No abstract

We studied the mechanism that may explain the relative resistance of thyrocytes to H 2 O 2 compared to other cell types. Ability to degrade H 2 O 2 , glutathione peroxidase (GPx) activity, heme oxygenase-1 (HO-1) expression, cell survival and capacity to repair DNA damage after H 2 O 2 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 H 2 O 2 exposure, rapidly degraded extracellular H 2 O 2 and presented a high basal seleno-dependent GPx activity. Only in thyrocytes, H 2 O 2 upregulated GPx activity and expression of HO-1 mRNA. These effects were not reproduced by irradiation. DNA damage caused by H 2 O 2 was more slowly repaired than that caused by irradiation and not repaired at all in Tcells. Our study demonstrates that the thyrocyte has specific protective mechanisms against H 2 O 2 and its mutagenic effects.