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In Vitro Toxicity and Inflammation Response Induced by Copper Nanoparticles in Rat Alveolar Macrophages
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Nanotechnology is a thriving industry and has the potential to benefit society in numerous ways. However, not all environmental and human health concerns of nanomaterials have been addressed. Thus, the purpose of this research was to investigate the toxicity and inflammation potential (using cytokines TNF-a and IL-6 as indicators) of various sized copper nanoparticles (40, 60, and 80 nm) in rat alveolar macrophages. Toxicity measurements were accomplished by means of in vitro techniques and toxicity mechanisms were studied by measuring reactive oxygen species (ROS) production. In addition, cyt...
Nanotechnology is a thriving industry and has the potential to benefit society in numerous ways. However, not all environmental and human health concerns of nanomaterials have been addressed. Thus, the purpose of this research was to investigate the toxicity and inflammation potential (using cytokines TNF-a and IL-6 as indicators) of various sized copper nanoparticles (40, 60, and 80 nm) in rat alveolar macrophages. Toxicity measurements were accomplished by means of in vitro techniques and toxicity mechanisms were studied by measuring reactive oxygen species (ROS) production. In addition, cytokine measurements used enzyme-linked immunosorbent assay (ELISA) methods. Results show copper nanoparticles as gravely toxic to rat alveolar macrophages; concentrations of only 10 µg/mL produced cell viability of less than 20 percent and membrane leakage increases of approximately 75 percent. However, the copper nanoparticles did not produce a significant degree of ROS (only 2.5 fold increases). Also, the toxicity showed a dose-dependent relationship, but not a significant size dependency between the various sized copper nanoparticles. Finally, minimal induction of cytokines occurred; however, stimulation of rat alveolar macrophages by lipopolysaccharide (LPS) and subsequent exposure to copper nanoparticles produced elevated levels of both cytokines.
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