Effects of zinc oxide nanoparticles on human coronary artery endothelial cells

Kai Jen Chuang; Kang Yun Lee; Chih Hong Pan; Ching Huang Lai; Lian Yu Lin; Shu Chuan Ho; Kin Fai Ho; Hsiao Chi Chuang

doi:10.1016/j.fct.2016.05.008

Effects of zinc oxide nanoparticles on human coronary artery endothelial cells

Kai Jen Chuang, Kang Yun Lee, Chih Hong Pan, Ching Huang Lai, Lian Yu Lin, Shu Chuan Ho, Kin Fai Ho, Hsiao Chi Chuang^*

^*Corresponding author for this work

Research output: Contribution to journal › Journal Article › peer-review

30 Scopus citations

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.

Original language	English
Pages (from-to)	138-144
Number of pages	7
Journal	Food and Chemical Toxicology
Volume	93
DOIs	https://doi.org/10.1016/j.fct.2016.05.008
State	Published - 01 07 2016
Externally published	Yes

Bibliographical note

Publisher Copyright:
© 2016 Elsevier Ltd.

Keywords

AGTR1
Inflammation
Nanoparticles
Nitric oxide
Oxidative stress

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.fct.2016.05.008

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title = "Effects of zinc oxide nanoparticles on human coronary artery endothelial cells",

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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author = "Chuang, {Kai Jen} and Lee, {Kang Yun} and Pan, {Chih Hong} and Lai, {Ching Huang} and Lin, {Lian Yu} and Ho, {Shu Chuan} and Ho, {Kin Fai} and Chuang, {Hsiao Chi}",

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doi = "10.1016/j.fct.2016.05.008",

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AU - Chuang, Kai Jen

AU - Lee, Kang Yun

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AU - Lai, Ching Huang

AU - Lin, Lian Yu

AU - Ho, Shu Chuan

AU - Ho, Kin Fai

AU - Chuang, Hsiao Chi

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N2 - 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.

AB - 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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KW - Inflammation

KW - Nanoparticles

KW - Nitric oxide

KW - Oxidative stress

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ER -

Effects of zinc oxide nanoparticles on human coronary artery endothelial cells

Abstract

Bibliographical note

Keywords

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