Genotoxic potential of copper oxide nanoparticles in human lung epithelial cells

Copper oxide nanoparticles (CuO NPs) are increasingly used in various applications. Recent studies suggest that oxidative stress may be the cause of the cytotoxicity of CuO NPs in mammalian cells. However, little is known about the genotoxicity of CuO NPs following exposure to human cells. This stud...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2010-05, Vol.396 (2), p.578-583
Main Authors: Ahamed, Maqusood, Siddiqui, Maqsood A., Akhtar, Mohd J., Ahmad, Iqbal, Pant, Aditya B., Alhadlaq, Hisham A.
Format: Article
Language:English
Subjects:
A549 cells
Catalase
Cell Line
Copper - toxicity
Copper oxide nanoparticles
DNA Damage
Genotoxicity
Humans
Lung - drug effects
Lung - metabolism
Nanoparticles - toxicity
Oxidative Stress
Respiratory Mucosa - drug effects
Respiratory Mucosa - metabolism
Tumor Suppressor Protein p53 - metabolism
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Summary:Copper oxide nanoparticles (CuO NPs) are increasingly used in various applications. Recent studies suggest that oxidative stress may be the cause of the cytotoxicity of CuO NPs in mammalian cells. However, little is known about the genotoxicity of CuO NPs following exposure to human cells. This study was undertaken to investigate CuO NPs induced genotoxic response through p53 pathway in human pulmonary epithelial cells (A549). In addition, cytotoxicity and oxidative stress markers were also assessed. Results showed that cell viability was reduced by CuO NPs and degree of reduction was dose dependent. CuO NPs were also found to induce oxidative stress in dose-dependent manner indicated by depletion of glutathione and induction of lipid peroxidation, catalase and superoxide dismutase. The expression of Hsp70, the first tier biomarker of cellular damage was induced by CuO NPs. Further, CuO NPs up-regulated the cell cycle checkpoint protein p53 and DNA damage repair proteins Rad51 and MSH2 expression. These results demonstrate that CuO NPs possess a genotoxic potential in A549 cells which may be mediated through oxidative stress. Our short-term exposure study of high level induction of genotoxic response of CuO NPs will need to be further investigated to determine whether long-term exposure consequences may exist for CuO NPs application.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2010.04.156