Bioactive nano-selenium antagonizes cobalt nanoparticle- mediated oxidative stress via the Keap1-Nrf2-ARE signaling pathway

Abstract BackgroundAt present, no effective treatment exists for the clinical toxicity of cobalt nanoparticles (CoNPs) after metal-on-metal (MOM) artificial joint replacement. As such, a better understanding of the CoNPs-toxicity mechanism is necessary and urgent for the development of effective and safe detoxification drugs. Our purpose was to explore the role of bioactive nano-selenium (BNS) in antagonizing the toxicity of CoNPs and its mechanism through the Keap1-Nrf2-ARE signaling pathway. MethodsTo examine BNS detoxification, we exposed HUVEC cells to CoNPs (400μmol/l) and BNS (50μg/ml) for 24h, before measuring cell activity, reactive oxygen species (ROS), inflammatory factors, and KNA signaling pathway related transcript and protein expression. ResultsCoNPs stimulate intracellular inflammation and ROS production to bring about significant downregulation of cellular activity. Conversely, BNS reduces ROS generation and suppresses inflammatory factors within cells to reduce CoNPs-mediated cytotoxicity, possibly via the KNA signaling pathway. ConclusionsBased on our results, BNS antagonizes CoNPs toxic effects by suppressing ROS production through the KNA pathway. Our research provides new insight into the clinical treatment of CoNPs toxicity and explores the potential of BNS in detoxification therapy.