The Fate of Human Lung Epithelial Cells – Death or Survival Induced by Sodium Arsenite

Arsenic as a toxic metalloid has been found to have potential carcinogenic effects of humans. However, pulmonary toxicity has not been fully elucidated. The purpose of this experiment is to test and observe the degree of toxicity of various concentrations of sodium arsenite (NaAsO2) on human lung epithelial cells (BEAS-2B cell line). In this experiment, BEAS-2B cells were plated and grown according to experimental requirements and treated with different concentrations of NaAsO2 for various exposure durations to study the biological responses of the human lung cells. MTT assay and ROS (reactive oxygen species) production were used to observe and visualize the effects of cytotoxicity on cell viability of BEAS-2B cells. Necrotic cell death was measured by lactic dehydrogenase (LDH) level. Western Blotting was used to detect LC3B-I and LC3B-II (autophagy related protein), cleaved PARP (apoptosis related protein), and surviving (apoptosis inhibitor related protein) to understand the biological responses of BEAS-2B cells after NaAsO2 exposure. This study supports that acute, in vitro exposure to NaAsO2 on BEAS-2B cells induced concentration-dependent decrease in cell viability and increase in ROS generation in BEAS-2B. For necrosis, it occurred at high concentrations of arsenite indicating the resistance of BEAS-2B to arsenite toxicity. It also supports that NaAsO2 exposure induces both autophagy and apoptosis, but autophagy occurred at much lower concentrations than apoptosis did in the arsenite-exposed BEAS-2B. *Corresponding authors: He Wang, School of Health Sciences, University of Newcastle, Callaghan, NSW2308, Australia, Tel: (02) 49217735; Email: [email protected] Received Date: April 11, 2017 Accepted Date: November 30, 2017 Published Date: December 3, 2017 Citation: Wang, H., et al. The Fate of Human Lung Epithelial Cells – Death or Survival Induced by Sodium Arsenite. (2017) J Med Chem Toxicol 2(2): 95-99. J Med Chem Toxicol | volume 2: issue 2 www.ommegaonline.org