Cell Viability and Immune Response to Low Concentrations of Nickel and Cadmium: An In Vitro Model

Ah-Ra, Kim; Park, sang-jin; Sung, Joo Hyun

doi:10.3390/ijerph17249218

Cited by 8 publications

(6 citation statements)

References 32 publications

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“…The data showed Ni had certain cytotoxicity at these concentrations and hindered cell proliferation; moreover, its toxicity increased with increasing concentrations. Kim A. et al (2020) explained that Ni generally enters cells through transferrin or divalent metal transporter 1 (DMT1) and exhibits cytotoxicity by inhibiting DNA repair processes or by inducing oxidative stress through the depletion of intracellular antioxidants such as glutathione [ 31 ], but the specifics need to be verified.…”

Section: Resultsmentioning

confidence: 99%

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

et al. 2022

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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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Section: Resultsmentioning

confidence: 99%

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

et al. 2022

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“…There are contradictory results regarding the immunomodulation capacity of nickel, yet solid evidence indicates that nickel potentially suppresses the host immune response [ 221 ]. The exposure of immune cells to a low concentration of nickel can influence the normal activity of the immune system [ 249 ]. Splenic NK cells were demonstrated to express IFN- γ as a direct or indirect response to nickel detection in the cell culture system.…”

Section: H Pylori and Mineralsmentioning

confidence: 99%

The Effects of Vitamins and Micronutrients on Helicobacter pylori Pathogenicity, Survival, and Eradication: A Crosstalk between Micronutrients and Immune System

Nabavi-Rad

Azizi

Jamshidizadeh

et al. 2022

Journal of Immunology Research

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Helicobacter pylori as a class I carcinogen is correlated with a variety of severe gastroduodenal diseases; therefore, H. pylori eradication has become a priority to prevent gastric carcinogenesis. However, due to the emergence and spread of multidrug and single drug resistance mechanisms in H. pylori, as well as serious side effects of currently used antibiotic interventions, achieving successful H. pylori eradication has become exceedingly difficult. Recent studies expressed the intention of seeking novel strategies to improve H. pylori management and reduce the risk of H. pylori-associated intestinal and extragastrointestinal disorders. For which, vitamin supplementation has been demonstrated in many studies to have a tight interaction with H. pylori infection, either directly through the regulation of the host inflammatory pathways or indirectly by promoting the host immune response. On the other hand, H. pylori infection is reported to result in micronutrient malabsorption or deficiency. Furthermore, serum levels of particular micronutrients, especially vitamin D, are inversely correlated to the risk of H. pylori infection and eradication failure. Accordingly, vitamin supplementation might increase the efficiency of H. pylori eradication and reduce the risk of drug-related adverse effects. Therefore, this review aims at highlighting the regulatory role of micronutrients in H. pylori-induced host immune response and their potential capacity, as intrinsic antioxidants, for reducing oxidative stress and inflammation. We also discuss the uncovered mechanisms underlying the molecular and serological interactions between micronutrients and H. pylori infection to present a perspective for innovative in vitro investigations, as well as novel clinical implications.

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“…Before exposure to contaminants, cells were starved for 24 h with culture medium FBS free. A549 cells were stimulated with a range of concentrations (0, 1 nM, 10 nM, 100 nM, 1 microM and 10 microM) as previously described in in vitro models of epithelial cells [24,25]. Furthermore, the cells were stimulated with single CdCl2 (100 nM) or CdCl2 (100 nM)/BDEs (47 or 209) (100 nM) mixtures.…”

Section: A549 Cell Cultures and Exposurementioning

confidence: 99%

Cadmium and Cadmium/BDE (47 or 209) Exposure Affect Mitochondrial Function, DNA Damage/Repair Mechanisms and Barrier Integrity in Airway Epithelial Cells

et al. 2022

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Heavy metals and Brominated diphenyl ether flame-retardants (BDEs) often coexist in the environment and are capable of inducing injury, cytotoxicity or genotoxicity in human epithelial cells of the lung. We studied the effects of single Cadmium chloride (CdCl2) or CdCl2/BDE (47 or 209) mixtures in airway epithelial cells, using A549 cell line cultured at submerged conditions and air–liquid interface (ALI) (an in vitro model described as physiologically relevant in vivo-like). We evaluated cell viability, oxidative stress, apoptosis, DNA damage/repair (Comet assay, γH2AX phosphorylation ser139), mitochondrial redox balance (NOX-4, Nrf2 and TFAM) and cell barrier integrity (TEER, ZO-1, Claudin-1, E-cadherin-1) in A549 cells exposed to CdCl2 (1 nM to 10 µM), or to CdCl2 (100 nM)/BDEs (47 or 209) (100 nM). CdCl2 (10 μM) reduced cell viability and increased apoptosis. CdCl2 (100 nM) significantly affected DNA-damage/repair (Olive Tail length production), γH2AX phosphorylation and oxidative stress (ROS/JC-1 production) in submerged cell cultures. CdCl2 (100 nM) decreased viability, TEER, ZO-1, Claudin-1 and E-cadherin-1 mRNA expression, and Nrf2 and TFAM while increased NOX-4, in ALI culture of cells. In both cell culture approaches, the cells stimulated with Cadmium/BDEs mixtures did not show a significant increase in the effects observed in the cells treated with CdCl2 alone. CdCl2 inhalation might exert cytotoxicity and genotoxicity, playing a pivotal role in the uncontrolled oxidative stress, damaging DNA and gene expression in airway epithelial cells. No additional or synergistic adverse effects of CdCl2/BDEs mixture were observed in comparison to CdCl2 alone in lung epithelium.

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Cell Viability and Immune Response to Low Concentrations of Nickel and Cadmium: An In Vitro Model

Cited by 8 publications

References 32 publications

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

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

The Effects of Vitamins and Micronutrients on Helicobacter pylori Pathogenicity, Survival, and Eradication: A Crosstalk between Micronutrients and Immune System

Cadmium and Cadmium/BDE (47 or 209) Exposure Affect Mitochondrial Function, DNA Damage/Repair Mechanisms and Barrier Integrity in Airway Epithelial Cells

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