Oxidative stress and its role in the development of autoimmune thyroid diseases.

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Abstract

Abstract


A large number of socially significant diseases is accompanied with oxidative stress and carry with tissue damage. Free radicals play a crucial role in the development of these diseases. Similar processes occur under the influence of ionizing radiation and bacterial infections. Recently, was indicated the significant role of oxidative stress in the development of autoimmune thyroiditis. It is assumed that the synthesis of thyroid hormones depends on the concentration of H2O2, which, due to its high toxicity, must be in strict accordance with the activity of antioxidant systems. Many biochemically negative processes occur on the apical membrane of the thyrocyte, which allows limiting the effect of free radicals and avoid cell destruction. However, in pathological conditions, enzymatic systems are disturbed and their components become abnormally activated in the cytoplasm, and it is leads to functional and morphological disorders. A deeper understanding of oxidative stress and its role in the development of autoimmune thyroiditis can contribute to the identification of new methods for its assessment, the expansion of therapeutic ranges for this disease. This review discusses oxidative stress, which is the accumulation of active damaging agents (free radicals, prooxidants, reactive oxygen species) that initiate cell damage and lead to the development of various pathological conditions.


About the authors

Anastasia Rybakova

Endocrinology Research Centre

Author for correspondence.
Email: aamamykina@gmail.com
ORCID iD: 0000-0002-1248-9099
SPIN-code: 8275-6161

Russian Federation, 11 Dm. Ulyanova street, 117036 Moscow, Russia

MD

Nadezhda Platonova

Endocrinology Research Centre

Email: doc-platonova@inbox.ru
ORCID iD: 0000-0001-6388-1544
SPIN-code: 4053-3033
11 Dm. Ulyanova street, 117036 Moscow, Russia

MD, ScD

Ekaterina Troshina

Endocrinology Research Centre

Email: troshina@inbox.ru
ORCID iD: 0000-0002-8520-8702
SPIN-code: 8821-8990
11 Dm. Ulyanova street, 117036 Moscow, Russia

MD, ScD, professor

References

  • Betteridge D. What is oxidative stress? Metabol. 2000;49(2):3-8. doi: 10.1016/s0026-0495(00)80077-3.
  • Frijhoff J, Winyard PG, Zarkovic N, et al. Clinical relevance of biomarkers of oxidative stress. // Antioxid Redox Signal. 2015;23(14):1144–1170. doi: 10.1089/ars.2015.6317.
  • Mancini A, Di Segni C, Raimondo S et al. Thyroid hormones, oxidative stress, and inflammation. // Mediators Inflamm. 2016;2016:1-12. doi: 10.1155/2016/6757154.
  • Rosen GM, Freeman BA. Detection of superoxide generated by endothelial cells. // Proc Natl Acad Sci USA. 1984;81(23):7269–7273. doi: 10.1073/pnas.81.23.7269.
  • Mancini A, Giacchi E, Raimondo S, Di C, Silvestrini A, Meucci E. Hypothyroidism, oxidative stress and reproduction. // Hypothyroidism - Influences and Treatments. 2012. doi: 10.5772/31939.
  • Dobrzynska MM, Baumgartner A, Anderson D. Antioxidants modulate thyroid hormone‐ and noradrenaline‐induced DNA damage in human sperm. // Mutagenesis. 2004;19(4):325-330. doi: 10.1093/mutage/geh037.
  • Kowaltowski A, Costa A, Vercesi A. Activation of the potato plant uncoupling mitochondrial protein inhibits reactive oxygen species generation by the respiratory chain. // FEBS Lett. 1998;425(2):213-216. doi: 10.1016/s0014-5793(98)00231-2.
  • Rebiger L, Lenzen S, Mehmeti I. Susceptibility of brown adipocytes to pro-inflammatory cytokine toxicity and reactive oxygen species. // Biosci Rep. 2016;36(2):e00306-e00306. doi: 10.1042/bsr20150193.
  • Hoang T, Kuljanin M, Smith M, Jelokhani-Niaraki M. A biophysical study on molecular physiology of the uncoupling proteins of the central nervous system. // Biosci Rep. 2015;35(4):e00226-e00226. doi: 10.1042/bsr20150130.
  • Petrovic N, Cvijic G, Davidovic V. Thyroxine and tri-iodothyronine differently affect uncoupling protein-1 content and antioxidant enzyme activities in rat interscapular brown adipose tissue. // J Endocrinol. 2003;176(1):31-38. doi: 10.1677/joe.0.1760031.
  • Branco M, Ribeiro M, Negrão N, Bianco A. 3,5,3′-Triiodothyronine actively stimulates UCP in brown fat under minimal sympathetic activity. // Am J Physiol. 1999;276(1):E179-E187. doi: 10.1152/ajpendo.1999.276.1.e179.
  • Hima S, Sreeja S. Regulatory role of estrogen-induced reactive oxygen species in the modulatory function of UCP 2 in papillary thyroid cancer cells. // IUBMB Life. 2015;67(11):837-846. doi: 10.1002/iub.1440.
  • Venditti P, Balestrieri M, Di Meo S, De Leo T. Effect of thyroid state on lipid peroxidation, antioxidant defences, and susceptibility to oxidative stress in rat tissues. // J Endocrinol. 1997;155(1):151-157. doi: 10.1677/joe.0.1550151.
  • Venditti P, Meo S. Thyroid hormone-induced oxidative stress. // Cell Mol Life Sci. 2006;63(4):414-434. doi: 10.1007/s00018-005-5457-9.
  • Venditti P, Daniele M, Masullo P, Di Meo S. Antioxidant-sensitive triiodothyronine effects on characteristics of rat liver mitochondrial population. // Cell Physiol Biochem. 1999;9(1):38-52. doi: 10.1159/000016301.
  • Huh K, Kwon T, Kim J, Park J. Role of the hepatic xanthine oxidase in thyroid dysfunction: effect of thyroid hormones in oxidative stress in rat liver. // Arch Pharm Res. 1998;21(3):236-240. doi: 10.1007/bf02975281.
  • Asayama K, Dobashi K, Hayashibe H, Megata Y, Kato K. Lipid peroxidation and free radical scavengers in thyroid dysfunction in the rat: a possible mechanism of injury to heart and skeletal muscle in hyperthyroidism. // Endocrinol. 1987;121(6):2112-2118. doi: 10.1210/endo-121-6-2112.
  • Ademoglu E, De Gokkusu C, Yarman S, Azizlerli H. The effect of methimazole on the oxidant and antioxidant system in patients with hyperthyroidism. // Pharmacol Res. 1998;38(2):93-96. doi: 10.1006/phrs.1998.0336.
  • Bianchi G, Solaroli E, Zaccheroni V et al. Oxidative stress and anti-oxidant metabolites in patients with hyperthyroidism: effect of treatement. // Horm Met Res. 1999;31(11):620-624. doi: 10.1055/s-2007-978808.
  • Mancini A, Raimondo S, Di Segni C, et al. Thyroid hormones and antioxidant systems: focus on oxidative stress in cardiovascular and pulmonary diseases. // Int J Mol Sci. 2013;14(12):23893–23909. doi: 10.3390/ijms141223893.
  • Haribabu A, Reddy V, Pallavi C et al. Evaluation of protein oxidation and its association with lipid peroxidation and thyrotropin levels in overt and subclinical hypothyroidism. Endocrine. 2012;44(1):152-157. doi: 10.1007/s12020-012-9849-y.
  • Azizi, F., Raiszadeh, F., Solati, M. et al. Serum paraoxonase 1 activity is decreased in thyroid dysfunction. // J Endocrinol Invest. 2003;26:703. doi: 10.1007/BF03347350.
  • Erdamar H, Demirci H, Yaman H, et al. The effect of hypothyroidism, hyperthyroidism, and their treatment on parameters of oxidative stress and antioxidant status. // Clin Chem Lab Med. 2008;46(7):1004-1010. doi: 10.1515/CCLM.2008.183.
  • Santi A, Duarte M, Moresco R, et al. Association between thyroid hormones, lipids and oxidative stress biomarkers in overt hypothyroidism. Clin Chem Lab Med. 2010;48(11):1635-1639. doi: 10.1515/CCLM.2010.309.
  • Nanda N, Bobby Z, Hamide A, Koner BC, Sridhar MG. Association between oxidative stress and coronary lipid risk factors in hypothyroid women is independent of body mass index. // Metabol. 2007;56(10):1350–1355. doi: 10.1016/j.metabol.2007.05.015.
  • Kebapcilar L, Akinci B, Bayraktar F, Comlekci A, Solak A, Demir T, Yener S, Küme T, Yesil S. Plasma thiobarbituric acid-reactive substance levels in subclinical hypothyroidism. // Med Princ Pract. 2007;16:432-436. doi: 10.1159/000107747.
  • Santi A, Duarte MM, de Menezes CC, Loro VL. Association of lipids with oxidative stress biomarkers in subclinical hypothyroidism. // Int J Endocrinol. 2012;2012:856359. doi: 10.1155/2012/856359.
  • Mancini A, Festa R, Donna V et al. Hormones and antioxidant systems: Role of pituitary and pituitary-dependent axes. // J Endocrinol Invest. 2010;33:422. doi: 10.1007/BF03346615.
  • Mancini A, Leone E, Silvestrini A et al. Evaluation of antioxidant systems in pituitary-adrenal axis diseases. // Pituitary. 2010;13:138. doi: 10.1007/s11102-009-0213-z.
  • Ozturk U, Vural P, Ozderya A, Karadag B, Dogru-Abbasoglu S, Uysal M. Oxidative stress parameters in serum and low density lipoproteins of Hashimoto's thyroiditis patients with subclinical and overt hypothyroidism. // Int Immunopharm. 2012;14(4):349–352. doi: 10.1016/j.intimp.2012.08.010.
  • Ohye H, Sugawara M. Dual oxidase, hydrogen peroxide and thyroid diseases. // Exp Biol Med. 2010;235(4):424–433. doi: 10.1258/ebm.2009.009241.
  • Varela V, Rivolta CM, Esperante SA, Gruneiro-Papendieck L, Chiesa A, Targovnik HM. Three mutations (p.Q36H, p.G418fsX482, and g.IVS19-2A>C) in the dual oxidase 2 gene responsible for congenital goiter and iodide organification defect. // Clin Chem. 2006;52(2):182–191. doi: 10.1373/clinchem.2005.058321.
  • Rigutto S. et al. Activation of dual oxidases Duox1 and Duox2: differential regulation mediated by camp-dependent protein kinase and protein kinase C-dependent phosphorylation. // J Biol Chem. 2009;284(11):6725–6734. doi: 10.1074/jbc.M806893200.
  • Weber G. et al. Genetic defects of hydrogen peroxide generation in the thyroid gland. // J Endocrinol invest. 2013;36(4):261–266. doi: 10.3275/8847.
  • Hulur I. et al. A single copy of the recently identified dual oxidase maturation factor (DUOXA) 1 gene produces only mild transient hypothyroidism in a patient with a novel biallelic DUOXA2 mutation and monoallelic DUOXA1 deletion. // JCEM. 2011;96(5):E841–845. doi: 10.1210/jc.2010-2321.
  • Guichard C. et al. The Nox/Duox family of ROS-generating NADPH oxidases. // Med Sci (Paris). 2006;22(11):953–959. doi: 10.1051/medsci/20062211953.
  • Ameziane-El-Hassani R. et al. Dual oxidase-2 has an intrinsic Ca2+-dependent H2O2-generating activity. // J Biol Chem. 2005;280(34):30046–30054. doi: 10.1074/jbc.M500516200.
  • Raad H. et al. Thyroid hydrogen peroxide production is enhanced by the Th2 cytokines, IL-4 and IL-13, through increased expression of the dual oxidase 2 and its maturation factor DUOXA2. // Free Radic Biol Med. 2012:1–10. doi: 10.1016/j.freeradbiomed.2012.09.003.
  • Karbownik-Lewinska M, Kokoszko-Bilska A. Oxidative damage to macromolecules in the thyroid - experimental evidence. // Thyroid Res. 2012;5(1):25. doi: 10.1186/1756-6614-5-25.
  • Zhang N, Wang L, Duan Q, et al. Metallothionein-I/II Knockout Mice Aggravate Mitochondrial Superoxide Production and Peroxiredoxin 3 Expression in Thyroid after Excessive Iodide Exposure. // Oxid Med Cell Longev. 2015;2015:267027. doi: 10.1155/2015/267027.
  • Vitale M, Matola TD, D’Ascoli F, et al. Iodide excess induces apoptosis in thyroid cells through a p53-independent mechanism involving oxidative stress. // Endocrinol. 2000;141(2):598–605. doi: 10.1210/endo.141.2.7291.
  • Corvilain B, Collyn L, Van Sande J, Dumont JE. Stimulation by iodide of H2O2 generation in thyroid slices from several species. // Am J Physiol. 2000;278(4):e692–e699. doi: 10.1152/ajpendo.2000.278.4.E692.
  • Seven A, Tasan E, Inci F, et al. Biochemical evaluation of oxidative stress in propylthiouracil treated hyperthyroid patients. Effects of vitamin C supplementation. // Clin Chem Lab Med. 2005;36(10):767-770. doi: 10.1515/CCLM.1998.136.
  • Baskol G, Atmaca H, Tanrıverdi F, Baskol M, Kocer D, Bayram F. Oxidative stress and enzymatic antioxidant status in patients with hypothyroidism before and after treatment. Exp Clin Endocrinol Diabetes. 2007;115(8):522-526. doi: 10.1055/s-2007-981457.
  • Chiu-Ugalde J. et al. Thyroid function is maintained despite increased oxidative stress in mice lacking selenoprotein biosynthesis in thyroid epithelial cells. // Antioxid Redox Signal. 2012;17(6):902–913. doi: 10.1089/ars.2011.4055.
  • Schmutzler C. et al Selenoproteins of the thyroid gland: expression, localization and possible function of glutathione peroxidase 3. // Biol Chem. 2007;388(10):1053–1059. doi: 10.1515/BC.2007.122.
  • Chakrabarti SK, Ghosh S, Banerjee S, Mukherjee S, Chowdhury S. Oxidative stress in hypothyroid patients and the role of antioxidant supplementation. // Indian J Endocrinol Metab. 2016;20(5):674–678. doi: 10.4103/2230-8210.190555.

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