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Oxidative stress enhances the immune response to oxidatively modified catalase enzyme in patients with Graves’ disease

BACKGROUND: Oxidative stress is associated with several autoimmune disorders and oxidative modification of proteins that may result in autoimmune response. This study aims to evaluate the catalase (CAT) activity and the autoimmune response against the native CAT and the oxidatively modified enzyme i...

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Detalles Bibliográficos
Autores principales: Gargouri, Bochra, Mseddi, Malek, Mnif, Fatma, Abid, Mohamed, Attia, Hamadi, Lassoued, Saloua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7031633/
https://www.ncbi.nlm.nih.gov/pubmed/31617239
http://dx.doi.org/10.1002/jcla.23051
Descripción
Sumario:BACKGROUND: Oxidative stress is associated with several autoimmune disorders and oxidative modification of proteins that may result in autoimmune response. This study aims to evaluate the catalase (CAT) activity and the autoimmune response against the native CAT and the oxidatively modified enzyme in patients with Graves' disease (GD) and healthy controls in a comparative way. METHODS: The CAT activity was evaluated via spectrophotometric method. Using enzyme‐linked immunosorbent assay, the reactivities of autoantibody toward native, malondialdehyde (MDA) and hydrogen peroxide (H(2)O(2)) modified CAT were evaluated in plasmas of patients and controls. RESULTS: Reduced CAT activity was found in patients compared with controls (P < .05). It was proved that levels of IgG antibodies against MDA‐modified CAT were higher than against unmodified ones (P < .001). No changes were found for the reactivities to H(2)O(2)‐modified CAT. Positive correlation was found between the reactivity to MDA‐modified CAT and the triiodothyronine level (P < .001, r = .6). CONCLUSION: Our findings incriminate the MDA in the autoantibodies reactivity to oxidatively modified CAT leading to a disturbed oxidative profile and/or the progression of GD pathology.