N‐acetylcysteine Attenuates Cobalt Nanoparticle‐Induced Cytotoxic Effects through Inhibition of Cell Death Reactive Oxygen Species‐related Signaling and Cytokines Expression

摘要

ObjectiveComplex cobalt‐chromium alloys, bearing surfaces of the second‐generation metal‐on‐metal (MoM) hip prostheses, are subject to wear and generate cobalt nanoparticles (CoNPs). CoNPs could reduce cellular viability, activate the mitogen‐activated protein kinase (MAPK) pathway and increase cell apoptosis via reactive oxygen species (ROS). However, the detailed mechanisms of ROS functioning on CoNP‐mediated signaling molecules and cytotoxicity has not yet been fully demonstrated. The present study investigated the functional role of N‐acetylcysteine (NAC) in reversing the activation of ROS signaling pathways triggered by CoNPs in normal mice kidney cells ( style="fixed-case">TCMK‐1 cells).