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

At present, no effective treatment exists for the clinical toxicity of cobalt nanoparticles (CoNPs, 30 nm) 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, > 97%) in antagonizing the toxicity of CoNPs and its mechanism through the Keap1-Nrf2-ARE signaling pathway. To examine BNS detoxification, we exposed HUVEC cells to CoNPs and BNS for 24 h, before measuring cell activity, reactive oxygen species (ROS), the GSH level, inflammatory factors, and KNA signaling pathway-related transcript and protein expression. CoNPs stimulate intracellular inflammation and ROS production to bring about significant downregulation of cellular activity and the GSH level. Conversely, BNS reduces ROS generation and suppresses inflammatory factors within cells to reduce CoNPs-mediated cytotoxicity, possibly via the KNA signaling pathway. Based 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. Trial registration: no human participant.

Synthesis of a magnetic C@Co material via the design of a MOF precursor for efficient and selective adsorption of water pollutants

3D metal-organic frameworks (MOFs) can be appropriate templates for the fabrication of nanomaterials due to they have active sites exposed on the channel or surface, which thus provide them with improved catalytic performance. In this study, a 3D cobalt-based MOF [Co(H2bpta)]n (Co-MOF), where H4bpta denotes 2,2′,4,4′-biphenyltetracarboxylic acid, has been constructed with the use of a ligand with a high carbon content. On this basis, a 2D magnetic carbon-coated cobalt nanoparticle composite (C@Co) was prepared by using the title MOF. Magnetic C@Co can readily absorb dye from the solution and can thus act as an inexpensive and fast-acting adsorbent. Moreover, we have explored the adsorption isotherms, kinetics and thermodynamics of the anion dyes in detail. The adsorption capacity of the C@Co for investigated methyl orange (MO) and congo red (CR) dyes were 773.48 and 495.66 mg g− 1, respectively. It is noteworthy that MO adsorption is higher in existing materials. Thermodynamic studies suggest that the adsorption processes are spontaneous and exothermic. This study opens a new insight into the synthesis and application of carbon-based materials that enable the selective removal of organic dyes.

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

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.