Protein oxidation and autoantibodies' reactivity against malondialdehyde and hydrogen peroxide-modified thyroid antigens in plasma of patients with Graves' disease and Hashimoto Thyroiditis.

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Protein oxidation and autoantibodies' reactivity against malondialdehyde and hydrogen peroxide-modified thyroid antigens in plasma of patients with Graves' disease and Hashimoto Thyroiditis.

Chem Biol Interact. 2017 Apr 18;:

Authors: Mseddi M, Ben Mansour R, Gargouri B, Mnif F, El Ghawi S, Hammami B, Ghorbel A, Abid M, Lassoued S

Abstract
The aim of this study was first to investigate the oxidative proteins modifications in the plasma of both autoimmune thyroid diseases (AITD), Graves' disease (GD) and Hashimoto Thyroiditis (HT). Then, the impact of these oxidative modifications on immune response was evaluated by measuring the reactivity of patients' autoantibodies against malondialdéhyde (MDA) and Hydrogen peroxide (H2O2) modified thyroid antigens (T.Ag) in comparison to native ones. Carbonyl and thiol groups, and MDA-protein adducts were first assessed among 74 AITD patients and 65 healthy controls. Then, the reactivities of AITD immunoglobulin (Ig)G autoantibodies towards MDA-modified, H2O2-modified and unmodified T.Ag proteins were compared using a standard enzyme-linked immunosorbent assay (ELISA). High levels of MDA bound to proteins and carbonyl groups, as well as reduced thiol level were observed among patients by comparison to healthy controls (p < 0.05). Enhanced reactivity of IgG circulating autoantibodies was found against H2O2-modified T.Ag compared to unmodified ones (p < 0.001). However, decreased reactivity to MDA-modified T.Ag compared to the native form was observed in GD patients (p < 0.05) and no changes were noted for HT. The reactivity's to H2O2-modified T.Ag correlate positively with free triiodothyronine level in GD and with thyroid stimulating hormone level in HT. High production of H2O2, probably during hormone synthesis, could contribute to protein oxidation during AITD diseases and to create neoepitopes responsible for antibody reactivity enhancement and as a consequence for AITD development and/or exacerbation.

PMID: 28431875 [PubMed - as supplied by publisher]

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