Protectıve Role Of Selenocompounds Agaınst DNA Damage An Oxıdatıve Stress Caused By Bısphenol A In Human Papıllar Thyroıd Cancer Cell Line


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Tan E., Özkemahlı K. G. , Bacanlı M., Balcı Özyurt A., Baysal E., Zeybek N. D. , ...More

13th International Symposium on Pharmaceutical Sciences (ISOPS), Ankara, Turkey, 22 - 25 June 2021, pp.213-214

  • Publication Type: Conference Paper / Summary Text
  • City: Ankara
  • Country: Turkey
  • Page Numbers: pp.213-214
  • Gazi University Affiliated: Yes

Abstract

Introduction: Bisphenol A (BPA) is a chemical compound that can bind to estrogen receptors with low affinity. BPA shows weak estrogenic activity and is classified as an “endocrine disrupting chemical” (Almeida et al., 2018). It may also disrupt thyroid homeostasis (Moriyama et al., 2002). Selenium has an essential role in thyroid homeostasis as a component of deiodinases. Additionally, it protects the thyroid gland against oxidative stress as a constituent of glutathione peroxidases (Schomburg 2011). In this study, we aimed to investigate the toxic effects of BPA and the modifying effects of selenium supplementation against BPA toxicity in human papillary thyroid cancer cell line (B-CPAP). We also evaluated the cytotoxicity, oxidant/antioxidant parameters, oxidative DNA damage and apoptosis caused by BPA. In addition, the protective roles of inorganic selenium (sodium selenite, SS) and organic selenium (selenomethionine, SM) were assessed. Materials and Methods: B-CPAP cell line was used throughout the experiments. The study groups were: Control, BPA, SM, SS, BPA+SM and BPA+SS. Cell viability was assessed by MTT assay. The oxidative stress parameters including malondialdehyde (MDA), glutathione (GSH) levels, intracellular reactive oxygen species (ROS) production and levels of apoptosis markers (caspase 3 and 8 l) were measured by using commercial kits. Oxidative DNA damage was determined by single cell gel electrophoresis (COMET) assay. Apoptotic cell count was evaluated using TUNEL assay. Results: Our results showed that BPA caused significant elevations of intracellular ROS and MDA levels and decreases in total GSH concentrations in B-CPAP cell line. Additionally, BPA also induced oxidative DNA damage and apoptosis. Conclusions: We can conclude that one of the underlying mechanisms of the toxic effects of BPA in B-CPAP cell line may be significant alterations of oxidant/antioxidant status which can lead to DNA damage. Physiological doses of selenocompounds might be partially protective against BPA toxicity in thyroid cell cancer cell lines. Acknowledgements 13th International Symposıum on Pharmaceutical Sciences, 22-25 June 2021, Ankara/Turkey 214 This study was supported by a grant of Hacettepe Scientific Research Projects Coordination Unit, Project number: TYL-2018-17076