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The involvement of oxidative stress was clarified more easily than apoptosis, which involved control experiments to confirm specific metabolites that could be used as standard markers for apoptosis based on this we tentatively propose methylnicotinamide as a generic metabolic marker for apoptosis. CuO NPs induced regulation of metabolites involved in oxidative stress, hypertonic stress, and apoptosis. Toxicity hypotheses were then generated based on the affected pathways, and critically tested using more conventional biochemical and cellular assays. We have used untargeted metabolome analysis to determine differentially expressed metabolites in human lung epithelial cells (A549) exposed to copper oxide nanoparticles (CuO NPs).
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These techniques thus provide the opportunity to identify specific toxicity pathways and to generate hypotheses on how to reduce or abolish toxicity. The use of omics technologies, including metabolomics, can play a vital role in this process by providing relatively fast, comprehensive, and cost-effective assessment of cellular responses. It is therefore important to develop methods which can provide high-throughput screening of biological responses.
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With this increasing, and ever changing, catalogue of NPs it is becoming more difficult to adequately assess the toxic potential of new materials in a timely fashion. The rapidly increasing number of engineered nanoparticles (NPs), and products containing NPs, raises concerns for human exposure and safety.