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Effects of Nickel at Environmentally Relevant Concentrations on Human Corneal Epithelial Cells: Oxidative Damage and Cellular Apoptosis

Nickel (Ni) is ubiquitous in the environment and evidence has suggested that Ni can cause ocular surface inflammation, especially in fine particulate matter and personal products. Continuous daily exposure to Ni-containing dust may adversely impact the human cornea, whereas the underlying mechanism...

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Autores principales: Zhang, Zhen-Ning, Liu, Hai, Liu, Mi-Mi, Yang, Dan-Lei, Bi, Jue, Chen, Qian-Qian, Chen, Wei, Xiang, Ping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9496594/
https://www.ncbi.nlm.nih.gov/pubmed/36139122
http://dx.doi.org/10.3390/biom12091283
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author Zhang, Zhen-Ning
Liu, Hai
Liu, Mi-Mi
Yang, Dan-Lei
Bi, Jue
Chen, Qian-Qian
Chen, Wei
Xiang, Ping
author_facet Zhang, Zhen-Ning
Liu, Hai
Liu, Mi-Mi
Yang, Dan-Lei
Bi, Jue
Chen, Qian-Qian
Chen, Wei
Xiang, Ping
author_sort Zhang, Zhen-Ning
collection PubMed
description Nickel (Ni) is ubiquitous in the environment and evidence has suggested that Ni can cause ocular surface inflammation, especially in fine particulate matter and personal products. Continuous daily exposure to Ni-containing dust may adversely impact the human cornea, whereas the underlying mechanism of this phenomenon remains not fully understood. Here, human corneal epithelial cells (HCEC) were employed to analyze the toxicity of Ni via detections of cell morphology, cell viability, reactive oxygen species production, cell apoptosis rate, and apoptotic gene expression levels after exposure for 24 h to uncover the damage of Ni to the cornea. A concentration-dependent inhibition of HCECs’ viability and growth was observed. In particular, Ni at 100 μM significantly decreased cell viability to 76%, and many cells displayed an abnormal shape and even induced oxidative damage of HCEC by increasing ROS to 1.2 times, and further led to higher apoptosis (24%), evidenced by up-regulation of apoptotic genes Caspase-8, Caspase-9, NF-κB, IL-1β, and Caspase-3, posing a risk of dry eye. Our study suggested that Ni induces apoptosis of HCEC through oxidative damage. Therefore, Ni pollution should be comprehensively considered in health risks or toxic effects on the ocular surface.
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spelling pubmed-94965942022-09-23 Effects of Nickel at Environmentally Relevant Concentrations on Human Corneal Epithelial Cells: Oxidative Damage and Cellular Apoptosis Zhang, Zhen-Ning Liu, Hai Liu, Mi-Mi Yang, Dan-Lei Bi, Jue Chen, Qian-Qian Chen, Wei Xiang, Ping Biomolecules Article Nickel (Ni) is ubiquitous in the environment and evidence has suggested that Ni can cause ocular surface inflammation, especially in fine particulate matter and personal products. Continuous daily exposure to Ni-containing dust may adversely impact the human cornea, whereas the underlying mechanism of this phenomenon remains not fully understood. Here, human corneal epithelial cells (HCEC) were employed to analyze the toxicity of Ni via detections of cell morphology, cell viability, reactive oxygen species production, cell apoptosis rate, and apoptotic gene expression levels after exposure for 24 h to uncover the damage of Ni to the cornea. A concentration-dependent inhibition of HCECs’ viability and growth was observed. In particular, Ni at 100 μM significantly decreased cell viability to 76%, and many cells displayed an abnormal shape and even induced oxidative damage of HCEC by increasing ROS to 1.2 times, and further led to higher apoptosis (24%), evidenced by up-regulation of apoptotic genes Caspase-8, Caspase-9, NF-κB, IL-1β, and Caspase-3, posing a risk of dry eye. Our study suggested that Ni induces apoptosis of HCEC through oxidative damage. Therefore, Ni pollution should be comprehensively considered in health risks or toxic effects on the ocular surface. MDPI 2022-09-12 /pmc/articles/PMC9496594/ /pubmed/36139122 http://dx.doi.org/10.3390/biom12091283 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Zhang, Zhen-Ning
Liu, Hai
Liu, Mi-Mi
Yang, Dan-Lei
Bi, Jue
Chen, Qian-Qian
Chen, Wei
Xiang, Ping
Effects of Nickel at Environmentally Relevant Concentrations on Human Corneal Epithelial Cells: Oxidative Damage and Cellular Apoptosis
title Effects of Nickel at Environmentally Relevant Concentrations on Human Corneal Epithelial Cells: Oxidative Damage and Cellular Apoptosis
title_full Effects of Nickel at Environmentally Relevant Concentrations on Human Corneal Epithelial Cells: Oxidative Damage and Cellular Apoptosis
title_fullStr Effects of Nickel at Environmentally Relevant Concentrations on Human Corneal Epithelial Cells: Oxidative Damage and Cellular Apoptosis
title_full_unstemmed Effects of Nickel at Environmentally Relevant Concentrations on Human Corneal Epithelial Cells: Oxidative Damage and Cellular Apoptosis
title_short Effects of Nickel at Environmentally Relevant Concentrations on Human Corneal Epithelial Cells: Oxidative Damage and Cellular Apoptosis
title_sort effects of nickel at environmentally relevant concentrations on human corneal epithelial cells: oxidative damage and cellular apoptosis
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9496594/
https://www.ncbi.nlm.nih.gov/pubmed/36139122
http://dx.doi.org/10.3390/biom12091283
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