Cerium oxide nanoparticles induce cytotoxicity in human hepatoma SMMC-7721 cells via oxidative stress and the activation of MAPK signaling pathways

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• 作者：Guilin Cheng^a ; ¹ ; Wei Guo^b ; ¹ ; Lu Han^a ; Erlei Chen^c ; Lingfang Kong^c ; Lili Wang^d ; Wenchao Ai^a ; Naining Song^a ; Haishan Li^a ; ^{lihs@aqsiqch.ac.cn} ; Huiming Chen^a ; ^{huimingchenchm@126.com}
• 关键词：CeO2 nanoparticles ; Cytotoxicity ; Oxidative stress ; MAPKs
• 刊名：Toxicology in Vitro
• 出版年：2013
• 出版时间：April, 2013
• 年：2013
• 卷：27
• 期：3
• 页码：1082-1088
• 全文大小：1332 K

文摘

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.