Oxidative stress in graves' disease - PubMed (original) (raw)

Oxidative stress in graves' disease

Claudio Marcocci et al. Eur Thyroid J. 2012 Jul.

Abstract

Increased reactive oxygen species (ROS) generation and the consequent oxidative damage are involved in the development of several diseases, including autoimmune diseases. Graves' disease is an autoimmune disorder characterized by hyperthyroidism and, less frequently, orbitopathy. Hyperthyroidism is characterized by increased oxidative stress. Untreated hyperthyroidism is associated with an increase of several parameters of oxidative stress and in most studies (but not all) by an increase of antioxidant defense enzymes. Restoration of euthyroidism with antithyroid drug is associated with a reversal of the biochemical abnormalities associated with oxidative stress. Animal and human studies suggest that increased ROS may directly contribute to some clinical manifestation of the disease, including orbitopathy. Antioxidants administered alone improve some clinical signs and symptoms of hyperthyroidism and, when associated with antithyroid drugs, induce a more rapid control of clinical manifestations and a faster achievement of euthyroidism. A large randomized clinical trial has shown that antioxidant supplementation (selenium) may also be beneficial for mild Graves' orbitopathy.

Keywords: Antithyroid drugs; Graves' orbitopathy; Hyperthyroidism; Selenium.

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Figures

Fig. 1

Fig. 1

Mechanisms responsible for oxidative stress and cell damage. An increased production of ROS and inactivation or excessive consumption of antioxidant defenses will be responsible for oxidative damage of biological membranes and molecules, such as lipids, proteins and nucleic acids.

Fig. 2

Fig. 2

Effect of treatment with methimazole (Group A) or Larotabe® (an antioxidant mixture containing vitamin E, β-carotene, vitamin C, Cu, Zn, Mn, selenium; Group B) on serum T3 levels and urinary MDA levels and clinical score (based on symptoms and signs of hyperthyroidism) in 36 patients with GD (derived from data of Guerra et al. [31]).

Fig. 3

Fig. 3

Changes of GO-specific quality of life score questionnaire (a) and overall eye evaluation (b) at 6 and 12 months in patients with mild GO randomly assigned to treatment with sodium selenite (100 μg twice daily) or placebo (twice daily). Changes of quality of life and overall eye evaluation were scored as improved, unchanged, or worsened according to predefined criteria (derived from data of Marcocci et al [45]).

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References

    1. Halliwell B, Gutteridge JM. Lipid peroxidation, oxygen radicals, cell damage, and antioxidant therapy. Lancet. 1984;1:1396–1397. - PubMed
    1. Valko M, Leibfritz D, Moncol J, Cronin MT, Mazur M, Telser J. Free radicals and antioxidants in normal physiological functions and human disease. Int J Biochem Cell Biol. 2007;39:44–84. - PubMed
    1. Song Y, Driessens N, Costa M, De Deken X, Detours V, Corvilain B, Maenhaut C, Dalton TP, Shertzer HG, Puga A. Regulation of gene expression by reactive oxygen. Ann Rev Pharmacol Toxicol. 1999;39:67–101. - PubMed
    1. Halliwell B, Gutteridge JMC. Free Radicals in Biology and Medicine. ed 4. New York: Oxford University Press; 2007. Cellular responses to oxidative stress: adaptation, damage, repair, senescence and death; pp. 187–267.
    1. Venditti P, Di Meo S. Thyroid hormone-induced oxidative strees. Cell Mol Life Sci. 2006;63:414–434. - PMC - PubMed

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