褪黑素（5 mM）或IPA（5 mM）。采用分光光度法测定丙二醛+4-羟基烯醛（MDA + 4-HDA）浓度（脂质过氧化指数）。NaClO增加了甲状腺和肝脏中的脂质过氧化，但褪黑素或IPA均未阻止这些促氧化作用。相反，两种吲哚类物质均阻止了在两个组织中观察到的NHSCN的促氧化作用。KSeCN和NaF仅增加了甲状腺中的脂质过氧化，而褪黑素和IPA阻止了这些促氧化作用。KNO、KClO和BPA未增加脂质过氧化，这可能是由于其溶解度受限导致浓度较低。总之，由于褪黑素可预防某些钠/碘同向转运体抑制剂引起的甲状腺膜脂质氧化损伤，这种吲哚胺应被视为一种潜在的保护剂，当它在生物体内适当产生时，也应被视为一种推荐给过度暴露于NIS抑制剂的个体的外源物质。
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