Cerium oxide nanoparticles induce cytotoxicity in human hepatoma SMMC-7721 cells via oxidative stress and the activation of MAPK signaling pathways
Autor: | Lingfang Kong, Lili Wang, Guilin Cheng, Huiming Chen, Naining Song, Lu Han, Haishan Li, Wenchao Ai, Wei Guo, Erlei Chen |
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Rok vydání: | 2013 |
Předmět: |
Carcinoma
Hepatocellular Cell Survival MAP Kinase Signaling System p38 mitogen-activated protein kinases Apoptosis Toxicology medicine.disease_cause Antioxidants Superoxide dismutase chemistry.chemical_compound Cell Line Tumor Malondialdehyde medicine Humans chemistry.chemical_classification Glutathione Peroxidase Reactive oxygen species biology Superoxide Dismutase Glutathione peroxidase Cerium General Medicine Catalase Acetylcysteine Cell biology Oxidative Stress chemistry Immunology biology.protein Nanoparticles Mitogen-Activated Protein Kinases Reactive Oxygen Species Oxidative stress |
Zdroj: | Toxicology in Vitro. 27:1082-1088 |
ISSN: | 0887-2333 |
DOI: | 10.1016/j.tiv.2013.02.005 |
Popis: | Background Lanthanide cerium oxide (CeO2) nanoparticles have extensive applications in industrial fields, and concerns regarding their potential toxicity in humans and their environmental impact have increased. We investigated the underlying molecular mechanisms by which CeO2 nanoparticles induce toxicity in human hepatoma SMMC-7721 cells. Results Our results demonstrated that CeO2 nanoparticles reduced viability, caused dramatic morphological damage, and induced apoptosis in SMMC-7721 cells. CeO2 nanoparticles significantly increased the production of reactive oxygen species (ROS) and malondialdehyde (MDA), and significantly reduced the activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-px) and catalase (CAT). The phosphorylation levels of ERK1/2, JNK and p38 MAPK were significantly elevated after treatment with CeO2 nanoparticles. Pretreatment with the antioxidant N-acetyl-cysteine (NAC): reduced the induction of ROS and MDA by CeO2 nanoparticles; recovered the activity of SOD, GSH-px and CAT; reduced the phosphorylation levels of ERK1/2, JNK and p38; and attenuated CeO2 nanoparticles-induced damage and apoptosis in SMMC-7721 cells. Conclusions Our data demonstrated that CeO2 nanoparticles induced damage and apoptosis in human SMMC-7721 cells via oxidative stress and the activation of MAPK signaling pathways. |
Databáze: | OpenAIRE |
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