ArticleOrthopaedic surgery2016
N-acetylcysteine Attenuates Cobalt Nanoparticle-Induced Cytotoxic Effects through Inhibition of Cell Death, Reactive Oxygen Species-related Signaling and Cytokines Expression.
Article in Orthopaedic surgery, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Navigating Transition Metal-Dependent Cell Death: Mechanisms, Crosstalk, and Future Directions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- The association of cobalturia with cobaltism symptoms a prospective blinded study of 229 post-arthroplasty patients.PloS one · 2023Article
- Different Strategies to Attenuate the Toxic Effects of Zinc Oxide Nanoparticles on Spermatogonia Cells.Nanomaterials (Basel, Switzerland) · 2022Article
- Intercellular transfer of mitochondria via tunneling nanotubes protects against cobalt nanoparticle-induced neurotoxicity and mitochondrial damage.Nanotoxicology · 2021Article
- An Overview of the Beneficial Role of Antioxidants in the Treatment of Nanoparticle-Induced Toxicities.Oxidative medicine and cellular longevity · 2021Review
- Alpha lipoic acid antagonizes cytotoxicity of cobalt nanoparticles by inhibiting ferroptosis-like cell death.Journal of nanobiotechnology · 2020Article
- The paradoxical role of tumor-infiltrating immune cells in lung cancer.Intractable & rare diseases research · 2017Review
- Melatonin counteracts cobalt nanoparticle‑induced cytotoxicity and genotoxicity by deactivating reactive oxygen species‑dependent mechanisms in the NRK cell line.Molecular medicine reports · 2017Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 (TCMK-1 cells).
methodsAfter being pretreated with NAC, TCMK-1 cells were treated with 300-700 μmol/L CoNPs, then, CCK-8 assay was used to verify the survival of TCMK-1 cells. Annexin V/PI staining was performed to investigate the apoptosis of TCMK-1 cells after NAC and different concentrations of CoNP treatments. In addition, western blot was performed to identify the cytokine (p-ERK, p-p38, and p-JNK) expression of the ROS-related MAPK signaling pathway.
resultsApoptosis rate of TCMK-1 cells was increased obviously after different concentrations of CoNP treatment. However, TCMK-1 cells, pretreated with NAC, exhibited a significantly decreased apoptosis rate. In addition, p-ERK, p-p38, and p-JNK expressions were increased with CoNP treatment, which indicated that CoNPs could activate the MAPK pathway. Interestingly, this entire stimulated phenomenon by CoNPs was reversed with NAC treatment.
conclusionsThese findings indicated that NAC could reverse CoNP-induced cytotoxicity by inhibiting ROS-induced cell death and cytokine expression. To our knowledge, this is the first report that describes how CoNP-induced cytotoxicity in TCMK-1 cells could be attenuated by anti-oxidative agents (NAC), which may function through inhibition of cell death and ROS.
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