ICEECE2012 Poster Presentations Thyroid (non-cancer) (188 abstracts)
Hospital of Qingdao University Medical College, Qingdao, China.
Objective: To investigate the influence of vitamin E (VE) and selenium (Se) on apoptosis of human thyrocyte induced by H2O2.
Methods: The human thyroid epithelium cells (TEC) from normal para-adenoma tissues of patients with thyroid adenoma resection were cultured. In prevention groups, vitamin E (50 μmol/l), selenium (107 mol/l) or serum-free medium was respectively added into thyrocytes of monolayer culture before H2O2 (200800 μmol/l) with different concentrations added, while in treatment groups H2O2 (200800 μmol/l) was added firstly. The survial rates of thyrocyte were detected by MTT stain, and the apoptosis rates by flow cytometry.
Results: When the thyroid epithelium cells exposed to H2O2 (200800 μmol/l) only for 24 h, the cell survial rates declined and cell apoptosis rates increased (P<0.01) in both prevention and treatment groups, with a relation of dose-effect response. Adding VE (50 μmol/l) and Se (107 mol/l) into cell culture for prevention and treatment, the cell survial rates increased and the thyrocyte apoptosis reduced compared to the corresponding simple H2O2 intervention groups. Above differences were particularly significant (P<0.05) when thyrocytes exposed to 400 and 800 μmol/l H2O2. The decrease of cell apoptosis rates in group with selenium pre-intervention was more significant than that in group with VE pre-intervention (P=0.018) when cells exposed to 400 μmol/l H2O2. While the decline in group with VE was more obvious than that in group with selenium (P<0.05) when cells exposed to 200 and 400 μmol/l H2O2 in treatment groups.
Conclusion: VE and selenium could have protective effect on apoptosis of human thyrocytes induced by H2O2 in human thyrocytes.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.