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Giulia Lanzolla Endocrinology Unit II, Department of Clinical and Experimental Medicine, University of Pisa and University Hospital of Pisa, Pisa, Italy

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Claudio Marcocci Endocrinology Unit II, Department of Clinical and Experimental Medicine, University of Pisa and University Hospital of Pisa, Pisa, Italy

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Michele Marinò Endocrinology Unit II, Department of Clinical and Experimental Medicine, University of Pisa and University Hospital of Pisa, Pisa, Italy

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likely multifactorial, and the complex pathogenetic interplay includes, among others, oxidative stress [ 4 , 6 ]. GO is observed in ∼25–30% of GH patients, making it the most common extrathyroidal manifestation of GD [ 7 ]. The pathogenesis of GO is

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Denise P. Carvalho Laboratório de Fisiologia Endócrina Doris Rosenthal, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil

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Corinne Dupuy Université Paris-Sud, UMR 8200 CNRS, Institute Gustave Roussy, Villejuif, France

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, indicating a relatively high level of this oxidizing agent in the thyroid gland. More recently, the observation that somatic mutations are present in higher levels in the rat thyroid gland has further confirmed that the thyrocyte is under oxidative stress [ 5

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Steen J. Bonnema Departments of Endocrinology, Odense University Hospital, Odense

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Elisabeth S. Stovgaard Laboratory of Clinical Pharmacology Q7642, Rigshospitalet

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Søren Fast Departments of Endocrinology, Odense University Hospital, Odense

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Kasper Broedbaek Laboratory of Clinical Pharmacology Q7642, Rigshospitalet

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Jon T. Andersen Laboratory of Clinical Pharmacology Q7642, Rigshospitalet

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Allan Weimann Laboratory of Clinical Pharmacology Q7642, Rigshospitalet

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Peter Grupe Departments of Nuclear Medicine, Odense University Hospital, Odense

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Laszlo Hegedüs Departments of Endocrinology, Odense University Hospital, Odense

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Henrik E. Poulsen Laboratory of Clinical Pharmacology Q7642, Rigshospitalet
Department of Clinical Pharmacology, Bispebjerg Hospital
Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark

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to increased intracellular oxidative stress, and eventually cell death [ 2 , 3 , 4 ]. Other organs than the thyroid gland are affected by 131 I therapy. Chromosomal alterations in peripheral lymphocytes are seen after 131 I therapy, with recovery

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Claudio Marcocci Department of Endocrinology and Metabolism, University of Pisa, Pisa, Italy

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Marenza Leo Department of Endocrinology and Metabolism, University of Pisa, Pisa, Italy

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Maria Antonietta Altea Department of Endocrinology and Metabolism, University of Pisa, Pisa, Italy

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(GSH) and vitamins (ascorbic acid and tocopherol). Any increase in the rate of ROS production or decrease in their scavenging ability will disrupt the oxidative stability of the cell, resulting in oxidative stress (fig. 1 ) [ 4 ]. Fig. 1

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Kamilla R Riis Department of Endocrinology, Odense University Hospital, Odense, Denmark
Department of Clinical Research, University of Southern Denmark, Odense, Denmark

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Camilla B Larsen Department of Endocrinology, Odense University Hospital, Odense, Denmark
Department of Clinical Research, University of Southern Denmark, Odense, Denmark

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Bjarke R Medici Department of Medicine, Copenhagen University Hospital – Herlev and Gentofte, Denmark

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Christian Z Jensen Department of Medicine, Copenhagen University Hospital – Herlev and Gentofte, Denmark

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Kristian H Winther Department of Endocrinology, Odense University Hospital, Odense, Denmark

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Emil L Larsen Department of Clinical Pharmacology, Bispebjerg-Frederiksberg Hospital, Copenhagen, Denmark

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Christina Ellervik Department of Laboratory Medicine, Boston Children’s Hospital, Harvard Medical School, Boston, United States of America
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Department of Data and Data Support, Region Zealand, Sorø, Denmark

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Jeppe L la Cour Department of Medicine, Copenhagen University Hospital – Herlev and Gentofte, Denmark

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Laszlo Hegedüs Department of Endocrinology, Odense University Hospital, Odense, Denmark
Department of Clinical Research, University of Southern Denmark, Odense, Denmark

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Thomas H Brix Department of Endocrinology, Odense University Hospital, Odense, Denmark

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Henrik E Poulsen Department of Endocrinology, Copenhagen University Hospital, Bispebjerg-Frederiksberg Hospital, Denmark
Faculty of Health Science, University of Copenhagen, Copenhagen, Denmark
Department of Cardiology, University Hospital Nordsjælland, Hillerød, Denmark

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Filip K Knop Department of Medicine, Copenhagen University Hospital – Herlev and Gentofte, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Steno Diabetes Center Copenhagen, Herlev, Denmark
Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark

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Birte Nygaard Department of Medicine, Copenhagen University Hospital – Herlev and Gentofte, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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Steen J Bonnema Department of Endocrinology, Odense University Hospital, Odense, Denmark
Department of Clinical Research, University of Southern Denmark, Odense, Denmark

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imbalance between oxidative and antioxidative processes, in favor of the oxidative processes, leads to a disruption of redox signaling and/or molecular damage, and is defined as oxidative stress ( 9 ). Prooxidants include reactive oxygen species (ROS) that

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Horea Ioan Ursu ‘C.I. Parhon' National Institute of Endocrinology

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Monica Livia Gheorghiu ‘Carol Davila' University of Medicine and Pharmacy, Bucharest, Romania

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significantly the course of mild GO [ 2 ]. There is good evidence that oxidative stress plays a role in GO: orbital fibroblasts of GO patients have higher contents of malondialdehyde, superoxide anions and hydrogen peroxide than control orbital fibroblasts [ 3

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Roberto Negro Division of Endocrinology, ‘V. Fazzi' Hospital, Lecce

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Giacomo Greco Faculty of Medicine, San Raffaele Hospital, Milan, Italy

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oxide (NO) availability that in turn regulates EPC self-renewal, viability, migration, proliferation and differentiation [ 10 , 11 ]. Hypothyroidism, as well as CV diseases like chronic HF, are associated with oxidative stress, in which altered levels of

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Maik Pietzner Institute of Clinical Chemistry and Laboratory Medicine, Berlin, Germany

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Georg Homuth Interfaculty Institute for Genetics and Functional Genomics, Berlin, Germany

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Kathrin Budde Institute of Clinical Chemistry and Laboratory Medicine, Berlin, Germany

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Ina Lehmphul Institut für Experimentelle Endokrinologie, Charité-Universitätsmedizin Berlin, Berlin, Germany

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Uwe Völker Interfaculty Institute for Genetics and Functional Genomics, Berlin, Germany

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Henry Völzke Institute for Community Medicine, University Medicine Greifswald, Ernst Moritz Arndt University, Greifswald, Germany

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Matthias Nauck Institute of Clinical Chemistry and Laboratory Medicine, Berlin, Germany

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Josef Köhrle Institut für Experimentelle Endokrinologie, Charité-Universitätsmedizin Berlin, Berlin, Germany

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Nele Friedrich Institute of Clinical Chemistry and Laboratory Medicine, Berlin, Germany

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glutathione after response to oxidative stress. Beside this redox cycle, glutathione synthesis is assured by the γ-glutamyl cycle, which at least in astrocytes [ 39 ] was assumed to be stimulated by TH. The γ-glutamyl cycle involves the formation of

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Leonidas Duntas Evgenideion Hospital, Unit of Endocrinology, Diabetes and Metabolism, National and Kapodeistrian University of Athens, Greece

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considerable diminishment of TPOAbs indicates a possible modulatory effect on oxidative stress, likely leading to co-regulation of TPOAb generation. It is an extremely important finding demonstrating that Se provides health benefits to patients with

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Hyun-Jin Lee Department of Otorhinolaryngology-Head and Neck Surgery, Gyeongsang National University College of Medicine, Jinju, South Korea
Department of Otorhinolaryngology-Head and Neck Surgery, Chung-Ang University College of Medicine, Seoul, South Korea

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Young-Sool Hah Biomedical Research Institute, Gyeongsang National University Hospital, Jinju, South Korea

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So Young Cheon Biomedical Research Institute, Gyeongsang National University Hospital, Jinju, South Korea

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Seong Jun Won Department of Otorhinolaryngology-Head and Neck Surgery, Gyeongsang National University College of Medicine, Jinju, South Korea
Department of Otorhinolaryngology-Head and Neck Surgery, Gyeongsang National University Hospital, Jinju, South Korea
Institute of Health Sciences, Gyeongsang National University, Jinju, South Korea

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Chae Dong Yim Department of Otorhinolaryngology-Head and Neck Surgery, Gyeongsang National University College of Medicine, Jinju, South Korea
Department of Otorhinolaryngology-Head and Neck Surgery, Gyeongsang National University Hospital, Jinju, South Korea
Institute of Health Sciences, Gyeongsang National University, Jinju, South Korea

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Somi Ryu Department of Otorhinolaryngology-Head and Neck Surgery, Gyeongsang National University College of Medicine, Jinju, South Korea
Department of Otorhinolaryngology-Head and Neck Surgery, Gyeongsang National University Hospital, Jinju, South Korea
Institute of Health Sciences, Gyeongsang National University, Jinju, South Korea

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Seung-Jun Lee Department of Convergence of Medical Sciences, Gyeongsang National University, Jinju, South Korea

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Ji Hyun Seo Institute of Health Sciences, Gyeongsang National University, Jinju, South Korea
Department of Pediatrics, Gyeongsang National University College of Medicine, Jinju, South Korea

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Jung Je Park Department of Otorhinolaryngology-Head and Neck Surgery, Gyeongsang National University College of Medicine, Jinju, South Korea
Biomedical Research Institute, Gyeongsang National University Hospital, Jinju, South Korea
Department of Otorhinolaryngology-Head and Neck Surgery, Gyeongsang National University Hospital, Jinju, South Korea
Institute of Health Sciences, Gyeongsang National University, Jinju, South Korea

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processes, including glucose and lipid metabolism, mitochondrial function, and oxidative stress responses ( 11 ). A possible link between SIRT4 and cancer progression was recently proposed ( 12 , 13 , 14 , 15 , 16 ). SIRT4 has been characterized as a

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