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Factors contributing to the resistance of the thyrocyte to hydrogen peroxide

We studied the mechanism that may explain the relative resistance of thyrocytes to H2O2 compared to other cell types. Ability to degrade H2O2, glutathione peroxidase (GPx) activity, heme oxygenase-1 (HO-1) expression, cell survival and capacity to repair DNA damage after H2O2 exposure or irradiation...

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Published in:Molecular and cellular endocrinology 2019-02, Vol.481, p.62-70
Main Authors: Ghaddhab, Chiraz, Kyrilli, Aglaia, Driessens, Natacha, Van Den Eeckhaute, Emmanuel, Hancisse, Olivier, De Deken, Xavier, Dumont, Jacques-Emile, Detours, Vincent, Miot, Françoise, Corvilain, Bernard
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Language:English
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Summary:We studied the mechanism that may explain the relative resistance of thyrocytes to H2O2 compared to other cell types. Ability to degrade H2O2, glutathione peroxidase (GPx) activity, heme oxygenase-1 (HO-1) expression, cell survival and capacity to repair DNA damage after H2O2 exposure or irradiation were measured in human thyrocytes in primary culture and compared to the values obtained in human T-cells and different cell lines. Compared to other cell types, thyrocytes presented a low mortality rate after H2O2 exposure, rapidly degraded extracellular H2O2 and presented a high basal seleno-dependent GPx activity. Only in thyrocytes, H2O2 up-regulated GPx activity and expression of HO-1 mRNA. These effects were not reproduced by irradiation. DNA damage caused by H2O2 was more slowly repaired than that caused by irradiation and not repaired at all in T-cells. Our study demonstrates that the thyrocyte has specific protective mechanisms against H2O2 and its mutagenic effects. •Resistance of the tested cell types against irradiation was relatively equal.•Resistance against H2O2 was largely dependent on the cell type, T-cells being the more fragile.•Thyrocyte is well protected against H2O2 and oxidative stress by several defense mechanisms.•In thyrocyte exposure to H2O2 leads to upregulation of antioxidant genes.•Disability of these protective mechanisms could be responsible for the appearance of mutations leading to thyroid cancer.
ISSN:0303-7207
1872-8057
DOI:10.1016/j.mce.2018.11.010