Abstract
Copper oxide nanoparticles (CuO NPs) are widely used as catalysts or semiconductors in material fields. Recent studies have suggested that CuO NPs have adverse genotoxicity and cytotoxicity effects on various cells. However, little is known about the toxicity of CuO NPs following exposure to murine lungs. The purpose of this fundamental research was to investigate whether CuO NPs could induce epithelial cell injury, pulmonary inflammation, and eventually fibrosis in C57BL/6 mice. Our studies showed that CuO NPs aggravated pulmonary inflammation in a dose-dependent manner. CuO NPs induced apoptosis of epithelial cells as indicated by TUNEL staining, flow cytometry and western blot analysis, which was partially caused by increased reactive oxygen species (ROS). In addition, CuO NPs exposure promoted collagen accumulation and expression of the progressive fibrosis marker α-SMA in the lung tissues, indicating that CuO NP inhalation could induce pulmonary fibrosis in C57BL/6 mice. All data provide novel evidence that there is an urgent need to prevent the adverse effects of CuO NPs in the human respiratory system.
Highlights
Copper oxide nanoparticles (CuO NPs) have attracted attention and have been commonly used in industrial and commercial fields for their photovoltaic and photoconductive properties[6]
The respiratory tract is one of the main routes that CuO NPs use to get into the body[13]
Respiratory toxicity has become the focus of CuO NPs on the biological effects of the body[26]
Summary
Copper oxide nanoparticles (CuO NPs) have attracted attention and have been commonly used in industrial and commercial fields for their photovoltaic and photoconductive properties[6]. In vitro studies have proven that CuO NPs induce the cytotoxic, genotoxic, and oxidative stress response in several cultured human lung epithelial cells[9,10,11,12,13]. Yokohira et al established a method through intratracheal instillation in F344 male rats to simulate nanoparticle inhalation in human being and found that CuO NPs induced pulmonary neoplastic lesions after intratracheal instillation[15]. Data are somewhat limited regarding murine exposure to CuO NPs. the genetic relationship between humans and rats is relatively close, and mice can be conveniently genetically manipulated using gene editing tools[17]. Reactive oxygen species (ROS) levels in pulmonary epithelial cells were assessed under control and exposure conditions
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