par Ghaddhab, Chiraz 
;Kyrilli, Aglaia ;Driessens, Natacha ;Van Den Eeckhaute, Emmanuel ;Hancisse, Olivier ;De Deken, Xavier ;Dumont, Jacques Emile ;Detours, Vincent ;Miot, Françoise ;Corvilain, Bernard
Référence Molecular and cellular endocrinology, 481, page (62-70)
Publication Publié, 2019-02-01
;Kyrilli, Aglaia ;Driessens, Natacha ;Van Den Eeckhaute, Emmanuel ;Hancisse, Olivier ;De Deken, Xavier ;Dumont, Jacques Emile ;Detours, Vincent ;Miot, Françoise ;Corvilain, Bernard Référence Molecular and cellular endocrinology, 481, page (62-70)
Publication Publié, 2019-02-01
Article révisé par les pairs
| Résumé : | 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. |
