Effects of zinc oxide nanoparticles on human coronary artery endothelial cells |
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| Affiliation: | 1. School of Public Health, College of Public Health and Nutrition, Taipei Medical University, Taipei, Taiwan;2. Department of Public Health, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan;3. Division of Pulmonary Medicine, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan;4. Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan;5. Institute of Labor, Occupational Safety and Health, Ministry of Labor, New Taipei City, Taiwan;6. School of Public Health, National Defense Medical Center, Taipei, Taiwan;7. Department of Internal Medicine, Division of Cardiology, National Taiwan University Hospital, Taipei, Taiwan;8. School of Respiratory Therapy, College of Medicine, Taipei Medical University, Taipei, Taiwan;9. Jockey Club School of Public Health and Primary Care, The Chinese University of Hong Kong, Hong Kong;10. Shenzhen Municipal Key Laboratory for Health Risk Analysis, Shenzhen Research Institute, The Chinese University of Hong Kong, Shenzhen, China;1. State Key Laboratory of Materials-Oriented Chemical Engineering, Nanjing Tech University, Nanjing 210009, China;2. Taiyuan Qiaoyou Chemical Industrial Co. Ltd., Taiyuan 030025, China;1. International Institute for Translational Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, PR China;2. Key Laboratory of Environment-Friendly Chemistry and Application of Ministry of Education, Lab of Biochemistry, College of Chemistry, Xiangtan University, Xiangtan 411105, PR China;3. Institute of Bast Fiber Crops, Chinese Academy of Agricultural Sciences, Changsha 410205, PR China;1. Healthy High Density Cities Lab, HKUrbanLab, The University of Hong Kong, Hong Kong Special Administrative Region, China;2. School of Respiratory Therapy, College of Medicine, Taipei Medical University, Taipei, Taiwan;3. School of Public and Community Health Sciences, University of Montana, Missoula, MT, USA;4. Key Laboratory of Aerosol, SKLLQG, Institute of Earth Environment, Chinese Academy of Sciences, Xi’an, China;5. Graduate Institute of Environmental Engineering, National Taiwan University, Taipei, Taiwan;6. The Jockey Club School of Public Health and Primary Care, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China;7. Shenzhen Institute of Research and Innovation, The University of Hong Kong, Shenzhen, China;1. Department of Medical Microbiology and Parasitology, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, 43400, Serdang, Selangor, Malaysia;2. Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, 43400, Serdang, Selangor, Malaysia;3. Department of Biological Sciences, National University of Singapore, 117543, Singapore;1. School of Environment, Guangzhou Key Laboratory of Environmental Exposure and Health, and Guangdong Key Laboratory of Environmental Pollution and Health, Jinan University, Guangzhou, 510632, China;2. Joint Genome Institute, Lawrence Berkeley National Laboratory, Walnut Creek, 94598, CA, USA |
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| Abstract: | Inhalation of zinc oxide (ZnO) metal fumes is known to cause metal fume fever and to have systemic effects; however, the effects of ZnO nanoparticles (ZnONPs) on the cardiovascular system remain unclear. The objective of this study was to investigate the cardiovascular toxicity of ZnONPs. Human coronary artery endothelial cells (HCAECs) were exposed to ZnONPs of different sizes to investigate the cell viability, 8-hydroxy-2’-deoxyguanosine (8-OHdG), interleukin (IL)-6, nitric oxide (NO), and regulation of cardiovascular disease-related genes. Exposure of HCAECs to ZnONPs resulted in decreased cell viability and increased levels of 8-OHdG, IL-6, and NO. Downregulation of cardiovascular-associated genes was observed in response to ZnONPs in HCAECs determined by qPCR, suggesting that the calcium signaling pathway, neuroactive ligand-receptor interaction, hypertrophic cardiomyopathy, dilated cardiomyopathy, and renin-angiotensin system are important affected pathways in response to ZnONPs. Furthermore, we observed a significant response of AGTR1 to ZnONP exposure in HCAECs. Our results suggest that ZnONPs cause toxicity to HCAECs, which could be associated with cardiovascular dysfunction. |
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| Keywords: | AGTR1 Inflammation Nanoparticles Nitric oxide Oxidative stress |
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