Selenium (sodium selenite) causes cytotoxicity and apoptotic mediated cell death in PLHC-1 fish cell line through DNA and mitochondrial membrane potential damage

Abstract

Elevated concentration of selenium poses a toxic threat to organisms inhabiting aquatic ecosystems influenced by excessive inputs from anthropogenic sources. Selenium is also an essential micronutrient in living things, particularly in fish, and provides antioxidant properties to tissues. Whole fish and hepatocytes in primary culture show selenite toxicity above threshold levels. The present study was designed to investigate the process by which selenite exposure causes cellular toxicity and apoptotic and necrotic cell death in fish hepatoma cell line PLHC-1. PLHC-1 cells were exposed to various selenite concentrations (1, 10, 50 and100μM) for 10, 20 and 40h intervals. The 24h inhibitory concentration 50 (IC50) of selenite in PLHC-1 cell line was found to be 237μM. Flow cytometery data showed that selenite exposed cells promote apoptotic and necrotic mediated cell death when selenite concentrations were ≥10μM compared to control. Selenite exposure was associated with a significant increase of caspase-3 activities suggesting the induction of apoptosis. Selenite exposure at high levels (≥10μM) and longer exposure times (≥20h) induces mitochondrial membrane potential damage (ΔΨm), DNA damage and elevated production of ROS which could be associated with cell death.